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A 



TEXT-BOOK OF MEDICINE 



FOR STUDENTS AND PRACTITIONERS 



Dr. ADOLF STKTTMPELL, 

FOEMERLY PROFESSOR AND DIRECTOR OF THE MEDICAL POLICLINIC AT THE UNIVERSITY OF LEIPSIC. 



TRANSLATED BY PER3IISSI0N FROM TEE SECOND AND THIRD GERMAN EDITIONS BY 

HERMAN F. YIOKERY, A. B., M. D., 

PHYSICIAN TO OUT-PATIENTS, MASSACHUSETTS GENERAL HOSPITAL ; ASSISTANT IN CLINICAL MEDICINE, HARVARD 
MEDICAL SCHOOL; FELLOW OF THE MASSACHUSETTS MEDICAL SOCIETY, ETC., 

AND 

PHILIP COOMBS KNAPP, A. M., M. D., 

PHYSICIAN TO OUT-PATIENTS WITH DISEASES OF THE NERVOUS SYSTEM, BOSTON CITY HOSPITAL; 
PHYSICIAN TO THE DEPARTMENT FOR DISEASES OF THE NERVOUS 8Y8TEM, BOSTON 
DISPENSARY ; FELLOW OF THE MASSACHUSETTS MEDICAL SOCIETY, ETC. 




WITH EDITORIAL NOTES BY 

FREDERICK C. SHATTUCK, A. M., M. D., 

VISITING PHYSICIAN TO THE MASSACHUSETTS GENERAL HOSPITAL, AND TO THE HOUSE OF THE GOOD SAMARITAN; 
INSTRUCTOR IN THE THEORY AND PRACTICE OF PHYSIC, HARVARD MEDICAL SCHOOL ; MEMBER OF THE 
ASSOCIATION OF AMERICAN PHYSICIANS ; FELLOW OF THE MASSACHUSETTS MEDICAL SOCIETY, ETC. 



WITH ONE HUNDRED AND ELEVEN ILLUSTRATIONS. 



y< "V OF CO 7?yC^ 

DEC IB 1886 , 

X/OP WASHING 

NEW YORK: 
D. APPLETON AND COMPANY, 

1, 3, and 5 BOND STREET, 
1887. 



COPYKIGHT, 1886, 

By D. APPLETON AND COMPANY. 



Ml rights reserved. 



LC Control Number 




tmp96 029105 



PEEFACE TO THE FIEST EDITION. 



1st the work which is now offered to the public I have made an attempt 
to give an account of our present knowledge in the field of the special 
pathology and treatment of internal diseases. This account, although brief, 
I have endeavored to make as complete as possible in regard to all impor- 
tant and certainly established facts. While everything hypothetical has 
been wholly omitted or only briefly referred to, I have tried, on the other 
hand, not only to enumerate the facts of clinical experience with sufficient 
accuracy, but also and especially to make the reader comprehend the develop- 
ment and the internal connection of the different morbid phenomena by 
constantly referring to the data of general pathological and anatomical 
research. In regard to treatment, the limits of our knowledge will often be 
apparent, but I believe that I have paid a sufficient regard to the needs of 
practice. In order to avoid repetitions, only a small number of complete 
prescriptions have been inserted in the text, but an abundant and well- 
arranged formulary has been added as an appendix at the end of the work.* 

Although in the composition of this text-book I have of course made very 
great use of the later literature of medicine, still the experienced reader 
will recognize in not a few places the results of the author's own experience 
and observation. These results are drawn from more than six years' active 
work in the medical clinique here, to the abundant material of which I have 
been fortunate enough to have access as assistant first to 0. Wunderlich 
and then to E. Wagner. 

Adolf Stkumpell. 

Leipsic, 1 March, 1883. 



[* Owing to the differences between our Pharmacopoeia and practice and those of Germany, it has 
been thought best to omit this appendix. — Trans.] 



PKEFACE TO THE SECOND EDITION. 



The accompanying second edition of my text-book has undergone many 
additions and improvements. In the first volume the sections on the aetiology 
of infectious diseases, especially typhoid fever, cholera, and diphtheria, have 
been materially enlarged on the basis of the later work of Koch and his 
pupils. In other chapters, too, many places will be noticed where the 
author has endeavored to adapt the work to the present standpoint of our 
latest knowledge. Many of the sections on the treatment of diseases have- 
had fuller statements added to them, so that they may be better adapted to 
the demands of the medical profession. In the second * volume of the text- 
book (the volume on nervous diseases), beside many smaller changes, several 
new sections in regard to the pathology of the nervous system have been 
added, especially the descriptions of saltatory reflex spasm, alcoholic neuritis, 
progressive ophthalmoplegia, and catalepsy. 

To friendly colleagues, who have called my attention to the errors and 
omissions in the first edition, I offer in this place my heartiest thanks. 

Adolf Strumpell. 

Leipsic, May, 1885. 

[* In the third edition of the volume on nervous diseases, various minor changes have been made, 
and a chapter has been added on general paralysis of the insane. — Trans.] 



TEANSLATOES' PEEFACE. 



This translation was made from the second German edition. After the 
work had been sent to the press in May, we learned that a third edition of 
the yolume on nervous diseases had appeared in Germany. We therefore 
recalled our manuscript, and incorporated into it all the changes and addi- 
tions that had been made in that edition. 

"We have tried to make the translation as exact as possible, but, in a few 
instances, we have taken the liberty of adding a word or a phrase to make 
the meaning clearer. With Dr. Shattuck's approval we have added a few 
foot-notes to the section on nervous diseases, embodying the results of investi- 
gations made subsequently to the appearance of the original. 

In regard to the nomenclature of physical signs in diseases of the lungs, 
we have departed somewhat from the original in order to have our nomen- 
clature conform to that proposed at the meeting of the American Medical 
Association in May, 1885, by the late Dr. Austin Flint, chairman of a com- 
mittee appointed to prepare such a nomenclature at the International Medi- 
cal Congress in 1881. This may explain certain unusual terms, such as 
" small rales." 

We have not attempted to adapt the treatment to the United States 
Pharmacopoeia. As a rule, when the preparation mentioned was described 
in Stille and Maisch's National Dispensatory (second edition, 1879), we have 
made no comment. In other cases we have added the formula of the prepa- 
ration either in a foot-note or in parenthesis. In a very few cases we have 
substituted an officinal (IT. S. P.) preparation which was almost identical. As 
the metric system is not yet in active use, we have substituted for it approxi- 
mate equivalents in the old system. We have considered it needlessly pre- 
cise, however, to give the exact equivalents in tenths of a degree or hun- 
dredths of a grain. In every instance we have retained the author's figures 
in parenthesis, and we have added tables of weights and measures in an 
appendix. Measures of length have been left in the metric system. 



vi 



TEANSLATOES' PEEFACE. 



In place of the original Fig. 101, page 721 — specimens of handwriting in 
general paralysis, in German script, and in the German language — we have 
substituted other specimens selected from a large number kindly sent us by 
Dr. E. P. Elliot, first assistant at the Danvers Lunatic Hospital. 

Our thanks are due to Dr. G. L. Walton, of this city, for his assistance at 
a critical moment in the work, and to other friends who have given us aid 
and encouragement during the progress of our labors. 

The Tea^slatoks. 

Boston, November, 1886. 



EDITOES PEEFACE. 



It is hoped that the following work may prove useful to practitioners 
and students alike. It has achieved great success in Germany, having very 
rapidly reached a third edition, and has been adopted as the text-hook in 
the Theory and Practice of Medicine in the Medical Department of Har- 
vard University. 

I am acquainted with no work which treats of the diseases of the nervous 
system, in our knowledge of which advance has been so rapid of late years, 
so fully, concisely, and clearly. While the work is perhaps less strong in the 
other branches of general medicine, the same qualities distinguish it through- 
out. Some of the details of treatment are not precisely those generally cur- 
rent in this country ; but this is a matter of minor importance, on the whole, 
than the presentment of a clear and accurate pathology. 

The addition of brief notes — which are bracketed — has been somewhat 
tentative, and the end in view has been mainly to make the book more 
useful in my own class-room. Short accounts of sunstroke, yellow fever, and 
dengue, affections which are almost or quite unknown in Germany, have been 
added. Should the book meet with a favorable reception demanding a sub- 
sequent edition, the notes will be so modified or developed as experience may 
show to be desirable. 

Frederick 0. Shattuck. 

Boston, September, 1886. 



ERRATA. 



Page 217, line 18 from bottom, for "sclerotic" read " sclerotinic." 

Page 354, line 16 from bottom, for "e stomacho" read " a stomacho." 

Page 390, line 4 from bottom, omit "best." 

Page 391, line 18 from top, for "two-grain" read "ten-grain." 

Page 408, note, for "calcic chloride" read "chloride of lime." 

Page 411, line 29 from top, for "in which" read "on which." 

Page 445, line 24 from top, for "some toxic" read "severe toxic." 

Page 445, line 35 from top, for "notion" read "motion." 

Page 579, line 7 from bottom, for "controlled" read "constipated." 



CONTENTS. 



Acute General Infectious Diseases. 

CHAPTER PAGE 

I. Typhoid Fever, 1 

Phenomena and Complications relating to the Separate Organs, ... 8 

Peculiarities in the Course of the Disease, 17 

Relapses of Typhoid Fever, 17 

II. Typhus Fever, 27 

III. Relapsing Fever, 30 

IV. Scarlet Fever, 34 

V. Measles 43 

VI. Rotheln, . • . 48 

VII. Small-pox, 49 

Variola Vera, 50 

Varioloid, 51 

VIII. Varicella, 57 

IX. Erysipelas, 57 

X. Diphtheria, 61 

XI. Dysentery, . 69 

XII. Cholera, 73 

XIII. Malarial Diseases, , 81 

Intermittent Fever, . 82 

Pernicious Intermittent Fever, 84 

Remitting and Continuous Forms of Malarial Fever, 85 

Chronic Malarial Cachexia, . . 85 

XIV, Typho-malarial Fever, 88 

XV. Dengue, 89 

XVI. Yellow Fever, . . . 90 

XVII. Epidemic Cerebro-spinal Meningitis, 93 

XVIII. Septic and Pyaemic Diseases, 98 

XIX. Hydrophobia (Rabies canina), 102 

XX. Glanders (Farcy) 104 

XXI. Malignant Pustule (Anthrax. Mycosis intestinalis), 106 

XXII. Trichinosis, 109 

Diseases of the Respiratory Organs. 

SECTION I. 

DISEASES OF THE NOSE. 

I. Coryza, 113 

II. Chronic Nasal Catarrh . . . . 114 

III. Nose-bleed, 116 



X 



CONTENTS. 



SECTION II. 

DISEASES OF THE LARYNX. 
CHAPTER PAGE 

I. Acute Laryngeal Catarrh (Acute Laryngitis), 117 

II. Chronic Laryngitis (Chronic Laryngeal Catarrh), 119 

III. Laryngeal Perichondritis, 121 

IV. (Edema of the Glottis, 122 

V. Tuberculosis of the Larynx (Consumption of the Larynx), 123 

VI. Paralyses of the Laryngeal Muscles, 125 

Paralyses in the Distribution of the Superior Laryngeal Nerve, .... 125 
Paralyses in the Distribution of the Inferior Laryngeal or Recurrent Nerve, . 126 

VII. Spasm of the Glottis, 129 

VIII. Disturbances of Sensibility in the Larynx, 130 

IX. New Growths in the Larynx, 130 

Benignant New Growths in the Larynx, 131 

Malignant New Growths. Carcinoma of the Larynx, 131 

X. Syphilis of the Larynx, 132 

SECTION III. 

DISEASES OF THE TRACHEA AND THE BRONCHI. 

I. Acute Catarrh of the Trachea and the Bronchi, 133 

Catarrh of the Larger Bronchi, 136 

Catarrh of the Finer Bronchi. Capillary Bronchitis, 136 

II. Chronic Bronchitis, 138 

III. Foetid Bronchitis (Putrid Bronchitis) 142 

IV. Croupous Bronchitis (Fibrinous Bronchitis), 145 

V. Whooping-Cough (Pertussis), 147 

VI. Bronchiectasis, 150 

VII. Stenosis of the Trachea and Bronchi, 152 

Tracheal Stenosis, 152 

Bronchial Stenosis, 153 

VIII. Bronchial Asthma, 154 

SECTION IV. 

DISEASES OF THE LUNGS. 

I. Pulmonary Emphysema, 159 

II. Pulmonary Atelectasis (Compression of the Lungs. Aplasia of the Lungs), . 167 

III. Pulmonary (Edema 169 

IV. Catarrhal Pneumonia (Broncho-pneumonia. Lobular Pneumonia), . . .170 
V. Croupous Pneumonia, 174 

Description of Single Symptoms and Complications, 178 

Special Peculiarities and Anomalies in the Course of Pneumonia, . . . 185 

VI. Tuberculosis of the Lungs (Pulmonary Phthisis. Pulmonary Consumption), . 191 

General Pathology and iEtiology of Tuberculosis, 191 

^Etiology of Tuberculosis in Man, ' . . . .193 

Pathological Anatomy of Tuberculosis, especially of Pulmonary Tuberculosis, . 196 
Clinical History of Tuberculosis in General, and of Pulmonary Tuberculosis in 

Particular, 198 

Special Symptoms and Complications, , 201 

Contraction of the Lungs (Fibroid Phthisis), 206 

Disseminated Pulmonary Tuberculosis, 208 

VII. Acute General Miliary Tuberculosis, 218 

VIII. Gangrene of the Lungs, 223 



CONTENTS. xi 

CHAPTER PAGE 

IX. Diseases from the Inhalation of Dust (Pneumonoconiosis) 227 

X. Embolic Processes in the Lungs (Hemorrhagic Infarction of the Lungs), . . 229 

XI. Brown Induration of the Lungs (Lungs of Heart Disease), 232 

XII. Tumors of the Lungs. Cancer of the Lungs. Echinococcus in the Lungs. 

Pulmonary Syphilis, 233 

SECTION V. 

DISEASES OF THE PLEURA. 

I. Pleurisy, 235 

Physical Signs, 240 

Different Forms of Pleurisy, 244 

II. Peripleuritis and Actinomycosis, 249 

III. Pneumothorax, 250 

IV. Hydrothorax. Hsematothorax, 253 

V. New Growths of the Pleura, 254 

VI. Mediastinal Tumors, 255 

Diseases of the Circulatory Organs. 

SECTION I. 

DISEASES OF THE HEART. 

I. Acute Endocarditis (Endocarditis verrucosa and ulcerosa), 257 

II. Valvular Disease of the Heart, 261 

General Pathology of Valvular Disease of the Heart, 262 

Insufficiency of the Mitral Valve, 264 

Stenosis of the Mitral Orifice (Mitral Stenosis), . . . . . . .266 

Insufficiency of the Semilunar Valves of the Aorta, . . . . . . 268 

Stenosis of the Aortic Orifice, . . . 271 

Insufficiency of the Tricuspid Valve, 272 

Stenosis of the Tricuspid Orifice, 273 

Insufficiency of the Pulmonary Valve, 273 

Stenosis of the Pulmonary Orifice (Pulmonary Stenosis), 274 

Combined Valvular Diseases of the Heart, 275 

General Comparison of the most Important Physical Signs in Valvular Disease 

of the Heart, . . . . . . 275 

General Sequelae and Complications of Valvular Disease of the Heart, . . 276 

General Course and Prognosis of Valvular Disease of the Heart, . . . 281 

Treatment of Valvular Heart Disease, 282 

III. Myocarditis (Indurated Degeneration. Myodegeneration), 287 

IV. Idiopathic Hypertrophy and Dilatation of the Heart (Over-exertion of the 

Heart. Weakened Heart), 291 

V. Fatty Heart, . ... . . 294 

VI. Neuroses of the Heart, 296 

Angina Pectoris (Stenocardia), 296 

Nervous Palpitation, 297 

Tachycardia, 298 

SECTION II. 

DISEASES OF THE PERICARDIUM. 

I. Pericarditis, . 299 

Pericarditis externa and Mediastino-pericarditis (Pleuro-pericarditis), . . 302 

Obliteration of the Pericardial Cavity (Adhesive Pericarditis), .... 303 

Tubercular Pericarditis, 304 



xii CONTENTS. 

CHAPTER PAGE 

II. Hydro-pericardium (Dropsy of the Pericardium), 306 

III. Hasmo-pericardium (Blood in the Pericardial Sac), ...... 307 

IV. Pneumopericardium (Air in the Pericardial Sac), 307 

SECTION III. 

DISEASES OF THE VESSELS. 

I. Arterio-sclerosis (Endarteritis chronica deformans. Atheroma of the Vessels), . 308 

II. Aneurism of the Thoracic Aorta, 311 

III. Aneurisms of the Other Vessels, . . .316 

IV. Rupture of the Aorta, 316 

V. Narrowing of the Aorta, 317 

Diseases of the Digestive Organs. 

SECTION I. 

DISEASES OF THE MOUTH, TONGUE, AND SALIVARY GLANDS. 

I. Stomatitis (Inflammation of the Mouth), 318 

II. Ulcerative Stomatitis (Stomacace), . 319 

III. Aphtha? (Aphthous Stomatitis), 320 

IV. Thrush (Soor. Muguet), 321 

V. Glossitis, 322 

VI. Noma (Water-cancer. Cancrum oris), 323 

VII. Parotitis (Mumps), 324 

Idiopathic, Primary Parotitis, 324 

Secondary, Metastatic Parotitis, 325 

VIII. Angina Ludovici, 326 

IX. Anomalies of Dentition, 326 

SECTION II. 

DISEASES OF THE SOFT PALATE, TONSILS, PHARYNX, AND NASO-PHARYNX. 

I. Sore Throat (Tonsillitis. Angina), 328 

Catarrhal Sore Throat, . 329 

Follicular Tonsillitis, 329 

Tonsillar Abscess (Parenchymatous Sore Throat), 330 

Necrotic Tonsillitis (Necrotic Sore Throat), 331 

Benign Croupous Sore Throat, 331 

II. Chronic Hypertrophy of the Tonsils, 333 

III. Chronic Pharyngitis, 334 

Chronic Catarrh of the Naso-pharynx, 335 

Pharyngitis Sicca, 335 

Hypertrophic Catarrh of the Pharynx and Naso-pharynx, 335 

IV. Retro-pharyngeal Abscess, 337 

SECTION III. 

DISEASES OF THE CESOPHAGUS. 

I. Inflammation and Ulcer of the (Esophagus, 338 

II. Dilatation of the (Esophagus, ' . . 339 

Diffuse Dilatation, 339 

Diverticula, 340 

III. Stenosis of the (Esophagus, 342 

IV. Cancer of the (Esophagus, 346 



CONTENTS. 



xiii 



CHAPTER PAGE 

V. Rupture of the (Esophagus, . . 347 

VI. Neuroses of the Oesophagus, 348 

Spasm of the (Esophagus, 348 

Paralysis of the (Esophagus, 348 

SECTION IV. 

DISEASES OF THE STOMACH. 

I. Acute Gastric Catarrh, 348 

II. Chronic Gastric Catarrh, 350 

III. Phlegmonous Gastritis, 357 

IV. Gastric Ulcer (Simple or Round Ulcer of the Stomach), 358 

V. Cancer of the Stomach, 364 

VI. Dilatation of the Stomach, 369 

VII. Gastric Haemorrhage, 374 

VIII. Nervous Affections of the Stomach, 375 

SECTION V. 

DISEASES OF THE INTESTINES. 

I. Intestinal Catarrh (Catarrhal Enteritis), . 377 

Different Forms of Intestinal Catarrh, 379 

II. Cholera Morbus (Cholera Nostras, Cholera Infantum), 384 

III. Intestinal Catarrh of Children (Pedatrophy), 387 

IV. Typhlitis and Perityphlitis (Inflammation of the Caecum), 391 

V. Perforating Ulcer of the Duodenum, 395 

VI. Tuberculosis of the Intestines, 395 

VII. Syphilis of the Rectum . 397 

VIII. Cancer of the Intestines, 398 

IX. Haemorrhoids, . 400 

X. Habitual Constipation, . 402 

XI. Stricture and Obstructions of the Intestines, 404 

XII. Intestinal Parasites, 411 

Tape-worms (Taenia and Bothriocephalus), . . . . . . .411 

Round- worms (Ascaris lumbricoides), 417 

Oxyuris vermicularis (Seat-worms), . 418 

Anchylostomum duodenale (Dochmius s. Strongylus duodenalis), . . . 419 

Trichocephalus dispar (Whip-worm), ......... 420 

SECTION VI. 

DISEASES OF THE PERITONEUM. 

I. Acute Peritonitis, 420 

II. Chronic Peritonitis. Tubercular Peritonitis, 429 

III. Ascites (Hydroperitoneum), . . . 432 

IV. Cancer of the Peritoneum, 434 

SECTION VII. 

DISEASES OF THE LIVER, BILE-DUCTS, AND PORTAL VEIN. 

1. Catarrhal Jaundice (Icterus catarrhal is. Gastro-duodenal Catarrh with Jaundice), 435 

II. Biliary Calculi (Hepatic Colic. Cholelithiasis), 440 

III. Suppurative Hepatitis (Hepatic Abscess), 446 

IV. Cirrhosis of the Liver (Chronic Diffuse Interstitial Hepatitis. Laennec's 

Cirrhosis. Gin-drinkers' Liver), 448 

V. Biliary and Hypertrophic Cirrhosis of the Liver, 453 



xiv 



CONTENTS. 



CHAPTER PAGE 

VI. Acute Yellow Atrophy of the Liver, 455 

Appendix. Pernicious Jaundice. Cholaemia and Acholia, .... 459 

VII. Icterus Neonatorum (Jaundice of the New-born), 460 

VIII. Hepatic Syphilis, 460 

IX. Cancer of the Liver and Bile-ducts, . . . 462 

X. Echinococcus of the Liver, 464 

XI. Circulatory Disturbances in the Liver, 466 

XII. Atrophy, Hypertrophy, and Degenerations of the Liver, 467 

XIII. Anomalies in the Shape and Position of the Liver, 469 

XIV. Suppurative Pylephlebitis (Purulent Inflammation of the Portal Vein and its 

Branches), . . 470 

XV. Thrombosis of the Portal Vein (Chronic Adhesive Pylephlebitis. Pylethrom- 

bosis), . . ....... . • 471 

Appendix. Diseases of the Pancreas, 473 



Diseases of the Nervous System. 

L The Diseases of the Peripheral Nerves. 
SECTION I. 

DISEASES OF THE SENSORY NERVES. 

I. General Eemarks upon the Disturbances of Sensibility, 475 

The Different Varieties of Cutaneous Sensibility and the Methods of testing 



them, 475 

The Sensibility of the Muscles and Joints, 479 

II. Anaesthesia of the Skin, 480 

Anaesthesia of the Trigeminus, 482 

III. Neuralgia in General, 485 

IV. The Individual Forms of Neuralgia, 491 

1. Neuralgia of the Trigeminus, 491 

2. Occipital Neuralgia, 493 

3. Neuralgias in the Region of the Brachial Plexus, 493 

4. Intercostal Neuralgia, 494 

5. Neuralgias in the Region of the Lumbar Plexus, 495 

6. Sciatica, 495 

7. Neuralgia of the Genitals and the Rectal Region, 497 

V. Neuralgia of the Joints, . . . . . 498 

VI. Habitual Headache, 499 

VII. Anomalies of the Sense of Smell, 501 

VIII. Anomalies of the Sense of Taste, 502 

SECTION II. 

DISEASES OF THE MOTOR NERVES. 

1. General Remarks upon the Disturbances of Motility, . . . . . . 503 

1. Paralysis, . . . . . . 503 

2. Symptoms of Motor Irritation, 508 

3. Ataxia, 510 

4. General Remarks upon testing the Reflexes and the Condition of them, . 511 
Mechanical Muscular Irritability and Paradoxical Contraction, . . 514 

5. General Remarks upon the Changes of Electrical Excitability in the Motor 

Nerves and Muscles, ........... 514 

II. The Different Forms of Peripheral Paralysis, 522 

1. Paralysis of the Ocular Muscles, . . . 522 



CONTENTS. xv 

CHAPTER PAGE 

2. Paralysis of the Motor Branch of the Trigeminus, ...... 525 

3. Facial Paralysis, 525 

4. Paralyses in the Region of the Muscles of the Shoulder, .... 529 

5. Paralyses of the Muscles of the Back, 531 

6. Paralyses in the Region of the Upper Extremity, 532 

Radial (Musculo-spiral) Paralysis, . 532 

Ulnar Paralysis, 533 

Median Paralysis, 534 

Combined Paralyses of the Arm, 534 

7. Paralysis of the Diaphragm, 535 

8. Paralyses in the Region of the Lower Extremity, 536 

9. Toxic Paralyses, 537 

Lead Paralysis, 537 

Arsenical Paralysis, ............. 538 

III. The Different Forms of Localized Spasms, 538 

1. Spasms in the Motor Distribution of the Trigeminus, 538 

2. Clonic Facial Spasm, 539 

3. Spasm in the Region of the Hypoglossal Nerve. Lingual Spasm, . . . 540 

4. Spasms in the Muscles of the Neck, 541 

5. Spasms in the Muscles of the Shoulder and Arm, . . . . * . . 542 

6. Spasms in the Muscles of the Lower Extremity, ■ 542 

Saltatory Reflex Spasm, 543 

Arthrogryposis, 543 

7. Spasms in the Respiratory Muscles, 543 

IV. Writers' Cramp and Allied Professional Neuroses, 544 

V. Simple and Multiple Degenerative Neuritis, 546 

Alcoholic Neuritis, 550 

VI. New Growths in the Peripheral Nerves, 551 

77. V A SO-MOTOR AND TROPHIC N EUR OSES. 

I. Preliminary Remarks upon Vaso-motor, Trophic, and Secretory Disturbances, . 553 

II. Hemicrania, 556 

III. Progressive Facial Hemiatrophy, 559 

IV. Exophthalmic Goitre, 560 

III. The Diseases or the Spinal Cord. 

I. Diseases of the Spinal Meninges, 564 

1. Acute Inflammations of the Spinal Meninges, . . . . . . . 564 

2. Chronic Spinal Leptomeningitis, 566 

3. Pachymeningitis cervicalis hypertrophica, . 567 

4. Haemorrhages of the Spinal Meninges, 568 

H. Disturbances of Circulation, Haemorrhages, Functional Disturbances, and Trau- 
matic Lesions of the Spinal Cord, 569 

1. Disturbances of Circulation, 569 

2. Spinal Apoplexy. Haematomyelia 569 

3. Functional Disturbances, 570 

4. Traumatic Lesions, 571 

5. Concussion of the Spine. Commotio Spinalis. Railway Spine, . . . 572 

6. Diseases of the Spinal Cord after a Sudden Reduction of the Atmospheric 

Pressure (Caisson Disease), 574 

III. The Pressure Paralyses of the Spinal Cord, 575 

IV. Acute and Chronic Myelitis, 581 

V. Multiple Sclerosis of the Brain and Spinal Cord, ....... 592 

VI. Locomotor Ataxia, . . . 596 

Appendix. Hereditary Ataxia. Friedreich's form of Locomotor Ataxia, . 612 



xvi CONTENTS. 

CHAPTER PAGE 

VII. Amyotrophic Lateral Sclerosis, 613 

VIII. Progressive (Spinal) Muscular Atrophy, 616 

Appendix. The Primary Myopathic forms of Muscular Atrophy, . . .621 

IX. The So-called Spastic Spinal Paralysis, . .' 625 

X. Acute and Chronic Poliomyelitis, 629 

1. Spinal Paralysis of Children, ■ . . . 629 

2. Acute Poliomyelitis of Adults, 633 

3. Subacute and Chronic Poliomyelitis, 634 

XI. Acute Ascending Spinal Paralysis, ......... 635 

XII. New Growths of the Spinal Cord and of its Membranes, 638 

XIII. The Formation of Cavities and Fissures in the Spinal Cord, .... 639 ■ 

Appendix. Spina Bifida, 640 

XIV. Secondary Degenerations in the Spinal Cord, 641 

XV. Unilateral Lesion of the Spinal Cord, 643 

IV. The Diseases of the Medulla Oblongata. 

I. Progressive Bulbar Paralysis, 646 

Appendix. The Rarer Forms of Chronic Bulbar Paralysis, and Progressive 

Ophthalmoplegia, 651 

II. Acute and Apoplectiform Bulbar Paralysis, 652 

1. Haemorrhage into the Medulla Oblongata and the Pons, 652 

2. Embolism and Thrombosis of the Basilar Artery, 654 

3. Acute or Inflammatory Bulbar Paralysis, 655 

III. Compression of the Medulla, 656 

V. The Diseases of the Brain. 
SECTION I. 

DISEASES OF THE CEREBRAL MENINGES. 

I. Hsematoma of the Dura Mater, 657 

II. Purulent Meningitis, 659 

III. Tubercular Meningitis, . 663 

Tubercular Meningitis in Children, 666 

IV. Thrombosis of the Cerebral Sinuses, 668 

SECTION II. 

DISEASES OF THE BRAIN-SUBSTANCE. 

I. Disturbances of Circulation in the Brain, 669 

II. General Preliminary Remarks upon the Localization of Cerebral Diseases 

(Topical Diagnosis of Cerebral Lesions), ....... 671 

1. The Motor Region of the Cortex Cerebri, 672 

2. The other Parts of the Cortex Cerebri, except the Center for Speech, . . 676 

3. The Centers of Speech and the Disturbances of Speech (Aphasia and Allied 

Conditions), 677 

4. The Centrum Ovale, Internal Capsule, Central Ganglia, and Region of the 

Corpora Quadrigemina, 681 

5. The Cerebellum, 683 

General Diagnostic Principles, 685 

III. Cerebral Haemorrhage, ' . . 686 

IV. Cerebral Embolism and Thrombosis, 698 

V. Inflammation of the Brain, 701 

1. Abscess of the Brain (Suppurative Encephalitis), 701 

2. Acute and Chronic Non-suppurative Encephalitis, 704 



CONTENTS. xvii 

CHAPTER PAGE 

Idiopathic Softening of the Brain, 704 

Curable Form of Encephalitis, 704 

Diffuse Cerebral Sclerosis, 704 

The Acute Encephalitis of Children (Cerebral Paralysis of Children), . . 704 
VI. Insolation. Sunstroke. Heat Prostration. Thermic Fever, . . . .706 

VII. Tumors of the Brain, . . . . .708 

Varieties of Cerebral Tumor, .... * 708 

Tumors in the Different Parts of the Brain. Their Focal Symptoms, . .711 

Appendix. Hydatids of the Brain, 715 

VIII. Cerebral Syphilis, 715 

IX. Progressive General Paralysis of the Insane (Paralytic Dementia), . . . 719 

X. Chronic Hydrocephalus, . 726 

XI. Meniere's Disease, 728 

VI. Neuroses without Known Anatomical Basis. 

I. Epilepsy, 729 

Appendix. Infantile Convulsions, 737 

II. Chorea, 739 

III. Paralysis Agitans, 742 

IV. Athetosis, . . 745 

V. Tetany, ............... 747 

VI. Tetanus, 749 

VII. Congenital Myotonia (Thomsen's Disease), 752 

VIII. Catalepsy, 754 

IX. Hysteria, 755 

X. Neurasthenia, 767 

Diseases of the Kidneys, the Pelvis of the Kidney, and the Bladder. 

SECTION I. 

DISEASES OF THE KIDNEYS. 

I. General Preliminary Remarks upon the Pathology of Renal Disease, . * . 771 

1. Albuminuria, 772 

2. Casts and other Abnormal Morphological Constituents of the Urine in Renal 

Disease, 775 

3. The Dropsy of Renal Disease, 777 

4. Uraemia, • . 778 

5. The Changes in the Circulatory Apparatus in Renal Disease, .... 783 
II. Acute Nephritis (Acute Bright's Disease), 784 

III. The Subchronic and Chronic Forms of Nephritis, with the Exception of the 

Genuine Contracted Kidney, 797 

IV. Contracted Kidney, 804 

V. Amyloid Kidney, • . .812 

VI. Purulent Nephritis and Perinephritis, 816 

Perinephritic Abscess. 818 

VII. Disturbances of Circulation in the Kidneys, 819 

1. The Congested Kidney, 819 

2. Embolic Infarction in the Kidneys, . . .819 

VIII. New Growths in the Kidneys, 820 

IX. Parasites of the Kidneys and of the Urinary Passages. Chyluria, , . . 822 

X. Movable Kidney (Floating Kidney. Ren Mobilis), 824 

Appendix. The Diseases of the Supra-renal Capsules and Addison's Dis- 
ease (Bronzed Skin), , 826 

JB 



xviii CONTENTS. 



SECTION II. 

DISEASES OP THE PELVIS OP THE KIDNEY AND OF THE BLADDER. 

CHAPTER PAGE 

I. Inflammation of the Pelvis of the Kidney. Pyelitis, 829 

II. Nephrolithiasis, 832 

III. Tuberculosis of the Genitourinary Apparatus 836 

IV. Hydronephrosis, 838 

V. Cystitis (Vesical Catarrh), 840 

VI. New Growths in the Bladder, • . . . 844 

VII. Enuresis Nocturna (Nocturnal Incontinence of Urine), 845 

Diseases of the Organs of Locomotion. 

I. Acute Articular Rheumatism, 847 

II. Chronic Articular Rheumatism (Chronic Polyarthritis) and Arthritis Defor- 
mans, . ' J" t ,1 . . . . 858 

III. Acute and Chronic Muscular Rheumatism, 863 

IV. Rachitis, 866 

V. Osteomalacia, 871 

Diseases affecting the Blood and Tissue-metamorphosis. 

(constitutional diseases.) 

I. Anaemia and Chlorosis, 874 

II. Progressive Pernicious Anaemia, 884 

III. Leukaemia, 890 

IV. Pseudo-leukaemia, 896 

V. Haemoglobinaemia and Haemoglobinuria, 898 

VI. Scurvy, 901 

VII. Purpura. Morbus Maculosis Werlhofii. Peliosis, 906 

VIII. Haemophilia, 907 

IX. Diabetes Mellitus, 910 

X. Diabetes Insipidus, . 926 

XI. Gout, . . . . . . 928 

XII. Obesity, 936 

XIII. Scrofula, 943 

Appendix I. Summary of the Symptoms and Treatment in Cases of Poisoning, . 946 

Appendix II. Table of Weights and Measures, . . . . . . . 953 

Index, 955 



LIST OF ILLUSTEATIOIsTS. 



PIG. PAGE 

1. Temperatures in typhoid fever, 6 

2. Example of the temperature-curve in relapsing fever, 32 

3. Spirilli of relapsing fever in the blood, 33 

4. Example of a normal scarlet-fever curve, 36 

5. Example of the temperature-curve in measles, ........ 45 

6. Example of the temperature-curve in true small-pox, 52 

7. Comma bacilli, 74 

8. Quotidian intermittent fever, . .83 

9. Tertian intermittent fever, 83 

10 a, 10 b. Anthrax bacilli, . 107 

11. Trichinae, ..... 0 110 

12. Paralysis of left vocal cord, 127 

13. Bilateral paralysis of the posticus, 127 

14. Paralysis of both internal thyro-arytasnoid muscles, 128 

15. Paralysis of the arytaenoideus, 128 

16. Paralysis of the thyro-arytaenoids and arytaenoideus, 128 

17. 18. Pediculated fibromata, 131 

19. Crystals of fat acids, 143 

20. Asthma crystals and Curschmann's spirals, 156 

21. Example of the temperature-curve in croupous pneumonia, 184 

22. Example of the temperature-curve in " intermitting " pneumonia, .... 184 

23. Cholesterine crystals, - . 188 

24. Elastic fibers, . . 203 

25. Tubercle bacilli in the sputum, 204 

26. Masses of actinomyces, 249 

27. Pulse-curve in marked mitral stenosis, 266 

28. Pulse-curve in aortic insufficiency, 270 

29. Pulse-curve in stenosis of the aortic orifice, 272 

30. Pulsus bigeminus, 278 

31. Plan of the dentition, '.. 327 

32. Sarcini ventriculi and yeast-cells, . . . . . . . . . 353 

33. Haemine crystals, 366 

34. Stomach-tube with Hegar's funnel, 372 

35. Washing out the stomach, 373 

36. Head of taenia solium, 412 

37. Head of cysticercus of the brain, . . . . 412 

38. Taenia solium, 412 

39. Eggs of intestinal parasites, 413 

40. Head of taenia mediocanellata, 414 

41. Taenia mediocanellata, . . . ... 414 

42. Head of bothriocephalus latus, 414 

43. Bothriocephalus latus, 414 

44. Embryo of bothriocephalus latus, .......... 415 

45. Ascaris lumbricoides, . . , 417 



XX 



LIST OF ILLUSTRATIONS. 



FIG. PAGE 

46, 47. Oxyuris vermicularis, 418 

48, 49. Anchylostomum duodenale, 419 

50. Trichocephalus dispar, 420 

51. Leucine and tyrosine crystals, . 458 

52. Taenia echinococcus, 464 

53. 54. Echinococcus scolices, . 465 

55. Echinococcus hooklets, 465 

56, 57. Distribution of the sensory cutaneous nerves in the head, 483 

58, 59. Distribution of the sensory cutaneous nerves in the trunk and upper extremities, 484 

60. Detailed distribution of the nerves to the dorsal surface of the fingers, . . . 485 

61, 62. Distribution of the sensory cutaneous nerves to the lower extremities, . . 485 

63. Horizontal section through the right cerebral hemisphere, 503 

64. Transverse section through the crura cerebri in secondary degeneration, . . 504 

65. Transverse section through the cervical enlargement, ...... 504 

66. Transverse section through the lumbar enlargement, 504 

67. Motor points of face, 515 

68. 69. Motor points of arm 516, 517 

70. Motor points of thigh, 518 

71, 72. Motor points of leg, 519, 520 

73. Right facial paralysis, 526 

74. Trunk of the facial, . 527 

75. Paralysis of the right serratus, 531 

76. Position of the hand in paralysis of the radial nerve, ...... 533 

77. Claw-shaped hand, main en griff e, 534 

78. Spasm of the right splenius capitis, 541 

79. Left facial hemiatrophy, 559 

80. Position of the hand in pachymeningitis cervicalis hypertrophica, . . . . 567 

81. Vertebral displacement in spondylitis, 576 

82. Example of disease of the cord in multiple sclerosis, 593 

83. Distribution of the sclerosed nodules on the surface of the pons, .... 593 

84. Transverse section through the lumbar region in locomotor ataxia, 598 

85. Transverse section through the cervical region in locomotor ataxia, . . . 598 

86. 87. Transverse section of cord in beginning locomotor ataxia, .... 598 

88. Positions of a child with pseudo-hypertrophic paralysis on rising, .... 622 

89. Pseudo-hypertrophy of the muscles, 623 

90. Section of the cord in anterior poliomyelitis, 629 

91. Secondary descending degeneration of the pyramidal tracts, ..... 642 

92. Secondary ascending and descending degeneration, 643 

93. Course of the main tracts in the cord, . 644 

94. Representation of the chief symptoms in unilateral lesion, ..... 645 

95. Diagram of focal diseases in the pons, 653 

96. 97. Lateral aspect of the brain, 673, 674 

98. Aspect of the median surface of the cerebrum, 674 

99. Topographical relations between the surface of the brain and the skull, . . 675 

100. Diagram of the course of the optic fibers in the chiasma, 676 

101. Examples of hand-writing in general paralysis, 721 

102. Characteristic position of the body in paralysis agitans, 437 

103. Example of the position of the fingers in the movements of athetosis, . . . 746 

104. Different forms of casts, 775 

105. Distoma haematobium, 823 

106. Embryos of filaria, 824 

107. Pelvic epithelium, . 830 

108. Crystals of triple phosphate and amnionic urate, 842 

109. Deformity of the hand in protracted arthritis deformans, 860 

110. Changes in the red blood-corpuscles in pernicious anaemia, . . . . . 888 

111. Anaemic blood 839 



ACUTE GENERAL INFECTIOUS DISEASES. 



CHAPTER I. 

TYPHOID FEVER. 

( Typhus abdominalis. Enteric Fever. Ileotyphits.) 

JEtiology. — According to our present views, the cause of typhoid fever must he 
sought in some specific, organized, pathogenetic poison. The later investigations 
in bacteriology have apparently revealed what this poison is. Koch and Eberth 
were the first to point out a clearly specific variety of short, rod-shaped bacteria 
(bacilli), which appear in this disease alone. They take up the aniline colors. 
Koch and Eberth, and later W. Meyer, Friedlander, and Gaffky, found them in 
the intestine, especially in its lymphatic apparatus, and also in the mesenteric 
glands, the spleen, liver, and kidneys. The subjects in whom these bacteria were 
detected had died in the beginning or during the fastigium of typhoid fever. 

The length of these bacilli is about one third the diameter of a red blood-glob- 
ule, and their breadth equals one third their length. Their ends are rounded off, 
and in their interior the formation of spores can sometimes be plainly recognized. 
They are found for the most part lying together in little clumps (foci of bacilli) in 
the organs. 

That these typhoid bacilli are specific is shown, however, as in the case of 
many micro-organisms, less by their external form than by their peculiarities, as 
observed in pure cultures of them. Gaffky, who first succeeded with such culti- 
vations, found that the colonies of these bacilli, reared in a mass of stiff gelatine, 
are made up of very minute, brownish-yellow clumps, and that in their growth 
they are always limited to the spots where they have been implanted, and never 
liquefy the jelly in which they grow. Examined in water, the typhoid bacilli 
exhibit quite an active individual motion. The formation of spores takes place 
only when the temperature is between 86° and 108° (30°-42° C), ceasing at lower 
temperatures. The attempt to rear the characteristic bacilli from portions of the 
fecal discharges or blood of typhoid patients has thus far failed. 

[The recent studies of Frankel and Simmonds are confirmatory of those of 
Gaffky. These observers find the bacilli nearly constantly in the spleens of pa- 
tients dying during the earlier stages of typhoid fever, and produced in rabbits 
changes similar to those seen in man by the injection into the blood of cultures of 
the organism. In three out of eleven cases they succeeded in obtaining cultures 
from fresh typhoid dejections.] 

Investigation of the aetiology of typhoid fever must consequently be directed to 
ascertaining in what manner and through what channels the specific typhoid 
bacilli penetrate * into the human body, and what circumstances are then essen- 

* Perhaps it is not useless once more to call attention expressly to the fact that typhoid fever can 
result only from an infection of the body with actual typhoid bacilli, and never through any other 
bacteria, through the products of decay and decomposition, tainted food, and the like ; nor does there 
yet exist the slightest proof that typhoid bacilli can be developed from any other micro-organisms. 
1 



2 



ACUTE GrENEEAL INFECTIOUS DISEASES. 



tial to their further development and to the display of their pathogenetic properties. 
It must be confessed that the ability to answer these questions accurately is a goal 
from which we are quite distant. 

It is almost universally believed that, as a rule, typhoid bacilli do not have any 
permanent, independent existence outside the human body. Often, however, the 
conditions essential to an abundant development of the bacilli arise in certain 
places, and thus make it possible for a greater or less number of persons to absorb 
the pathogenetic poison, and, as a result, to be attacked by typhoid fever. In this 
way arise the numerous greater or smaller epidemics of typhoid fever in contrast 
to the sporadic cases, which are likewise possible, and are not infrequent. If 
an epidemic of typhoid appears in a place till then entirely free from the disease, 
we must always refer it to an importation of the disease-germs, and seek their 
source in some previous case of typhoid. We must, therefore, take for granted 
that the poison of typhoid can in some way escape from the body of the patient 
into the outer world. If we believe this, we shall be sure to think, first of all, of 
the intestinal discharges as the source of infection. In all probability, these con- 
tain the typhoid bacilli or their spores ; but this fact has not yet been fully dem- 
onstrated, because of the presence of numerous other micro-organisms in the con- 
tents of the intestine. 

As to the exact manner of infection, views are still widely different. Up to 
the present time there are chiefly two contrasted theories, called, respectively, the 
" ground-soil" and the " drinking-water " * theories. According to the former, 
which is maintained principally by Pettenkofer and his pupils, the ground-soil is 
to be regarded as the chief place of development for the schizomycetic fungus of 
typhoid fever. Whether this will flourish depends chiefly on the condition of the 
soil (varying at different times and in different places), and this alone should ex- 
plain all the peculiarities observable in the spread of the disease — e. g., that single 
houses, streets, or wards of a city should suffer. According to Pettenkofer, a soil 
that air and water easily penetrate — e. g., one made up of alluvial or detrital depos- 
its — is most favorable for the spread of the disease, while a firm, rocky bottom 
makes its further development impossible ; and, where this " tendency of the 
ground-soil " is wanting, the disease can neither be introduced nor, if brought in, 
spread any further ; for, according to Pettenkofer, the typhoid poison is seldom if 
ever transferred directly from one person to another. The poison in the stools 
must first be changed by the soil before it becomes infectious. The " ground-air," 
which is continually rising, carries the poison not only into the open atmosphere, 
but into the air of dwelling-rooms, and, being then inhaled, produces infection. 
We can thus understand why Pettenkofer regards typhoid fever as not directly 
contagious. The chief support of the ground-soil theory, beyond the results of 
comparing the character of the soil with the extent of the epidemics, consists in 
the proof which Buhl and Pettenkofer have given (taking Munich as an example) 
that a relation exists between the variations of the standing water in the soil and 
the frequency of typhoid cases. It appears that, when the water stands high (near 
the surface), fewer cases occur, and when it falls below the mean height cases are 
more numerous. This relation, which is said to hold true also for Berlin and some 
other places, is not yet, we may add, explained with certainty. 

To be contrasted, or rather compared, with the soil-gas theory is the view held 
by many physicians, despite the vigorous protest of Pettenkofer, that drinking- 
water plays an important role in the origin of many epidemics of typhoid. In 
fact, in the case of numerous epidemics, whose extent bears an unmistakable rela- 

* Compare with what follows the statements concerning the aetiology of cholera, where the same dis- 
puted points are considered. 



TYPHOID FEVER. 



3 



tion to the water-supply, we seem perfectly justified in supposing that the typhoid 
germs are brought into the body by means of water used in drinking or otherwise. 
Even then we are by no means wholly to disregard the character of the soil, for 
the disease-producing poison — not to speak of direct pollution — is probably often 
communicated to the well-water from the soil. The possibility of this will be 
especially great if the wells are near drains or cess-pools containing typhoid dis- 
charges. 

We believe the idea is continually gaining ground that no single u theory " 
can fully explain all the facts, and that the possibility of infection occurring in 
several different ways must be considered. Beside the possible inhalation of the 
poison, or the ingestion of polluted water, it may be that sometimes the disease is 
conveyed by food. For example, it has been remarked in England, and lately in 
Cologne, that the fever in certain epidemics was limited to individuals who had 
their milk from one common source. In such cases, however, the probable cause 
is not a disease in the cows, but a pollution of the milk or the milk-cans by water. 
It is as yet doubtful if animals can have typhoid fever ; at any rate, all attempts 
at artificial inoculation have had a negative result. This fact makes it uncertain 
whether the illnesses which have been observed to follow the ingestion of the flesh 
of diseased calves (e. g., the epidemic of Kloten) are actually to be considered 
typhoid fever, although the pathological changes are said by Huguenin to be very 
similar to those found in typhoid. Finally, it seems very probable that persons 
who come into direct contact with typhoid discharges are thereby exposed to the 
danger of infection. Many deny this {vide supra), but it would explain why 
nurses and laundresses, who have to handle clothing soiled by the discharges of 
patients, are comparatively often attacked by typhoid fever. Through the agency 
of dirty linen, utensils, etc., the poison may be spread even further. 

[It is not probable that sewer-gas in itself is an exciting cause of typhoid fever. 
Especially in large cities typhoid dejections are constantly finding their way into 
the sewers, which afford all the conditions favorable to the further growth and 
development of the poison. If, then, the drainage of any house is defective, the , 
seeds of the disease can readily gain access to the interior of the house and infect 
susceptible individuals. 

One of the most instructive epidemics on record is that in Plymouth, Pennsyl- 
vania, a town of eight thousand inhabitants. In the spring of 1885 a disease, at 
first supposed to be of a strange character, broke out in the place, and, before it 
ceased, affected twelve hundred persons, causing one hundred and thirty deaths. 
It was soon found that the malady was typhoid fever, which arose from one case, 
briefly in this wise : In January, February, and March there was a case of typhoid 
in a house on a hill sloping toward a water-supply of the town. The dejections 
were thrown out on the snow, under which the ground was deeply frozen. On 
March 25th a sudden and great thaw occurred, the water did not sink into the 
ground, but ran immediately into the natural surface channels, and on April 10th 
the epidemic began. There were reasons, which it is not necessary here to detail, 
why the above source of water-supply was drawn upon to an unusual degree just 
at that time, but it has been shown that those who derived their water from other 
sources were spared by the disease. The original case came from Philadelphia, 
which was at that time unprovided with a board of health ; but the lessons of 
this epidemic, most carefully studied by competent physicians, have secured such a 
board, and will strengthen the position of every board of health in the country.] 

In almost all cases the intestine seems to be the actual gate of entrance for the 
typhoid poison into the human system. This is shown by the fact that in all 
cases which come to autopsy in early stages of the disease, the typhoid bacilli are 
mainly confined to the lymphatic tissues of the intestine. The typhoid poison 



4 



ACUTE GENEKAL INFECTIOUS DISEASES. 



(bacilli or spores) is probably swallowed, either directly with, water or polluted 
food, or after being inhaled or in some other way introduced into the mouth. If 
not destroyed in the stomach, it passes on in viable condition into the alkaline con- 
tents of the intestine, and here finds the conditions essential to its further develop- 
ment. It penetrates at first into the follicles and Peyer's patches, and thence goes 
on into the mesenteric glands, the blood-current, the spleen, and other organs. 

As in the case of most other infectious diseases, the occurrence of infection is 
dependent not only on outward conditions, but also on an individual predisposi- 
tion. Details of the circumstances attending this latter are as yet not at all accu- 
rately understood. Even in the worst typhoid centers, where the possibility of 
infection must be universal, many escape the disease. 

Age has an indubitable influence upon the liability to the disease. Typhoid is 
especially a disease of youthful, vigorous individuals, of fifteen to thirty years. 
Above that age, it is noticeably less frequent, although cases do occur at sixty and 
even seventy years. Formerly it was often said that young children were never 
attacked ; but this was because the disease was not recognized, for in reality it is 
only children under one year old who seem to be seldom infected. At a later age, 
cases are by no means rare. 

Sex can not be shown with certainty to have an especial predisposing influence 
upon the frequency of typhoid fever. 

Mental excitement and gross errors in diet seem to predispose to the disease. 
On the other hand, a certain immunity has been alleged to be given by many cir- 
cumstances, especially pregnancy, the puerperal state, and other diseases already 
existing (tuberculosis, heart disease). Most of these statements are shown, how- 
ever, by more extended experience, to be very doubtful. It does seem to be certain 
that the occurrence of typhoid fever gives very probable though not absolute 
immunity against any later new attack. 

Finally, it must be mentioned that the necessary conditions for an abundant 
development and conveyance of the typhoid germs are beyond doubt dependent 
on the season. According to statistics, most of the typhoid epidemics come in the 
months from August to November, while generally the number of cases greatly 
diminishes from December to spring. 

General Course of the Disease. — Extended experience shows that, after infection 
with the typhoid poison has taken place, a certain ' time must elapse before the 
symptoms of the disease appear. The length of this time, the " stage of incuba- 
tion," is, unlike that of many other infectious diseases, not perfectly definite. On 
the average, it lasts two to three weeks, sometimes less time, sometimes longer. 
During this period the patient either feels perfectly well, or has certain slight 
symptoms, to which he pays more or less attention, according to his individual 
susceptibility. These prodromata consist of languor, disinclination to exertion, 
anorexia, slight headache, pain in the limbs, etc. Often they last only a few days. 
Not infrequently the patients state afterward that they had felt the disease coming 
on for weeks. 

The transition of the prodromata into the regular disease takes place sometimes 
so gradually that it is utterly impossible to take any one day as the first of the 
illness, in order to reckon from it its duration. It is usually, however, the first 
symptoms of a high temperature, chilliness, feverishness, and the accompanying 
increase in general discomfort, which allow one to fix, with at least some accuracy, 
the beginning of the disease. A decided initial rigor is certainly exceptional.* 
After the fever begins, most patients soon take to their beds, although it happens 



* According to the representations of many authors, a marked initial rigor seems to occur rather 
often in some places. With us in Leipsic it is very rare. 



TYPHOID FEVER. 



5 



often enough that the sick feel either unable or unwilling" to give up, and keep on 
at work for days ! 

There have been manifold attempts to divide the whole course of the disease into 
separate periods. The most natural division seems to be into the three stages of 
development, height or fastigium, and decline {stadium increment!, s. acmes, s. 
decrementi). Usually, however, physicians reckon according to the week of the 
disease. The first week corresponds to the developmental stage, the second, and 
in all severer cases the third as well, to the fastigium, the fourth (in light cases 
the third) to the decline. The course of the disease is very variable, however, and 
naturally there is the greatest diversity in the departures from this general plan. 

In the first week, the initial period, the general symptoms augment rapidly. 
The patients become, in severe cases, very languid and feeble, have generally an 
intense headache, and complete anorexia, with great thirst. The fever, which is 
all the time gradually rising, is recognizable subjectively by alternating sensations 
of heat and cold, and objectively by the hot, dry skin, the parched lips, and the 
dry and coated tongue. The sleep is disturbed. For the most part there are no 
prominent thoracic or abdominal" symptoms, except that at times there is a sense of 
oppression in the chest, or some cough. The pulse is quickened, sometimes even 
now dicrotic. There is often a temporary epistaxis. The belly is not much 
swollen as a rule, and but little if at all tender. There is generally constipation. 
Usually the spleen, even at this time, exhibits a swelling that can be easily 
demonstrated. 

Generally the fastigium has begun before the end of the first week. The 
severe general symptoms persist or even increase. The fever maintains constant- 
ly a considerable elevation. The patients become more stupid. Often delirium 
appears, especially at night. In the lungs there is developed a more or less 
intense and extensive bronchitis. The abdomen becomes more swollen. On the 
skin of the trunk appear, generally at the beginning of the second week, a number 
of small, pale-red spots, roseolse. Instead of constipation, there is a moderate 
diarrhoea. There are daily about two to four soft, thin, bright-yellow dejections. 

The third week, during which in the severe cases the symptoms already men- 
tioned persist, is the chief time of the numerous complications and of especial 
clinical events about which we shall speak below at length. If the disease takes 
a favorable course, there comes at the end of the third week a decline of the 
fever ; and then the general symptoms also improve as a rule. The mind be- 
comes clearer, the patient sleeps better, and gains some appetite. The pulmonary 
and digestive symptoms abate, and convalescence gradually begins. 

This short sketch of the course of the disease corresponds to most of the cases of 
medium severity. There are, however, besides these, so many forms and so many 
variations from the usual picture, that it seems almost impossible to enumerate 
completely all the events of typhoid fever. And, besides, the separate epidemics 
vary in their general character according to the time and place of their occur- 
rence. In many epidemics the cases run a peculiar course and have certain special 
complications not seen in others. 

We will begin the presentation of the chief peculiarities by speaking of the 
course of the fever. 

Course of the Fever. — Observation of the temperature in typhoid is so abso- 
lutely essential for the estimation of each individual case that no scientific physi- 
cian ought to treat a case without regular measurement of the temperature. The 
measurements should be taken, if possible, in the rectum. Their frequency must 
of course be modified by circumstances, but it will probably be possible to have two 
to four measurements daily. At night, especially if the patients are asleep, it is 
generally not requisite to take the temperature. A general idea of the course of 



6 



ACUTE GENERAL INFECTIOUS DISEASES. 



the fever can be gained only by representing the separate measurements graphic- 
ally in a continuous "temperature curve." 

The typical curve of typhoid fever (see Fig. 1) falls naturally into three or four 

divisions. The first division is the 
initial period, or the pyrogenetic stage, 
and is seldom observed, since at this 
time the patients are generally not 
yet under the doctor's care. The ini- 
tial period of the fever lasts, as a 
rule, some three or four days, seldom 
longer ; and during this time the tem- 
perature rises, generally by gradual 
steps, so that the morning as well as 
the evening temperature is each day 
2° or 3° (l°-l-5° C.) higher than on the 
day before. A sudden and consider- 
able rise of temperature, such as occurs 
in many other diseases, is very rarely 
seen in the beginning of typhoid fever. 

The second division of the curve 
represents the so-called fastigium, and 
corresponds to the height of the dis- 
ease. During this time the fever pre- 
sents, in most of the severer cases, the 
general character of "febris contin- 
ua " — i. e., the spontaneous remissions 
of the fever seldom exceed 2° (1° C). 
Almost always the lower temperatures 
come in the morning hours and the 
higher in the evening. In cases of 
average severity the morning remis- 
sions touch 102°-103° (39°-39'5° C), 
and the evening exacerbations 104°- 
105° (40°-40-5° C). Temperatures 
which reach or exceed 106° (41° C.) 
are seen only in very severe cases. 
Considerable morning remissions are 
always a favorable symptom, while 
morning temperatures of 104° (40° C.) 
or higher generally show the case to 
be severe. The duration of the fas- 
tigium varies with the severity and 
obstinacy of the case. It may last 
only a few days or one and a half to 
two weeks; in violent cases longer 
yet. 

In many cases of slight or average 
severity the period of decline follows 
directly on the fastigium ; but in 
severe cases there frequently inter- 
venes another stage, which Wunder- 
lich has graphically named the "ambiguous" period. The temperature curve 
becomes irregular and more variable. The morning remissions may be great, 




TYPHOID FEVEE. 



7 



even reaching the normal, while the evening temperatures are often still very 
high. This stage has accordingly been termed the "period of the steep curves." 
It may be said that in general the longer a case of typhoid lasts the more irreg- 
ular will be the course of the fever. 

The last stage — i. e. , in cases of slight or average severity the third stage, and 
in severe cases commonly the fourth — is the period of defervescence or recovery. 
The peculiarity of this period in typhoid fever is that the fall of the fever is never 
by crisis, but always gradually, by lysis. Commonly the temperature descends by 
degrees, so that on each new day the morning remissions as well as the evening 
exacerbations are 1° to 2° (0*5°-l° C.) lower. The zigzag form of curve, in which 
there are of course very frequently slight irregularities, must be taken as the rule. 
The duration of the defervescence generally exceeds that of the initial period. 
It lasts five to eight days, often longer. It is not very seldom that in defervescence 
the morning remissions become from the first very marked, even reaching the 
normal temperature, while the evening exacerbations become daily less and less, 
until they too are not above the normal. A third form of decline is much less 
frequent, in which the morning remissions become every day greater, while the 
evening temperature persists for some days at about the same height. Several 
times we have seen the fever take on a tertian type during recovery. 

To this outline must be added a number of observations of practical importance. 

The initial period does not exhibit especial variations from the course we have 
stated. Its entire duration is bounded by certain relatively narrow limits. 

The fastigium presents, as already mentioned, the greatest varieties in its dura- 
tion. In light cases it is wholly wanting, so that these consist only of a period of 
gradually rising fever, and of a gradual defervescence almost immediately con- 
secutive to the rise. The entire duration of such light cases is only one and a half 
to two weeks. In other and tolerably frequent cases, which are often tedious, but 
still for the most part are light, the fever is not continuous, but remittent. We 
have seen in Leipsic, notably in the autumn epidemic of 1878, a number of cases 
where the fever was even perfectly intermittent during almost the entire illness, 
and where for two to three weeks afternoon elevations reaching 104° (40° C.) or 
more daily succeeded normal morning temperatures. These cases had the general 
course of light attacks. 

Various influences, not to speak of therapeutic interference, may produce a 
considerable temporary remission of temperature in the course of the fastigium. 
Such a remission sometimes occurs spontaneously on the seventh to tenth day of 
the disease. If a marked intestinal haemorrhage occurs {vide infra), the tempera- 
ture generally falls several degrees centigrade, and the less frequent instances of 
severe epistaxis have the same effect. If, in female patients, abortion or prema- 
ture delivery occurs, we often observe a similar considerable fall of temperature, 
even without severe attendant haemorrhage. Perforation of the intestine often 
causes the temperature to fall rapidly. At times the occurrence of mental dis- 
turbances effects a moderate though noticeable lowering of temperature. Those 
great and sudden depressions of temperature remain to be mentioned which are 
accompanied by a very small but exceedingly rapid pulse and general prostration. 
Every such collapse, if severe, is a most dangerous event, and demands prompt 
and energetic medical treatment {vide infra). 

The occurrence of local complications, such as pneumonia or inflammation of 
the parotid gland, is generally accompanied by a considerable rise of temperature. 
The fever in such cases often becomes more irregular. 

The period of defervescence departs most frequently from its typical behavior 
by being lengthened out into a " stage of retardation. " The morning temperature 
is then generally normal, while in the evening slight or moderate elevations con- 



8 



ACUTE GENERAL INFECTIOUS DISEASES. 



tinue. The reason for this long continuance of the fever may frequently be found 
in some not yet completely healed local complication, but often no such lesion 
can be demonstrated. Then we are commonly inclined to surmise sluggish intes- 
tinal ulcers which will not heal, or trouble in the mesenteric glands, etc. This 
sluggish fever may continue for weeks. It is prone to follow severe cases, but 
lighter attacks, especially in elderly or feeble patients, may also take on this slug- 
gish character at a relatively early period. 

Entrance into complete convalescence is shown with far greater certainty by 
the absence of elevations of temperature than by any other single symptom. 
There sometimes come, however, temporary elevations of temperature during con- 
valescence, following some error in diet, long-continued constipation, or mental 
excitement. In other cases the new fever depends on some local sequela, e. g., a 
boil or a glandular abscess. Often, however, the most accurate investigation fails 
to demonstrate a cause. Especially in the beginning of convalescence there some- 
times comes a high fever, or even a rigor, which may recur several times, but 
soon gives place to a normal temperature. Generally no certain cause for these 
brief but decided elevations of temperature can be pointed out. Perhaps we might 
consider the possibility of some affection of the mesenteric lymph-glands. These 
sudden and great elevations have seldom any grave significance. 

This new fever which we have just .described is best termed recurrent fever- 
attack, in contrast with the proper typhoid relapse. That is, after typhoid fever 
has ended, the whole process may be repeated ; and this occurrence is called a 
relapse. Particulars as to the behavior of the fever in such cases will be consid- 
ered below in connection with all the other peculiarities of typhoid relapses. 

Phenomena and Complications relating to the Separate Organs.* 

1. Digestive Organs. — We think it best to begin our consideration of the more 
special symptoms with the phenomena referable to the intestinal canal, for the 
reason that the anatomical changes in the intestine are pathognomonic. Indeed, 
these alterations may sometimes become of surpassing import in a clinical point 
of view, although in the majority of cases the intestinal symptoms are clinically 
not nearly so prominent as the general symptoms that result from the infection 
of the system as a whole. 

The characteristic typhoid lesion of the intestine consists of an affection of 
Peyer's patches, most marked in the lower part of the ileum. In the first week 
the patches swell gradually (stage of medullary in filtration). The rest of the 
mucous membrane exhibits at the same time more or less marked symptoms of 
simple catarrhal inflammation. In the second week, necrotic crusts form on the 
surface of the patches, which are cast off in the third week, leaving behind the 
typhoid ulcers. Toward the end of the third week the ulcers clean up, and then 
in the fourth week, if the case takes a favorable course, the ulcers heal. Smooth 
scars are formed, often diffusely pigmented. Experience shows that these scarcely 
ever lead to stricture of the intestine. The same process also goes on in a greater 
or less number of the solitary follicles as well as in the Peyer's patches themselves. 
We may add that probably in lighter cases of typhoid {vide infra) there is often 
no actual ulceration. The swelling of the lymphatic tissue subsides in this case 
before sloughing occurs. We have already stated all that is essential with regard 
to the characteristic typhoid bacilli. 

The number and severity of the ulcers formed have no direct relation whatever 
to the severity of the case. Although very extensive lesions in the intestine are 



* To avoid repetition, we have in what follows united a description of the anatomical changes with 
the presentation of the clinical symptoms. 



TYPHOID FEVER. 



9 



often found in cases that end fatally, yet, on the other hand, we observe fatal 
cases in which only a few ulcers are found in the intestine. In cases with exten- 
sive intestinal lesions we often see follicular ulcers in the colon as well as in the 
small intestine (colo-typhoid). 

The clinical symptoms referable to the intestinal canal are, as we have said, 
prominent only in exceptional cases. In the beginning of typhoid fever there is 
usually constipation. This may last throughout the illness, so that the patients 
have but one dejection in every two or three days, or often none at all unless an 
enema be given. As a rule, a moderate diarrhoea begins during the second week. 
There are two to four stools, or sometimes more, each day. They usually have 
a characteristic bright-yellow color. On standing, they divide into an upper, 
cloudy, . and quite liquid layer, and a lower layer composed of yellow, crumby 
masses. They have generally an alkaline reaction, and we often find in them 
with the microscope numerous crystals of triple phosphate. 

Severe diarrhoea (ten to twenty stools daily) is relatively infrequent. In some 
severe cases we have seen the stools take on a dysenteric character. The autopsy 
showed in these cases unusually severe lesions of the colon and a diphtheritic 
inflammation of its mucous membrane. 

Gaseous distention affecting the intestine, and especially the colon, is very 
frequent, but in most cases is not excessive. Indeed, severe cases of typhoid are 
observed in which the abdomen always remains concave. Marked tympanites is 
always an unpleasant complication. We saw one case, which ended fatally, with 
very great tympanites, in which the lesions were almost exclusively in the colon, 
and it was the enormous distention of its entire length which had so swollen 
the abdomen. The noise that can often be produced by pressure in the ileo-caecal 
region (gurgling) used to be regarded, but probably erroneously, as especially 
characteristic of typhoid fever. Abdominal pain is often entirely absent. Some 
patients, however, complain of abdominal pain during almost the entire illness. 
On pressure, the belly is generally somewhat sensitive, but the tenderness is sel- 
dom extreme. It is more apt to be marked when there is constipation. Often 
such tenderness is due to a participation of the peritoneum in the disease, even 
when there is no perforation (vide infra). 

There still remain two symptoms of the greatest practical importance, both of 
which have a direct connection with the intestinal lesions. They are intestinal 
haemorrhage and perforation. 

Intestinal haemorrhages in the course of typhoid are almost always due to the 
erosion of the walls of blood-vessels in connection with the formation and throw- 
ing off of the crusts of the ulcers. The haemorrhages occur, therefore, most fre- 
quently toward the end of the second and during the third week. The blood pours 
out into the intestine, and is passed with the stools. It may amount to one or two 
pints, or even more. Its color is generally rather dark. The later discharges are 
generally tarry. Liebermeister states that he has observed intestinal haemor- 
rhages in 7'3 per cent, of typhoid patients, and Griesinger in 5*3 per cent. We 
have ourselves seen, in the last few years, in the medical clinique at Leipsic, 45 in- 
testinal haemorrhages in 472 cases, i. e., in 9'5 per cent. In individual epidemics 
the frequency varies greatly. It rose in 1880 to eighteen per cent. 

Intestinal haemorrhage is always a grave symptom. Even slight haemorrhages 
deserve consideration, for they may be the precursors of severer ones. And yet 
intestinal haemorrhage, even if profuse, is not necessarily fatal. Of the above 
forty-five cases of typhoid with haemorrhage, twenty-six ended in complete recov- 
ery. In eight cases, death occurred as the immediate result of the loss of blood. 
Eleven ended fatally after a time. 

After every considerable intestinal haemorrhage, the symptoms of general 



10 



ACUTE GENEEAL INFECTIOUS DISEASES. 



anaemia, often even of collapse, appear. The fall of the bodily temperature has 
been already mentioned. The haemorrhage has sometimes a favorable influence 
on severe cerebral symptoms, for consciousness succeeds to the previous stupor 
or delirium. Often the haemorrhage is directly followed by recovery from the 
disease. 

Much more ominous than the intestinal haemorrhage is the occurrence of per- 
foration, as a result of the breaking through of a typhoid ulcer into the abdominal 
cavity, because, almost without exception, this is followed by a purulent or even 
ichorous peritonitis. The occurrence of perforation is sometimes marked by a vio- 
lent pain suddenly felt by the patient ; but it may also, even in severe cases, take 
place insidiously. The abdomen is generally (not always) greatly distended and 
very tender on pressure, so that even in stupor patients groan while being exam- 
ined. If gas has entered through the opening into the peritoneal cavity, we often 
observe absence of the ordinary dullness over the liver ; but this symptom is to 
be employed cautiously as a factor in diagnosis, for absence of hepatic dullness 
may also result from distended intestines lying in front of the liver. When per- 
foration has occurred, the patient soon looks collapsed, with cheeks fallen in and 
sharp, cool nose. Frequent eructations and vomiting often follow. The pulse 
becomes small and very frequent. The temperature generally falls as the peri- 
tonitis begins, and later it usually undergoes great variations. 

Perforation of the intestine occurs most frequently in the third or fourth week 
of the disease. In sluggish cases, however, we can not be without apprehensions 
of it till a late period. The perforation generally takes place in a coil of the lower 
part of the small intestine, and with marked relative frequency in the right side 
of the pelvis — seldom in the vermiform appendix or in the colon. With few 
exceptions, death comes quickly, after a few days at latest. Out of fifty-six fatal 
typhoid cases in the Leipsic medical clinique we lost* five, or nine per cent., from 
peritonitis following perforation. Here and there a case of recovery has been 
reported, probably resulting from a limitation of the peritonitis through speedy 
adhesion of the intestines. 

It should be mentioned here that sometimes in typhoid fever a local or general 
peritonitis may occur through direct extension of the process to the serous mem- 
brane without actual perforation. We have seen in one case, as a result of the 
peritonitic bands and false membranes, complete occlusion of the intestine (ileus), 
and death. 

Swelling of the mesenteric lymph-glands (less often of the retro-peritoneal 
glands as well) is found in typhoid almost as constantly as the anatomical changes 
in the intestine. Sometimes they break down, i. e., suppurate. In cases that have 
passed through the disease we often find considerable deposits of lime in the 
glands. These changes have a certain clinical importance ; for, as already men- 
tioned, we may often venture to refer a more or less tedious recurrent febrile state 
which has no other demonstrable cause to this lesion of the mesenteric glands. 
In some rare cases a general peritonitis has been observed as a result of the burst- 
ing of a suppurating gland. 

The swelling of the spleen (acute splenic tumor) is, in typhoid fever as well as 
in many other acute infectious diseases, one of the most constant symptoms. The 
enlargement of the spleen can often be demonstrated as early as the end of the 
first week, and is therefore of considerable diagnostic importance ;* but percussion 
of the spleen is sometimes decidedly difficult and deceptive in this disease because 
of the existence of tympanites. The surest demonstration of splenic enlargement 
is therefore always by means of palpation, which, after a little practice, gives a 
positive result in the majority of cases. Absence of splenic tumor is most fre- 
quently observed in elderly typhoid patients. The spleen may also diminish con- 



TYPHOID FEVER. 



11 



siderably in size after severe intestinal haemorrhage. Pain in the splenic region, 
resulting from tearing of the distended capsule, is comparatively rare. The splenic 
infarctions which sometimes occur may, in exceptional cases, prove the starting- 
point of a peritonitis. 

Hepatic symptoms are seldom seen in typhoid fever. The anatomical changes 
of "parenchymatous degeneration," and the frequent formation in the liver of 
the small lymphomata which Wagner discovered, have no clinical significance. 
The bile secreted is generally pale and scanty. This is a partial explanation of the 
light color of the stools. A very rare complication, which we ourselves observed 
in one case, is acute yellow atrophy of the liver. 

The stomach presents no especial anatomical changes in typhoid. Anorexia 
is an almost invariable symptom in the beginning and during the course of all 
severer cases. There is seldom any desire for food till recovery begins ; but then, 
if convalescence is undisturbed, the appetite soon attains an enviable keenness. 
Vomiting in the beginning or course of the disease is an exception, unless after 
some error in diet. We have already mentioned it as a symptom of peritonitis. 

The changes in the mouth and throat of typhoid patients deserve the careful 
attention of the physician. The lips and tongue are in severe cases dry and fis- 
sured. The lips are often covered with dry, black crusts, sometimes described as 
a "fuliginous coating." The tongue is apt to be thickly coated at first, but later 
cleans off from the edges and tip. In severe cases, especially if the mouth is not 
properly cleansed, a rather severe stomatitis may occur and produce superficial 
ulceration of the buccal mucous membrane and of the edges of the tongue. The 
gums sometimes become spongy, and are apt to bleed, as if scorbutic. 

Actual sore throat, at least with us in Leipsic, occurs but seldom at the begin- 
ning of typhoid fever. The difficulty in swallowing, often complained of by 
patients, is generally due to dryness of the pharynx. In certain epidemics, how- 
ever, the occurrence of sore throat at the beginning of the illness has been fre- 
quently observed. It may even happen that this early sore throat is accompanied 
by an erythema diffused over the body, so that at first suspicions of scarlet fever 
arise. In rare cases (so-called tonsillo-typhoid or pharyngo-typhoid) there are 
seen upon the tonsils peculiar whitish elevations, which later ulcerate. These are 
probably to be regarded as a specific typhoid lesion of the tonsils. It should also 
be mentioned that in severe cases there is often an extensive growth of thrush in 
the mouth and throat, and this may spread quite a distance down the oesophagus. 

The changes in the mouth and throat are of especial interest, for the reason 
that they may be directly propagated to important neighboring organs. Starting 
from the pharyngeal cavity, the pathogenetic agent may penetrate through the 
Eustachian tube into the middle ear. Thus arise those inflammations of the 
middle ear which are not very rare in severe cases of typhoid, and which lead to 
perforation of the membrana tympani and to purulent discharges from the ear. 
The not infrequent inflammation of the parotid gland is also, as we believe, occa- 
sioned in a similar way, the inflammatory agent reaching the parotid gland from 
the mouth by way of Steno's duct. We do not regard the otitis and parotitis as 
especial localizations of the typhoid poison, but as genuine complications (second- 
ary disease), for the occurrence of which typhoid fever merely furnishes the 
occasion, as when the mouth is imperfectly cleansed. The parotitis appears most 
frequently in the third week, and generally on one side, though sometimes on 
both. It almost always becomes purulent and discharges either externally or into 
the external auditory meatus, unless there is a timely incision. 

2. Organs of Respiration. — Affections of the lungs are among the most frequent 
and important complications of typhoid fever, but are for the most part not a 
direct result of the typhoid infection. The bronchitis very often found in severe 



12 



ACUTE GENERAL INFECTIOUS DISEASES. 



cases, and especially in patients who do not come till late under proper care, cer- 
tainly is chiefly dependent on the imperfect expectoration of the bronchial secre- 
tions and on the inhalation of inflammatory agents coming from the mouth and 
throat. 

Numerous cases of typhoid of slight or average severity, under proper care, 
run their course without any demonstrable bronchitis. In many other cases, and 
even severe ones, the bronchitis remains within moderate bounds, especially if the 
patient is brought promptly under proper care and treatment ; but in severe 
cases, where marked disturbances of the nervous system arise, and the patient in 
his stupor expectorates little, swallows things the wrong way, and lies all the 
time on his back, passive and collapsed, the occurrence of a severe, diffuse 
bronchitis, especially in the lower lobes of the lungs, can hardly be avoided. Nor 
in such cases is there generally a mere bronchitis, but a more or less extensive 
catarrhal, lobular pneumonia, to be classed therefore under the so-called inhala- 
tion pneumonias (cf. chapter on lobular pneumonia). What was formerly termed 
" hypostatic pneumonia " is also almost invariably to be put in this group. 

From the way in which these pulmonary disorders arise, we can understand 
why the bronchitis sometimes takes on a putrid character, and why the lobular in- 
filtrations are, in severe cases, transformed into genuine gangrene. If such spots 
touch the pleura, they occasion the development of a pleurisy which is almost 
always purulent. In rare cases, pneumothorax may arise as a sequel to the per- 
foration of a gangrenous infiltration into the pleural cavity. Various circum- 
stances promote the occurrence of pulmonary symptoms. Thus we find it espe- 
cially easy for a severe bronchitis and its sequelae to be developed, in the case of 
elderly persons, or the kyphoskoliotic, or the corpulent, or patients who have 
previously suffered from emphysema or cardiac disease. 

The subjective thoracic symptoms, in typhoid patients who have pulmonary 
complications, are generally not very prominent. It is only occasionally that 
patients complain in the early stages of typhoid fever of pain, and of a sense of 
oppression in the chest, or of cough, or of a stitch in the side ; and even when 
such symptoms exist, the physical examination may give comparatively insignifi- 
cant results. The severer pulmonary complications are seen mainly in those 
whose intelligence is more or less blunted, and who, therefore, make little com- 
plaint, are not much disturbed by the dyspnoea, and cough and expectorate little. 
A careful physical examination alone can enlighten us as to their condition. On 
auscultation, sibilant rhonchi are the chief signs observed in the milder cases. In 
the severer ones there are moist, fine, and coarse rales, especially numerous 
toward the base of the chest. If there are abundant moist rales, we may infer 
that there is a lobular pneumonia, although this can not be demonstrated with 
certainty till the separate islets of infiltration unite into a more extensive solidifi- 
cation, so as to afford dullness on percussion. 

In addition to the pulmonary lesions already mentioned, genuine croupous or 
lobar pneumonia does occur in typhoid fever. Probably this must be regarded as 
a direct result (localization) of the typhoid poison, although the croupous pneu- 
monia is not anatomically distinguishable from the common, genuine pneumonia. 
It often appears as early as the second week, and attacks the lower as well as the 
upper lobes. Liebermeister states that he has sometimes observed it during con- 
valescence. In cases where the pneumonia comes on early, the diagnosis between 
typhoid and primary lung-fever may be very difficult. If in such a case there is 
an actual attack of typhoid fever, of which the pneumonia is to be regarded as 
the most prominent early localization, we may speak of it as pneumo-typhoid.* 

* See what is said in the chapter on croupous pneumonia about "pneumo-typhoid" and "typhoid 
pneumonia." 



TYPHOID FEVER. 



13 



Laryngeal Lesions. — The same causes which produce the bronchitis result also 
in a simple catarrhal laryngitis, with hoarseness. This is in severe cases accom- 
panied by superficial ulcers on the vocal cords or the posterior wall of the larynx. 
The disorders which attack the less superficial structures of the larynx are fortu- 
nately rare. Chief among them is a laryngeal perichondritis of the arytenoid 
cartilages. This complication is justly regarded as of bad omen, and may lead to 
the rapid development of oedema of the glottis, with great laryngeal obstruction 
and threatening suffocation. These severe laryngeal affections in typhoid are 
regarded by some authorities, especially by Klebs, as always the direct effect of 
the infecting poison. We have several times seen laryngeal croup in typhoid 
fever, and it is a very dangerous symptom. We are inclined, however, to the 
belief that it was in every case a secondary disease. 

Among symptoms referable to the mucous membrane of the nose, epistaxis is 
important. It occurs in the beginning of typhoid with tolerable frequency, and 
is in one way not unfavorable, for it often mitigates the patient's headache. At a 
later period nose-bleed may become a very unpleasant complication, as it is some- 
times very difficult to check. We have even seen one fatal case due to persistent 
nose-bleed. Other nasal symptoms are exceptional. There is even an old saying 
that typhoid never begins with a coryza. 

3. Nervous System. — The old term "nervous fever," which is still used by the 
laity, shows how frequent and severe are the nervous derangements which occur 
in typhoid. In cases of any severity there is almost always a certain dullness of 
intellect, often amounting to apathy and somnolence. The patients give mono- 
syllabic and incomplete answers to all questions, and their statements about 
their previous history are often disordered and contradictory. There may even 
be sopor or a deep coma in the worst cases. All cases of this sort in which 
there was a condition of intellectual enfeeblement were termed by the old 
physicians "febris nervosa stupida" in contrast to the " febris nervosa ver- 
satilis^ that form in which abnormal mental activity or delirium predominates. 
In severe cases delirium is very frequent. It is generally worst at night, and at 
times when the patient happens to be left alone. Very often he tries to leave his 
bed, because of his delusions, and talks of persons and things with which he was 
formerly familiar; or he is very noisy and restless, sometimes shrieking from 
groundless fears. We may add that these diverse nervous symptoms frequently 
succeed each other, or appear in combination. Sometimes a soporose patient may 
be heard softly whispering to himself in "muttering delirium." 

Certain motor disturbances are often combined with considerable impairment 
of consciousness. There is a slight twitching of the muscles of the face and ex- 
tremities. The old authorities gave the name subsultus tendinum to the sudden 
leaping into prominence of the sinews thus caused. It is best seen on the back 
of the hands. In severe cases the patient is sometimes observed to grind the teeth 
together ; this is due to a cramp-like condition of the muscles of mastication, and 
is justly regarded as ominous. We often see persistent tremor of the extremities 
and lower jaw; and it is especially in these cases, as we have demonstrated upon 
numerous patients, that the tendon reflexes and the mechanical excitability of the 
muscles are much increased. If deep coma comes on, the muscles become lax, 
the motions of the eye are not co-ordinated, and reflex excitability diminishes, or 
is wholly extinguished. 

Headache is one of the most constant symptoms in the beginning of the dis- 
ease. It is usually referred to the forehead or temples. The pain may be very 
violent, and sometimes takes on almost a neuralgic character. It almost always 
subsides in the second week. 

If we seek the cause of these nervous symptoms, which are often so severe, we 



ACUTE GENERAL INFECTIOUS DISEASES. 



find that the anatomical changes in the nervous system, including the brain, bear 
no relation whatever to the severity of the symptoms observed during life. We 
sometimes meet with minute haemorrhages in the cerebral meninges, or meningeal 
opacity or oedema, or a moist condition of the cerebral parenchyma ; but the con- 
nection of these and similar changes with the symptoms of the disease is often 
more than doubtful. Nor can the microscopic alterations in the brain, which 
have been reported, be regarded as important and authoritative. It is only in 
very rare cases that large cerebral haemorrhages or purulent meningitis have 
been found. As to this last, we should always be very cautious in making a diag- 
nosis, as symptoms which would seem to be most conclusively meningeal — such as 
stiffness of the neck, rigidity of the whole spinal column, and occipital headache — 
may appear in typhoid patients, and yet the autopsy show no trace of meningitis. 

One theory, which has Liebermeister for its chief supporter, and which has 
won a tolerably wide-spread acceptance among physicians, is that the nervous 
symptoms are chiefly a direct result of the febrile temperature. It is impossible, 
however, for us to regard this view as universally true. The unprejudiced con- 
sideration of a large number of personal observations prevents it. Although it is 
undeniable that elevated temperature has a harmful influence on the nervous sys- 
tem, yet in numerous cases there is no relation between the height of the fever 
and the severity of the nervous derangements. There are cases in which the fever 
remains continuously high for days, while the patient feels perfectly comfortable 
and presents no symptoms of any important cerebral disturbance. The opposite 
class of cases is still more numerous, in which from the very start there is always 
a low temperature, and, notwithstanding, the most severe nervous symptoms 
arise. Frantzel has lately published very striking cases of this sort. 

It follows that we must seek for some other special cause of the severe nerv- 
ous symptoms. This can be found only in the specific typhoid infection. The 
severity or mildness of the cerebral symptoms in each case will correspond com- 
pletely to the varying intensity of all the other effects of the typhoid poison. As 
to the exact way in which the typhoid infection causes the symptoms we are dis- 
cussing, we have as yet little information. There seems to be constantly increas- 
ing evidence in favor of the theory that certain substances similar to the alkaloids 
are formed, as a result of the chemical processes inseparable from the life of all 
organized infectious agents ; and that these have a pronounced toxic action. This 
view is especially supported by the fact which Bouchard, Lepine, and others dis- 
covered, that the urine in typhoid fever, as well as in other infectious diseases, 
contains certain alkaloids possessing very pronounced poisonous properties. If 
such substances appear in the urine, we must conclude that they are formed in the 
body — perhaps in the intestine (?) or in the blood. According to this idea, the 
infection of the system is followed by intoxication. We may add that in certain 
cases an especial predisposition of the patient to severe nervous disturbances may 
be assumed to exist. This is especially true of hard drinkers, and of persons who 
have had a period of great mental excitement just before their illness. 

Actual insanity is not very infrequent during the course of typhoid, or in con- 
valescence. It generally takes the form of melancholia. We have repeatedly 
seen patients in such a state that they would lie almost motionless in bed, with 
eyes open, and perhaps assert that they were dead ! In other cases there is 
mental excitement, sometimes combined with hallucinations, or there is confu- 
sion of ideas. In one case, in a girl who was evidently predisposed to nervous dis- 
orders, we saw typical hysterical insanity break out during the fever. Sometimes 
the mental excitement at the beginning of a relapse terminates in actual insanity. 
Few of the psychoses which arise during or at the end of typhoid outlast con- 
valescence. 



TYPHOID FEVER. 



15 



We have still to mention a number of nervous diseases that develop in the 
course of typhoid or after its decline. Neuralgia is sometimes seen, as well at the 
beginning as at the end of the disease. It is most frequent in the regions supplied 
by the trigeminus and the occipital nerves. Great hyperesthesia of the skin 
and muscles is not rare during convalescence. It attacks the lower extremi- 
ties by preference. Paralysis of single muscles (e. g., of the serratus magnus), or 
paralysis of a single extremity, has been repeatedly observed as a sequela. The 
paralysis is generally of the atrophic variety, and is probably, as a rule, due to 
neuritis. Ataxia and spastic paralysis of the lower extremities are rare sequelae. 

4. Circulatory System. — Disturbances of the heart such as to produce striking 
anatomical changes are very rare. Endocarditis and pericarditis are, however, 
possible. The slight mitral endocarditis sometimes found at the autopsy has no 
clinical significance. On the other hand, great weight is laid by some authors 
upon the parenchymatous or fatty degeneration of the heart. They say it is often 
the cause of cardiac failure. We can not admit this, for experience shows that 
the two do not stand in any constant relation to each other. 

The pulse is almost always rapid, although often not so much so as the height 
of the temperature might lead one to expect. It averages from 90 to 110, and 
often more. When it keeps at 140 or higher, in adults, it is always an unfavorable 
symptom. This abnormal frequency is often in part due to the high temperature ; 
but there are other factors. Temperature and pulse do not correspond in all cases. 
Sometimes the pulse will have a normal or even subnormal frequency throughout 
the entire attack, despite the fever. Temporary accelerations are easily produced 
by mental excitement or bodily exertion, as by sitting up in bed. In convalescence 
the rate is frequently subnormal. 

Slight irregularities of the pulse are not rare, either in the acme or the decline 
of typhoid. Marked irregularity is always a grave symptom, although in many 
cases it passes off and the patient recovers. 

Dicrotism is so frequent that many elderly physicians still regard it as charac- 
teristic of the disease. It is often, however, equally marked in other acute dis- 
eases. Its cause is diminished arterial tension. 

The diminished cardiac activity may result in venous thrombosis, especially 
in the lower extremities. This sometimes causes swelling of one of the lower 
extremities during convalescence. The swollen member generally regains its 
normal size after some weeks. In other cases the thrombosis occurs earlier, and 
in patients who are still too vigorous to suffer from cardiac weakness, so that we 
are forced to the conclusion that there is some local specific cause. A possible, but 
fortunately infrequent, result of these thrombi in the lower limbs is pulmonary 
embolism and sudden death. 

In severe cases, which end in death, cardiac thrombi are sometimes found, 
with emboli in the lungs, spleen, kidneys, or other organs. 

(Edema of the ankles and legs is very often seen in convalescents, especially 
when they first get out of bed. It is due to the weakness of the heart and the 
imperfect circulation of the blood. Once we saw a general dropsy develop at the 
end of a severe attack in a girl of fourteen. The autopsy disclosed no other 
possible cause for it than the extreme atrophy and flabbiness of the heart. 

5. Skin. — The eruption seen in typhoid fever is characteristic. The rose-spots 
appear at the beginning of the second week, usually on the trunk, and chiefly on 
the abdomen. The number varies greatly. Rarely they are entirely absent, 
especially in elderly persons. Sometimes they are very abundant and extend 
to the thighs, the arms, and even to the neck and face. Often they vanish after a 
few days, but they may persist much longer. In the latter case they may become 
to a very slight degree petechial, so that they will not entirely disappear on press- 



16 



ACUTE GENEEAL INFECTIOUS DISEASES. 



ure. They often occur in successive crops. "We have even seen several cases 
where new rose-spots kept coming for some days after the fever had disappeared. 

As to other cutaneous eruptions, we may mention first of all that herpes la- 
bialis is so rare in typhoid that in cases of doubtful diagnosis it is a factor in 
excluding that disease. Miliaria, urticaria, and superficial pustules are some- 
times observed. Sometimes little bluish spots appear, especially on the trunk. 
These used to be called " taches bleudtres " (pelioma typhosum) ; but later observa- 
tions show that they are not connected with typhoid fever particularly. They are 
due to pediculi. We might use the term pelioma typhosum to designate the kind 
of vesicles which we have repeatedly seen on the abdomen in severe cases. They 
are about the size of peas, and have sero-haemorrhagic contents. Boils and super- 
ficial abscesses are frequent, especially as disagreeable sequelae in convalescence 
from severe cases. There are often abscesses of the sweat-glands in the skin of 
the axilla during convalescence. Extensive ecchymoses are very rare, and are 
symptomatic of a general haemorrhagic diathesis. Petechiae are frequent during 
recovery. They are generally seen in the follicles of the skin below the knee. 
There have been a few cases of gangrene in the lower extremities, especially in the 
toes. We saw in one patient an extensive gangrene of the skin of the abdomen. 
Its cause could not be determined. 

Finally, we must mention that bed-sores are prone to develop in severe or 
neglected cases. The localities most often attacked are the nates, the furrow 
between them, and the heels. A bed-sore may be so extensive, and accompanied 
by such undermining of the skin, as to be a dangerous or even fatal complication. 

The epidermis often scales off to a considerable extent during convalescence 
after a severe attack of typhoid. Everybody knows how the hair falls out after 
the fever. The nails also are not infrequently affected. 

6. Muscles, Bones, Joints. — Zenker has discovered a degeneration of the volun- 
tary muscles which occurs in typhoid as well as in' other severe diseases. It is 
called the " granular " or " waxy " degeneration. Whether it has clinical symp- 
toms can not be determined. Perhaps it may explain the great muscular hyper- 
esthesia which is often observed, and the muscular pains, which may be very 
severe. Severe cases sometimes have haemorrhages into the muscles, particularly 
the rectus abdominis. 

Lesions of the bones and joints occur but seldom. We have seen periostitis of 
the tibia, and of a rib, during convalescence. Swelling of the joints is equally rare. 

7. Genito-urinary Apparatus.— Genuine, acute, haemorrhagic nephritis is a 
very rare complication. It does occur, however, and has even given rise to the 
establishment of a special "renal form of typhoid fever" (nephro-typhoid). This 
name applies especially to those cases in which a severe acute nephritis is the pre- 
dominant symptom at the start, while at a later period the course of the fever, the 
intestinal symptoms, the rose-spots, etc., show the disease to be typhoid fever. 
Nephro-typhoid is analogous to pneumo-typhoid and tonsillo-typhoid. A simple 
so-called febrile albuminuria occurs very frequently at the acme of typhoid, and 
is not to be interpreted unfavorably. It is probably the result of that slight par- 
enchymatous degeneration of the kidneys which occurs in typhoid with the same 
frequency as in most of the other severe infectious diseases. There does not seem 
to be a direct relation between the albuminuria and the fever, although some 
authors assume it to exist. Cystitis is not a rare development toward the end of 
the illness. It is probably always secondary. 

In men orchitis is sometimes observed. Women often have their catamenia 
at the beginning of typhoid. Later in the course of the disease, and in convales- 
cence from severe attacks, the menses are often absent for several periods. In 
pregnant women there is considerable danger of abortion or miscarriage. 



TYPHOID FEVEK. 



17 



Peculiarities in the Course of the Disease. 

The above statements show an almost inexhaustible variety in the possible com- 
plications of typhoid. The course of the disease as a whole may likewise present 
many diverse forms and peculiarities. We shall attempt merely to cite the most 
essential. 

The numerous light and rudimentary attacks {typhus levissimus) are first to 
be mentioned. It was not recognized till lately that they belonged to typhoid 
fever at all (Griesinger). They used to have all sorts of names applied to them, 
the favorite term being "gastric fever." This light form lasts eight to fourteen 
days. The fever is moderate and often decidedly remittent. There is almost no 
proper fastigium. The typhoid symptoms are but slightly developed. There 
are no severe pulmonary or cerebral symptoms. There is generally a moderate 
diarrhoea, the spleen is plainly enlarged, and often rose-spots can be found. The 
diagnosis of these cases is of course difficult in proportion to the scanty develop- 
ment of typhoid symptoms. It is best established by demonstrating an aetiological 
relation between these cases and others which are plainly typhoid fever. 

Abortive typhoid is justly distinguished by Liebermeister from typhus levis. 
The name belongs to cases which begin with severe symptoms and high fever, as 
if they were going to be grave, but in which these violent symptoms disappear 
after a few days and give place to a rapid convalescence. 

On the other hand, there are cases which for a long time cause so little subjec- 
tive discomfort that the patient does not even go to bed (walking typhoid). It is 
not till quite late that there occurs a sudden change for the worse, or some severe 
complication. Thus it has happened that people who were apparently healthy 
have suddenly had all the symptoms of a severe peritonitis due to perforation and 
have died, the autopsy disclosing the lesions of the third week of typhoid fever. 

The individual circumstances are very important in weighing each case, for 
they may modify the disease in many ways. 

In children it is a remarkable fact that typhoid ulcers are much less frequent 
than in adults. This explains why intestinal haemorrhage and peritonitis are 
much rarer in children. Severe cerebral symptoms are, on the other hand, very 
frequent. In severe cases children sometimes exhibit the peculiar symptom of 
a continuous penetrating screaming. In other mild cases the children are sop- 
orose. 

In the aged the diagnosis of typhoid is often very difficult, since the course of 
the disease is frequently irregular. Generally the fever is not very high, and it 
very seldom exhibits distinctly the type described above. The pulmonary or cere- 
bral symptoms predominate as a rule. 

In the corpulent, typhoid fever is often very severe, so that our prognosis must 
always be rather grave, especially if pulmonary symptoms arise. 

Hard drinkers are also in especial peril in this as in all other acute diseases. 
Dangerous cardiac weakness is prone to appear. Severe cerebral symptoms are 
frequent. It is, however, surprising that true delirium tremens is relatively 
infrequent, although so common in pneumonia. 

The influence of previous strong mental excitement and of certain already ex- 
isting diseases (cardiac disease, emphysema, kyphoskoliosis, etc.) has been already 
mentioned. 

Eelapses of Typhoid Fever. 

Typhoid fever exhibits in many cases the peculiarity of repeating itself com- 
pletely after having run its entire course and disappeared. This process is called 
a relapse. It is in all probability the result, not of a fresh infection of the system 
2 



IS 



ACUTE GENEEAL INFECTIOUS DISEASES. 



from without, but of a renewed development, or possibly of a second generation, 
of the infectious germs already present. A typical relapse is like a first attack in 
all clinical and anatomical particulars, with this difference, that everything is 
more condensed, and lasts a shorter time than in the first attack. The interval 
between the two, during which there is no fever, lasts seven to ten days. It may 
be longer, and is often shorter. Sometimes the relapse follows immediately upon 
recovery. Indeed, it may even happen that, before the patieut has completely 
recovered, his temperature begins to rise again in the characteristic step-like way. 
To such cases as this last the term recrudescence is applied. Except in the time of 
its beginning, it may be just the same as a genuine relapse. In the interval be- 
tween the two attacks many persons are perfectly comfortable, and appear to be 
fully convalescent. There is often, however, a slight evening rise of temperature. 
It is noticeable that the splenic tumor does not completely disappear after the first 
attack in many cases which are followed by a relapse. 

The relapse is generally briefer, as we have said, than the first attack, seldom 
lasting more than fifteen to eighteen days. The temperature rises more rapidly, 
perhaps in two or three days. The fastigium is shorter, the decline more abrupt. 
The absolute height of the temperature may be very considerable, even exceeding 
that in the first attack. Rose-spots appear as soon as the third or fourth day. The 
stools become liquid, the spleen enlarges again, and all sorts of complications may 
arise. The danger occasioned by a relapse may, however, be overestimated. It is 
true that ligl^t primary attacks may be followed by severe relapses ; but, on the 
other hand, the relapse is often rudimentary. 

The frequency of relapses varies considerably in different epidemics. Here in 
Leipsic, of late years, we have had relapses in about nine per cent, of all cases, but 
in separate years the percentage varied between four and sixteen. Out of about 
five hundred cases we have seen three in which there were two successive and 
typical relapses. 

Diagnosis. — The diagnosis of typhoid fever may be perfectly easy, but, if the 
case be anomalous, or come under observation at a late period, it may be ex- 
tremely difficult. Important factors are the gradual onset, then the height and 
course of the fever, with no demonstrable localized disease, and the rose-spots. 
Less characteristic, but still of value, are the stools, the tympanites, and the 
swelling of the spleen. ^Etiological factors, such as the occurrence of undoubted 
cases of typhoid in the neighborhood, are of great diagnostic value in obscure 
cases. Sometimes the diagnosis can not be established till the appearance of 
certain symptoms, like intestinal haemorrhage, a characteristic mode of conva- 
lescence — viz., by lysis — or a relapse. It is an important rule not to make a 
diagnosis of typhoid after a single examination. It is generally necessary to ob- 
serve the case accurately for several days before the diagnosis can be established. 
The differential diagnosis from other acute diseases, such as miliary tuberculosis, 
acute endocarditis, meningitis, etc. , will be considered in discussing these diseases. 

Prognosis. — A perfectly favorable prognosis should never be made. Cases 
which seem the mildest may become dangerous. Yet, if there are good nursing 
and good treatment, typhoid fever is not a particularly dangerous disease, and we 
may hope for recovery even in very severe attacks. The danger lies, first, in the 
severity of the infection, as shown chiefly (though not wholly) by the height of the 
fever and the intensity of the general symptoms. A further danger is the appear- 
ance of the complications already enumerated and discussed. Thirdly, the con- 
stitution and condition of the individual are important. The circumstances com- 
ing under this head have likewise been repeatedly mentioned above. All these 
factors must be carefully estimated before we decide as to the danger in each case 
and make our prognosis. 



TYPHOID FEVER. 



19 



The mortality in typhoid varies greatly in the separate epidemics. The severe 
cases are undoubtedly more frequent at some times than at others. This renders 
it difficult to give statistics which are universally applicable. We may in general 
reckon on an average mortality of about ten per cent., and measure the severity 
of separate epidemics by this standard. Numerous observers agree that the treat- 
ment now in vogue has decidedly diminished the mortality. It was formerly not 
rare for it to reach twenty or twenty-five per cent. 

Treatment. — A specific cure for typhoid — i. e., some remedy to destroy the 
specific cause of the disease within the system, or to render it harmless — is as yet 
unknown. Antiseptic and antizymotic drugs, such as quinine and salicylic acid 
(vide infra), do have a certain influence upon the fever, but they are not 
capable of essentially modifying the course of the disease as a whole, at least 
not in such doses as we dare administer. The continued internal use of car- 
bolic acid (grains five to ten, gramme 0*30-0 "50, or more, in the course of 
twenty-four hours) is the means chiefly recommended lately for this purpose; 
but we doubt if it is of much benefit. Liebermeister ascribes to iodine a demon- 
strable, although slight, beneficial influence. Other physicians had previously 
recommended it. Four to five drops of the following solution are given every 
two hours . in a wineglass of water : Iodine, one part ; iodide of potassium, two 
parts ; distilled water, ten parts. We have had no personal experience with this 
remedy. 

Calomel is also said to have a specific effect on typhoid. Wunderlich and 
others have noticed that if a few rather large doses of calomel be given at the 
beginning of the disease, it will on the average run a lighter and more favorable 
course than otherwise would have been the case. Wunderlich believed that 
typhoid fever may sometimes be aborted by this method. Although we can hardly 
expect this, it is really an efficient means of procedure, which we have often 
found satisfactory, to give two or three powders, of five grains (0*30 gramme) each, 
of calomel, as the first prescription, to patients who come under treatment in the 
first week or the beginning of the second. As there is generally constipation, the 
laxative effect is also beneficial. Moreover, it often lowers the temperature some- 
what. A moderate diarrhoea is not a contra- indication, but, if the bowels be very 
loose, the calomel should be omitted. 

Ergotine may be mentioned as another drug which is said to act specifically. 
It has been lately used, chiefly by French physicians, in doses of twenty to forty- 
five grains (1*50-3 grammes) in twenty-four hours. We doubt if this remedy will 
be popular long. 

In the present state of our knowledge the treatment of typhoid must still be 
chiefly general and symptomatic, and in one sense prophylactic. We must fight 
the symptoms already present, and further seek, as far as possible, to defend the 
patient from the attack of certain dangerous secondary disorders. Starting out 
with this view, the proper treatment of typhoid fever is a task of the highest im- 
portance, and by no means a thankless one. 

We will begin by considering the general treatment. The sick-room must not 
be too warm, and must be frequently and thoroughly aired. The sick-bed must 
be well cared for. If pains be taken to prevent bed-sores, we shall obviate one 
source of pain and danger (vide supra), and save ourselves and the nurse much 
trouble. Those who are very sick should therefore be laid on an air-cushion, or, 
if possible, a water-bed. The patient should be told not to lie always upon his 
back, but to change now and then upon his side. The back, the region of the sa- 
crum, and the heels are to be often bathed with spirits of camphor or brandy. The 
minutest bed-sore is to be treated carefully. It should be cleansed twice a day 
(rinsed off with a solution of salicylic acid, 1-300), and done up with an ointment 



20 



ACUTE GENERAL INFECTIOUS DISEASES. 



containing Peruvian balsam, 1-30.* If the bed-sore be extensive, dusting with 
iodoform is very efficient treatment. We should be particularly careful not to let 
the skin be undermined. If this has already occurred, we must be prompt in the 
use of the knife or drainage-tube. 

We can not recommend too strongly that the mouth should be kept clean. In 
a light case the patient can see to this himself, but otherwise the mouth and 
tongue must be frequently cleansed with a linen cloth wet in cold water or a solu- 
tion of borax (1 to 30). Perhaps we need hardly repeat the reason for this exces- 
sive cleanliness. It lies in the causative relation between stomatitis and inflam- 
mation of the parotid gland, and of the middle ear. If the tongue and lips be 
dry, they may be touched with glycerine. 

The diet must be at once liquid and nourishing. Milk is excellent, and should 
always be ordered, but will, unfortunately, be taken by very few patients continu- 
ously. It is often better borne if coffee or a little brandy be added to it. Cocoa 
made with milk may also be given for a change. In severe cases Nestle's food 
(Kindermehl) has been often employed by us with benefit. Broth and soup, thick- 
ened with sago or rice, are also good. They may be made more nourishing by 
adding an egg to them. If the patient is very anxious to have more solid food, 
as often happens, we need not hesitate to give him a roll or rusk (Zwieback) 
that has been softened by soaking. If a patient becomes exceedingly enfeebled, 
we should give him fine shavings of raw beef, regardless of the fever. A little 
dilute hydrochloric acid might be given with the meat. Beef -tea would be still 
better than the raw meat, and is to be strongly recommended. The various prep- 
arations of meat which are now made (meat-solution, meat-peptones, etc.) may be 
sometimes useful. Where the fever takes a sluggish course, we must often begin 
to give stronger nourishment before the fever has ended. The best drink is cold 
water, which the patient would often not think of using unless we offered it to 
him. Lemonade and similar preparations generally become distasteful in time. 
Drinks containing carbonic dioxide are to be avoided, because they increase the 
meteorism. Cold tea with milk is good. In all severer cases we should give 
some good strong wine, such as port, Malaga, or Hungarian wine. If the patient 
desires beer, we need not hesitate to give it in moderate amount. During conval- 
escence we should be very careful about diet, since errors often have disagreeable 
consequences. We must wait till there has been no fever at all for seven to ten 
days before we allow a solid, animal diet, and return by degrees to common sorts 
of food. 

[The chief indication of beginning convalescence is the absence of febrile move- 
ment. It is not customary with us to wait so long as the author advises before 
allowing the patient to take solid food. Simple articles of food simply cooked 
should be selected, and the change from liquid to solid food should be made cau- 
tiously ; but beef-steak and the like can be safely given in very many cases from 
the beginning of convalescence. There is little or no reason to think that proper 
solid food has any influence on the occurrence of relapses, though an error in diet 
may cause a temporary recrudescence of the fever.] 

The general and dietetic treatment which we have thus far discussed is very 
important. Outside of this, it is our opinion that there is only one method of 
treatment to be chiefly considered — at least under the present limitations of our 
therapeutic ability. This method consists in the persistent use of cool baths, as 
first practiced by Brand in Stettin. We do not indeed believe that the indications 
for this method of treatment are exactly what its original promoter held them to 



* The unguentum balsami peruviani is made by mixing one part of balsam very exactly with thirty 
parts of the glycerite of starch (B. P.). It is not officinal in Germany. — Trans. 



TYPHOID FEVER. 



21 



be, and we think some of the minutiae of the treatment should be changed. Yet 
there is at present no other single method of treating typhoid fever which has so 
numerous and evident advantages for the patient. To carry it out in private prac- 
tice may often be more difficult than in a well-appointed hospital. However, even 
in private houses it will generally be possible to manage it, and we regard it as 
the duty of every physician who undertakes to treat a severe case of typhoid to 
try his best to have the baths employed. 

The great advantages of the treatment by baths are : 1. The baths diminish 
the fever, if their temperature be only sufficiently low, by direct absorption of 
heat. The baths thus obviate, as far as possible, all the bad effects which might 
result from a rise of temperature. 2. The direct influence of the baths upon the 
nervous system is still more important. The intellect becomes clearer, the apathy 
and dullness diminish. In fact, if baths be used, we do not see nearly so often as 
formerly the grave " typhoid condition." It is thus evident that bathing not only 
causes an improvement in the subjective sensations of the patient, but brings in 
its train many other beneficial effects. The patient takes his nourishment better, 
does not so often swallow the wrong way, coughs more effectively, is easier to 
move, and his body and his mouth can be better cleansed. 3. The influence of 
the baths ui>on the respiratory organs is of the greatest importance. We refer 
especially to the stimulation to deeper inspirations, and the promotion of expec- 
toration. The best proof of the benefit of this influence is the circumstance 
that, if patients are subjected to baths from the start, it is comparatively a rare 
thing for severe bronchitis, atelectasis, and catarrhal pneumonia to develop. 
4. The good care of the skin, which the bathing makes possible, is not to be 
despised. Since this treatment has been introduced, bed-sores are much rarer in 
typhoid than before. 5. Lastly, the baths are sometimes observed to have a 
diuretic effect. 

What has been said shows that the height of the fever is by no means the sole 
indication for the employment of baths, at least in our opinion. The condition 
of the nervous system and of the respiratory organs is also to be considered. It 
is true that numerous mild cases run a favorable course without a single bath ; 
but we should always remember that this treatment is not only directed against 
the symptoms already existing, but has also a prophylactic importance, since it 
tends to prevent any severe cerebral or pulmonary manifestations. 

We will pass on to the special method of carrying out balneo-therapeutics in 
typhoid. Full baths are generally employed, immersing the patient to his neck. 
The tub must stand, if possible, by the bedside. In hospitals, where there are 
beds on rollers, it is a better way to wheel the patients into the bath-room. All 
who are severely ill should be lifted into the bath and there held and supported, 
to avoid any bodily fatigue. During the bath the skin should be gently rubbed. 
This averts unpleasant sensations of chilliness. The temperature of the water 
should not be set too low, especially for the first baths. We begin at 85° to 90° 
(24° to 26° R.), or, if the individual be elderly or sensitive, and timid, at even 
warmer temperatures. When the patient has become accustomed to the tempera- 
ture of the water, we can cool off the bath still further. Baths below 73° (18° 
to 20° R.) have scarcely ever been used by us, and we believe that they are seldom 
needed. A very satisfactory average temperature is 80° to 85° (20° to 24° R.). 
A bath lasts on the average ten minutes. If the patient feels very cold or very 
uneasy in the bath, it must be cut short. After the bath the patient is at once 
lifted into bed, wrapped up in a sheet previously made ready, and wiped dry, with 
rather vigorous rubbing of the extremities and back. The moist sheet is then 
removed. The patient is covered up rather warmly, and is given some hot broth 
or a sip of good strong wine. The effect of the bath upon the temperature is 



22 



ACUTE GENEEAL INFECTIOUS DISEASES. 



measured about half an hour later by the rectum. If the temperature be 2° to 3° 
(1° to 2° C.) lower than before, the result is deemed satisfactory. Often the differ- 
ence is greater, but in severe cases the fever may be so obstinate that the tem- 
perature remits only a small fraction of a degree. In such cases it is sometimes 
permissible to lower the temperature of the bath still more, or continue it a little 
longer. If cool baths are ill-borne, protracted baths of lukewarm water are some- 
times very efficient (Biess, and others). 

In so far as the height of the fever furnishes an indication for baths, we may 
accept, say 103 '6° (39 "8° C.) in the rectum, as the temperature calling for a bath. 
As a rule, baths should not be given oftener than every three hours, as otherwise 
they exhaust the patient. In many cases three or four baths a day are enough. 
At night we have given baths very seldom, when forced to by extremely high 
temperatures or other bad symptoms. It must be a mistake to wake a patient who 
is quietly sleeping, and put him into cold water, even if his temperature is above 
104° (40° C). Likewise, in cases where the temperature shows considerable spon- 
taneous remissions, there may be no use in inflicting a cold bath upon a patient 
who has high fever only temporarily. On the other hand, even if the temperature 
be not excessive, or even if it be normal, there is, as we have said, no better remedy 
than the baths for severe pulmonary or cerebral symptoms. In such cases we 
often raise the temperature of the baths a little, and during them we have colder 
water poured upon the head and back. If we do this, the ears must be stopped 
with cotton- wool, lest the cold water find its way into them. 

It is not always advisable to use baths, however advantageous this treatment 
may be in typhoid fever. There are a number of contra-indications which can 
not be disregarded. First, the occurrence of intestinal haemorrhage, however 
slight, and likewise the suspicion that peritonitis is developing, prohibit bathing. 
In these cases quiet is the very first requirement of the patient, and the baths 
must be at once discontinued. Further contra-indications are great weakness or 
great sensitiveness, such that the excitement caused by the bath might do harm. 
Sometimes baths are followed by severe rheumatic (" rheumatoid ") pains in the 
limbs, and often the baths seem to promote the occurrence of furunculosis. In 
such cases it is often necessary to omit the baths, or at any rate to employ them 
less often and at a warmer temperature. The same is true if a severe laryngeal 
affection develops, or otitis or nephritis. Nothing seems to us a greater mistake 
than to attempt to establish a scheme for the treatment of typhoid by baths that 
shall be always applicable. Here, if anywhere, the only correct way is to treat 
each individual case according to its special symptoms and circumstances. 

We shall now pass on to the consideration of the further symptomatic treat- 
ment of typhoid. The first question is whether the fever — that is, the elevation of 
bodily temperature, as such — demands special consideration. In general, we are 
of the opinion that the internal antipyretics are seldom indispensable. It is true 
that by giving quinine (single doses of fifteen to twenty grains, gramme 1 to 
1'50) or salicylate of soda (in amounts of a drachm or a drachm and a half, 
grammes 4 to 6), the elevated temperature may often be considerably dimin- 
ished; but whether the patient is thereby benefited is at least doubtful. Cer- 
tainly the unpleasant accessory symptoms caused by the drugs mentioned — viz., 
vomiting, ringing in the ears, vertigo, and profuse perspiration — make the patient 
feel decidedly more uncomfortable than he was before. There is also some dan- 
ger that these medicines may have an unfavorable influence upon the cardiac 
activity. Antipyrine is decidedly better borne than quinine or salicylic acid. It 
was first recommended by Filehne. The dose is fifteen to thirty grains (grammes 
1 to 2) dissolved in water, to be repeated every one to three hours, according to 
circumstances, until about seventy-five or ninety grains (grammes 5 to 6) have 



TYPHOID FEVEE. 



23 



been used. Its effect is almost always a lowering of the temperature by several 
degrees centigrade, generally accompanied by sweating. Vomiting is sometimes 
observed after antipyrine, but unpleasant cerebral effects are rarely seen. It 
should, nevertheless, be considered that the effect of all internal antipyretics is 
limited to an influence upon the temperature, while the baths not only affect the 
fever, but have numerous other advantages (vide supra). If we had to choose 
whether to treat typhoid fever exclusively with baths or with quinine, and the like, 
we should certainly choose the baths. We do not by any means desire to banish the 
use of internal antipyretics from the treatment of typhoid, but only to make their 
employment more limited than has often been the case. We consider that they 
are actually indicated only where the fever is high and the employment of baths 
is for some reason impossible or contra-indicated, or where the fever remains con- 
tinuously high, despite bathing. In such cases it is often advantageous to com- 
bine the bath-treatment and the internal antipyretics, especially in the evening. 
If patients with a moderately high fever are made to take large doses of quinina 
and the like, without any satisfactory reason for it, we regard such treatment as 
at any rate useless and often really injudicious. This is, unfortunately, a com- 
mon practice, and frequently its only permanent result is a disordered stomach. 

[In spite of the German reports, the cold-bath treatment of typhoid and other 
fevers has never had any great following in this country, a conservatism which 
seems to have been wise in view of all the facts. A recent paper by Senator may 
here be cited. This observer, namely, compares the mortality statistics of the Ber- 
lin hospitals for ten years (1875-'84), and shows that the lowest typhoid rate — 12*3 
per cent. — was obtained in the Augusta hospital, which draws its material from 
the same class of the community as the others. In this hospital no methodical 
antipyretic treatment is carried out, while it was so done in the others. Senator 
thinks the special use of the cold bath is in cases with early stupor and profound 
nervous symptoms ; as an antipyretic he prefers quinine and antipyrine. The 
treatment he advocates coincides with that which is most in vogue in this country 
— a symptomatic and expectant treatment. 

Cool spongings with alcohol and water can be repeated several times during 
the day, and, in the hands of a skillful nurse, add greatly to the comfort of the 
patient, at the same time that they strengthen the nervous system and decidedly 
moderate the fever. Their use is highly to be recommended. Of the most modern 
internal antipyretics, the safest seems to be antipyrine. When well borne, as it is 
in the majority of cases, it promotes comfort and quiets the restlessness due to 
high fever. According to Beyer, it acts by increasing heat radiation, and neither 
weakens the heart, as do kairin, thallin, hydrochinon, and resorcin, nor does it 
damage the blood and the muscular tissues generally as do the two former of these 
remedies. 

Alcoholic stimulation is often required at some period in the course of the dis- 
ease, and the chief indication for its use is deficient heart-power, as shown by the 
pulse and the first sound at the apex. Large quantities of brandy, and the like, 
are seldom required, and the least toxic effect shows that the limit of toleration 
has been exceeded. 

Water or an acid drink should be given frequently by the nurse without wait- 
ing for the patient to ask for it, unless the mind is unusually clear.] 

Another important symptom which needs special treatment is intestinal 
haemorrhage. It has been already mentioned that if this occurs, the baths should 
cease at once. Further than this, the chief remedies are ice and opium. Flat 
ice-bags are laid upon the abdomen. They should not be too heavy, and should, 
if possible, be fastened to a hoop. Internally, the patient is given every two hours 
a powder of one half grain or one grain (gramme 0'03 to 0'05) of opium, either 



ACUTE GENEEAL INFECTIOUS DISEASES. 



pure or combined with acetate of lead (opii, gr. grm. 0'03; plumbi acetatis, gr. j, 
grm. 0-05; sacchari albi, gr. j, grm. 0*05). The object of the opium is to check 
peristalsis, and thus promote the formation of a clot in the bleeding vessel. Liquor 
f erri chloridi (five to ten drops in water every hour) is often employed, but is of 
extremely doubtful value. The baths can not be resumed till there has been no 
bleeding for at least three or four days— and then only cautiously. 

If peritonitis occurs, the treatment is much the same. Above all, opium 
must be used in still larger doses, but, unfortunately, as a rule, in vain. Per- 
haps surgical treatment is destined eventually to be useful, viz., incision, 
cleansing, and drainage of the peritoneum. Its results thus far are not very 
encouraging. 

If there is considerable diarrhoea, we can give mistura gummosa [P. Gr., gum 
arabic and sugar, each 15 parts ; water, 170 parts], tannin, subnitrate of bismuth, 
or small doses of opium. Constipation at the beginning of the disease is over- 
come by calomel (vide supra). In later stages we always try enemata first, to 
produce an operation. If this does not succeed, then we must employ rhubarb or 
castor-oil. Great tympanites may be diminished by laying cold wet cloths or 
ice-bags upon the belly. Considerable amounts of gas may often be removed by 
introducing a long rectal tube. As to puncturing the greatly inflated intestines, 
a method practiced by some physicians, we have no personal experience. 

If there are severe pulmonary symptoms, baths and pouring on cool water 
are, as we have said, the best remedies. Internally we may try liquor ammonii 
anisatus [P. G., olei anisi, 1 part; aquae destillatae, 24 parts; aquae ammoniae, 5 
parts] and benzoic acid (grains ij to iij, gramme 0*1 to 0*2, in powder). If the 
pulse be very rapid, we can put an ice-bag over the heart. If at the same time 
the pulse is small and weak, we give stimulants, of which the best is camphor 
(vide infra). Digitalis (one half grain of the leaves, gramme 0*03, two or three 
times daily) may also be employed if the pulse be rapid ; but it should be used 
with great caution. 

For nervous symptoms the baths and douching are the most effective reme- 
dies. The head is meanwhile covered by an ice-bag. If there be great excite- 
ment, as shown by excessive restlessness or delirium, small doses of morphine are 
often very useful. 

The conditions of collapse and cardiac failure, which sometimes appear rather 
suddenly, demand prompt and energetic treatment. Stimulants to be given in- 
ternally are some stronger kind of wine, camphor (two to five grains, gramme 
0*10 to 0 - 30, in the form of a powder), musk (one half grain to one grain, gramme 
0*03 to 0*05 at each dose), or spiritus aetheris [P. G., aether, one part ; alcohol, 
three parts]. Subcutaneous injections act quicker and are much more conveni- 
ent. We may use either ether or camphor (one part camphor to four parts olive- 
oil, seven to fifteen minims, c. c. 0'5 to 1*0, every one to two hours). To start up 
respiration, the best means is to pour cold water on the back of the neck. Artifi- 
cial respiration also succeeds, in many cases, in reviving the breathing when it 
is about to stop. 

The numerous other complications and sequelae which may occur, but which 
can not all be mentioned here, should be treated on general principles. 

The prophylactic measures to avoid the spreading of the disease can be only 
briefly referred to. Of chief importance is careful disinfection of the excreta, 
which can be accomplished by pouring upon the stools a not too small amount of 
five-per-cent. carbolic solution. We should also take care that bed-pans, bed- 
clothes, linen, etc., are handled by other people as little as possible. If there 
seems reason to suspect that the disease arose from bad water, of course the source 
of such suspected water must be cut off. 



TYPHOID FEVER. 



25 



[Recent experiments tend to show that the above solution of carbolic acid does 
not kill spores except after prolonged contact. 

The following' are the measures of disinfection recommended by the American 
Public Health Association. It will be observed that they apply to all infectious 
diseases, and it seems well to give them here nearly in extenso, as the directions 
for disinfection in most text-books are far too vague. 

Disinfection of Excreta, etc. — The infectious character of the dejections of 
patients suffering from cholera and from typhoid fever is well established ; and 
this is true of mild cases and of the earlier stages of these diseases as well as of 
severe and fatal cases. It is probable that epidemic dysentery, tuberculosis, and 
perhaps diphtheria, yellow fever, scarlet fever, and typhus fever, may also be 
transmitted by means of the alvine discharges of the sick. In cholera, diphtheria, 
yellow fever, and scarlet fever, all vomited material should also be looked upon 
as infectious ; and in tuberculosis, diphtheria, scarlet fever, and infectious pneu- 
monia, the sputa of the sick should be disinfected or destroyed by fire. It seems 
advisable also to treat the urine of patients sick with an infectious disease with 
one of the disinfecting solutions below recommended. 

Chloride of lime, or bleaching powder, is, perhaps, entitled to the first place 
for disinfecting excreta, on account of the rapidity of its action. The following 
standard solution is recommended : 

Standard Solution No. 1. 

Dissolve chloride of lime, of the best quality,* in pure water, in the proportion 
of four ounces to the gallon. Use one quart of this solution for the disinfection 
of each discharge in cholera, typhoid fever, etc. Mix well and leave in vessel for 
at least one hour before throwing into privy -vault or water-closet. The same 
directions apply for the disinfection of vomited matters. 

Standard Solution No. 2. 

Dissolve corrosive sublimate and permanganate of potash in pure water, in 
the proportion of two drachms of each salt to the gallon. This is to be used for 
the same purposes and in the same manner as Standard Solution No. 1. It is 
equally effective, but must be left a longer time in contact with the material to be 
disinfected — at least four hours. The only advantage this solution has over No. 1 
consists in the fact that it is odorless. It costs about two cents a gallon. It is 
very poisonous, and will injure lead pipes if passed through them in considerable 
quantities. Solutions of corrosive sublimate should not be placed in metal re- 
ceptacles. 

Disinfection of the Person. — The surface of the body of a sick person, or of 
his attendants, when soiled with infectious discharges, should be at once cleansed 
with a suitable disinfecting agent. For this purpose solution of chlorinated soda, 
diluted with three parts of water, or Standard Solution No. 1, diluted with three 
parts of water, may be used. A two-per-cent. solution of carbolic acid is also 
suitable for this purpose, and, under proper supervision, the use of a solution of 
corrosive sublimate (1-1000) is to be recommended. 

In diseases like small-pox and scarlet fever, in which the infectious agent is 
given off from the entire surface of the body, occasional ablutions with solution 
of chlorinated soda, diluted with twenty parts of water, will be more suitable than 
the stronger solution above recommended. 

In all infectious diseases the body of the dead should be enveloped in a sheet 



* Good chloride of lime should contain at least twenty -five per cent of available chlorine. The cost 
of the solution is less than one cent a gallon. The sediment does no harm. 



26 



ACUTE GENERAL INFECTIOUS DISEASES. 



saturated with Standard Solution No. 1, or with a five-per-cent solution of car- 
bolic acid, or a 1-500 solution of corrosive sublimate. 

Disinfection of Clothing. — Boiling for half an hour will destroy the vitality 
of all known disease-germs, and there is no better way of disinfecting clothing or 
bedding which can be washed than to put it through the ordinary operations of 
the laundry. No delay should occur, however, between the time of removing 
soiled clothing from the person or bed of the sick and its immersion in boiling 
water, or in one of the following solutions ; and no article should be permitted to 
leave the infected room until so treated. 

Standard Solution No. 3. 

Dissolve four ounces of corrosive sublimate and one pound of sulphate of 
copper in a gallon of water. Two fluid ounces of this standard solution to the 
gallon of water will make a suitable solution for the disinfection of clothing. 
The articles to be disinfected must be thoroughly soaked with the disinfecting 
solution, and left in it for at least two hours, after which they may be wrung out 
and sent to the wash. 

Clothing may also be disinfected by immersing it for four hours in a two-per- 
cent, solution of carbolic acid. Soiled mattresses, pillows, feather beds, and articles 
of this nature can not be effectually disinfected by sulphur fumigation, owing to 
the fact that the gas does not penetrate to their interior in sufficient amount. 
For articles of this kind, and in general for articles of little value, which have 
been soiled by the discharges of the sick, destruction by fire will be advisable. 

Disinfection of the Sick-Room. — No disinfectant can take the place of free 
ventilation and cleanliness, and it is impracticable to disinfect an occupied apart- 
ment. Neutralizing bad odors is not disinfection. 

All surfaces should be thoroughly washed with Standard Solution No. 1, diluted 
with three parts of water, or with a 1-1,000 solution of corrosive sublimate. 
Standard Solution No. 3, diluted in the proportion of four ounces to the gallon of 
water, may be used. 

The walls and ceiling, if plastered, should be brushed over with one of these 
solutions, and subsequently washed over with a lime-wash. 

Especial care must be taken to wash away all dust from window ledges and 
other places where it may have settled, and thoroughly to cleanse crevices and 
out-of-the-way places. After this application of the disinfecting solution, and an 
interval of twenty-four hours or longer for free ventilation, the floors and wood- 
work should be well scrubbed with soap and hot water, and this should be followed 
by a second more prolonged exposure to fresh air, admitted through open doors 
and windows. 

As an additional precaution, fumigation with sulphurous-acid gas is to be 
recommended, especially for rooms which have been occupied by patients with 
small-pox, scarlet fever, diphtheria, typhus fever, and yellow fever. All apertures 
into the room should be carefully closed, and not less than three pounds of sul- 
phur for each thousand feet of air-space should be burned. To secure complete 
combustion, the sulphur, in powder or small fragments, and moistened with 
alcohol, should be placed in a shallow iron pan, and this should be placed on 
bricks in a tub partly filled with water to guard against fire.] 



TYPHUS FEVER. 



27 



CHAPTER II. 

TYPHUS FEVER. 

{Spotted Fever. Ship Fever.) 

Typhus fever is an acute infectious disease, perfectly distinct from typhoid 
fever, but formerly often confounded with it. The similarity of the two dis- 
eases, which led to their similar names, consists only in the grave general con- 
dition, with fever, and in a number of complications, which may appear in both. 
There is, however, an essential difference in the whole course of the diseases, and 
especially in the circumstance that the intestinal lesion which is characteristic of 
typhoid is never seen in typhus. The chief distinction between the two affections, 
which must undoubtedly lie in the difference in their causes, can not yet be 
demonstrated. We do not yet know with certainty the organized pathoge- 
netic agents of typhus fever, although it must be presupposed that they exist. 

JEtiology. — As to the way in which infection occurs, we have much less infor- 
mation even than in relation to typhoid. We regard it as an established fact that 
the disease never arises spontaneously, and that its appearance in a place previ- 
ously free from the disease is always to be referred to an importation of the patho- 
genetic poison. It is likewise determined, through numerous observations, that 
typhus is one of the contagious diseases — that is, that the specific poison can be 
directly transferred from the patient to others around him. How it is transferred 
we have no certain knowledge. Perhaps the poison is contained in the expired 
air; or, as is still more probable, in the scales of epidermis; or, perhaps, in the other 
excretions and secretions of the patient. We are equally ignorant through what 
channel the infectious agent enters the system — whether it is inspired or swallowed. 
It is certain that the poison may be transferred in the clothes, etc., of the patient 
(fomites). 

Favorable hygienic surroundings decidedly diminish the contagiousness of 
typhus fever. For example, in the well-ventilated pavilions of the Leipsic hos- 
pital there have rarely been cases of transfer of the disease to physicians, nurses, 
or other patients. On the other hand, if the hygienic influences be unfavorable, 
typhus fever may appear in very widespread epidemics. Those terrible epidemics 
which have been described under the names of " famine fever," " camp fever " 
(Hungertyphus, Kriegstyphus), etc., were for the most part typhus fever. In the 
smaller epidemics it is often possible to trace the disease to some wretched, over- 
filled tenement-house. 

At present typhus fever appears constantly in Great Britain. Ireland has been 
notorious for many years as a breeding-place of the disease. It is also frequent in 
the eastern part of Germany (Posen, East Prussia and West Prussia, Silesia), in 
Poland, Galicia, Russia, and in parts of southern Europe. The isolated cases 
which occur every year here and there in central Germany, though more or less 
numerous, are, almost without exception, to be referred to an importation of the 
disease. 

Typhus fever attacks by preference young adults of twenty to forty years ; but 
it occurs in children, and is comparatively frequent in elderly persons. There is 
no marked dependence of the epidemics upon any particular season of the year. 
As in the case of typhoid fever, a person who has once had the disease seems to 
enjoy immunity from any fresh attack. 

[The practical acquaintance of American physicians with typhus fever is, f ortu- 



28 



ACUTE GENERAL INFECTIOUS DISEASES. 



nately, limited. Many of the outbreaks which have occurred were traceable to im- 
migrants, especially from Ireland. 

During our civil war the disease broke out neither among the armies in the 
"field nor among the prisoners of war. A number of cases were reported at the 
time, but great doubt has since been thrown upon the correctness of the diagnosis. 

Murchison, among other authorities, maintained that the disease can be devel- 
oped de novo under the influence of overcrowding, insufficient food, and defect- 
ive hygiene in general. The possibility of the correctness of this view can not 
be denied as yet, and it may perhaps be stated that the arguments in its favor are 
stronger than those in favor of a similar development of the poison of typhoid 
fever. It may be that this and some other diseases and morbid conditions depend 
on auto-infection from an accumulation of alkaloidal substances developed in the 
living body. G-autier, of Paris, has made some most interesting studies of these 
substances, which he calls leucomaines, to distinguish them from analogous sub- 
stances developed in the dead body — ptomaines. This whole subject is still in em- 
bryo, but may have a great future.] 

Course and Symptoms of the Disease.— If we try to sketch the characteristic 
behavior of typhus fever, especially as contrasted with typhoid, we may say that 
the disease begins much more abruptly and rapidly, and that the fever quickly 
becomes very high and the general disturbance very severe, but the illness lasts 
a shorter time, seldom more than two weeks, and generally passes by crisis into 
recovery. 

The length of incubation seems to vary. Murchison thinks it is usually 
more than nine days. Sometimes, though not invariably, slight prodromata 
precede by some days the actual outbreak of the disease. These are languor, 
anorexia, headache, and pain in the limbs. Then the regular illness begins, as a 
rule, rather suddenly, and often with a pronounced rigor. With this the tem- 
perature rises quickly, and may on the very first evening reach 104° or 105°. 
(40°-40'5° C). Vomiting is not rare, and may be repeated. A grave general 
condition, with fever, is developed in a few days. The patient feels exhausted. 
There is often violent pain in the loins and extremities. Nervous symptoms 
soon appear : persistent and intense headache, vertigo, spots before the eyes, 
ringing in the ears, and in very severe cases quickly increasing stupor and de- 
lirium. In severe cases the fever often reaches 106° (41° C), and may be even 
higher, and it is almost constant, with but slight morning remissions. The skin 
is hot and dry, the tongue dry and thickly coated, the respiration moderate, 
the pulse very rapid. We very frequently find in the chest the signs of an 
extensive bronchitis. Nasal catarrh and conjunctivitis also occur. Serious in- 
testinal symptoms are generally absent, although there may be slight tympanites 
or diarrhoea. The spleen is almost always greatly enlarged. Only in a few epi- 
demics is the splenic tumor said to have been wanting (?). The urine is concen- 
trated and scanty, and sometimes has a trace of albumen. 

On the third to the seventh day of the disease the characteristic eruption ap- 
pears. To this the disease owes its name of "spotted fever." The eruption con- 
sists of rose-spots, generally very numerous and widespread, upon the trunk and 
extremities, often also on the face. Sometimes the spots are larger, and may then 
bear great resemblance to a fresh eruption of measles. The skin between the sep- 
arate rose-spots is not infrequently diffusely reddened. After two or three days the 
roseolse become hemorrhagic, and change into lighter or darker petechise. It is 
commonly only in the lighter cases that the rose-spots fade away without first 
becoming petechial. In rare though well-substantiated cases the eruption has been 
scanty, or even wholly wanting. Herpes does occur, but only seldom. 

The fever begins to abate in light cases as early as the second week, coincidently 



TYPHUS FEVER. 



29 



with an improvement in the general symptoms. Often this change is indicated 
about the seventh day by a considerable remission in the temperature. On the 
other hand, in severe cases, all the symptoms grow worse. The weakness in- 
creases. The nervous derangement reaches the extreme of a severe "typhoid 
state," expressed either by marked stupor, which sometimes passes into complete 
coma, or by violent delirium. Lobular pneumonia attacks the lungs, and the 
fever continues with unabated violence. These symptoms may end with death, 
but in favorable cases they decline rapidly. Sometimes this decline is preceded 
by a great rise in temperature (perturbatio critica) on the fourteenth to seven- 
teenth day, rarely a few days earlier or later. In such cases the temperature is 
apt to fall by crisis, sinking in a day or two, with but slight interruption, down to 
the normal level. Even in those cases in which the descent is by gradations it is 
always decidedly more abrupt than in typhoid. The eruption quickly fades, the 
patients gradually improve, and, as a rule, become completely and permanently 
convalescent. It is true that some observers have seen relapses, but they are, at 
least in our present epidemics, extremely rare. 

Complications and Varieties in the Course of the Disease.— From what we have 
said of its course, it is evident that the symptoms are essentially those of an intense 
general infection of the system. The sole demonstrable local lesion which is 
almost invariably present, is the characteristic eruption, and this has evidently no 
causal relation to the severe symptoms of the disease. It is likewise extremely 
probable that most of the complications, which not infrequently arise in severe 
cases, are secondary, and occur in the way already described with considerable 
detail in the preceding chapter. They are just such complications as are possible 
in every severe general disease, and embrace otitis, parotitis, extensive lobular 
pneumonia, more rarely gangrene of the lungs, and pleurisy ; also furunculosis, 
cellular hyperplasia, bed-sores, dysentery, icterus, etc. Whether some of the 
local lesions which are observed may not be direct results of the pathogenetic 
poison, we can not at present decide. Among these would come, first of all, the 
rare cases of lobar pneumonia and nephritis. Sequelae are, on the whole, rare, 
though sometimes there is a tedious anaemic condition, or neuralgia, paralysis, etc. 

The separate epidemics of typhus present considerable variety, not only as 
regards the occurrence of individual complications, but more especially in the 
general course and character of the cases. For instance, some epidemics are dis- 
tinguished by the greater frequency of light attacks (typhus exanthematicus 
levissimus, unsuitably termed by some " febricula "). Here the entire attack runs 
its course in five to eight days. The fever is generally comparatively moderate ; 
there are no severe general symptoms, and complications are exceptional. 

Diagnosis. — It may be very difficult for a time to distinguish typhus from 
typhoid. The following factors are of chief importance : 1. The onset is much 
more abrupt in typhus than in typhoid, and is often accompanied by a pronounced 
rigor. 2. In typhus, the nervous disturbances usually appear earlier and are more 
severe than in typhoid. 3. The rash is seldom so extensive in typhoid as in ty- 
phus, and in typhoid it hardly ever becomes petechial. 4. In typhus the pains in 
the loins and limbs are generally much more pronounced. 5. If we still find it 
hard to decide, the manner of recovery will almost always settle the question. 
Recovery in severe cases of typhoid is, on the average, much more tardy and 
gradual, by lysis. In typhus it occurs generally by the seventeenth day, and by 
crisis. 

The prognosis is chiefly determined by the severity of the fever and of the 
nervous symptoms. Extensive lobular pneumonia is the most frequent dangerous 
complication. The mortality varies greatly in the separate epidemics. It is some- 
times only six or seven per cent., but may rise to twenty per cent. 



30 



ACUTE GENERAL INFECTIOUS DISEASES. 



Treatment is based on the same principles as in typhoid fever. There is no 
specific remedy. Besides good nursing, a judicious employment of baths is cer- 
tainly our chief reliance for lessening the severity of many of the symptoms, such 
as febrile, nervous, and pulmonary disturbances, as well as for averting many dan- 
gerous complications. For all details of treatment we may refer to the preceding 
chapter. 



CHAPTER III. 

RELAPSING FEVER. 

{Typhus, seu Febris, recurrens.) 

iEtiology. — This disease was first named by English pathologists relapsing 
fever, and by Griesinger febris recurrens. It has a peculiar course, made up of 
separate attacks, and is further of great interest because it is one of the first infec- 
tious diseases in which the specific pathogenetic organisms became known, and, 
being easily demonstrable in each separate case, were utilized for the speedy and 
certain diagnosis of the disease. Obermeier discovered in Berlin, in the year 1873, 
that in relapsing fever the blood, at certain times, invariably contains peculiar, 
thread-like micro-organisms. This discovery has since been universally confirmed ; 
and it may be maintained that if once the presence of these " spirilli " be demon- 
strated in the blood, we are justified in making an absolute diagnosis of relapsing 
fever. Any one who has had opportunity to observe a considerable epidemic of 
relapsing fever will not only be compelled to regard this disease as parasitic, but 
will be conscious of the goal to be striven for in regard to the aetiology, pathology, 
and treatment of all the infectious diseases. 

In Germany the disease did not become epidemic till the year 1868. In 1872 
and 1873 there were considerable epidemics in Breslau and Berlin. Its last exten- 
sive appearance was in 1879 and 1880, when it spread over most of northern and cen- 
tral Germany, and was accurately studied by numerous observers. People of the 
poorer classes were almost exclusively attacked, and especially the " tramps." The 
uncleanly dens where these people lodge were found everywhere to be the chief 
centers of infection. 

The precise manner of infection is as yet almost wholly unknown. All ob- 
servers agree that the disease is directly contagious ; but it can not be very con- 
tagious if the hygienic influences be good. At least the results of our late epidemics 
would imply this. In the Leipsic hospital, where over two hundred and fifty cases 
were treated, and isolation could not be at all perfectly carried out, not one case 
of infection occurred. It is certain that the disease can be transmitted by direct 
inoculation with the blood of patients. This has been established by a Russian 
physician by the experimental inoculation of healthy persons. Doctors have been 
repeatedly inoculated at the autopsy of those who have died of relapsing fever. 
The disease may likewise be transferred by inoculation to monkeys, while other 
mammals seem to enjoy an immunity from it. 

[The first cases of relapsing fever observed in this country were in Irish immi- 
grants coming over in the same vessel in the year 1844. At several periods since 
then more or less limited outbreaks traceable to immigration have occurred, but 
the disease has never acquired any foothold with us, and comparatively few physi- 
cians have ever seen it. As far as I can learn, only one case has ever been seen 
in Boston, and that was in the person of a physician from another city, who 



RELAPSING FEVER. 



31 



brought the disease with him and passed through it in the Massachusetts General 
Hospital.] 

Clinical History. — The stage of incubation lasts about five to eight days. It is 
only exceptionally that some slight prodromal symptoms present themselves just 
before the outbreak of the disease proper. As a rule, it begins suddenly, with a 
more or less pronounced chill and intense constitutional symptoms. There are 
violent headache, great languor, anorexia, and especially marked pains in the loins 
and extremities. The temperature rises rapidly, reaching generally 106° (41° C.) 
or higher as early as the first or second day. The skin is hot and dry, and usually 
quickly assumes a very characteristic dirty-yellowish color. Here, in Leipsic, 
we have often seen herpes labialis, which seems, however, to have been rarer 
in epidemics elsewhere. The tongue becomes dry and thickly coated. Some- 
times there is vomiting. The bowels are constipated, or there is a slight diarrhoea. 
The spleen becomes rapidly enlarged, being, as a rule, even larger than in typhoid 
or typhus. The liver is slightly enlarged. The chest presents the signs of a bron- 
chitis, generally moderate, but in exceptional instances severe. The pulse is much 
quickened. It is seldom that there are severe cerebral symptoms beyond a certain 
apathy and stupor. We have seen delirium tremens sometimes, in drunkards. A 
very characteristic symptom, already mentioned, is the marked hyperesthesia of 
the muscles, especially in the calves. 

After these symptoms, accompanied by persistent and generally very high 
fever, have lasted five days to a week, there is a critical decline of temperature, 
with profuse sweating. The patient now improves so rapidly and decidedly that 
he thinks himself completely cured, and generally gives little credence to the 
physician's prophecy of a relapse. In rare but well-attested cases there has been 
really but one attack. The rule is that, after about a week, a second attack occurs, 
often a third after that, and, infrequently, even a fourth and fifth. In each of 
these, the above-mentioned symptoms are repeated more or less completely and 
violently. As the only certain and constant sign of the recurring attacks (the 
so-called relapses) is a fresh rise of temperature, it will be well to consider their 
peculiarities at the same time that we describe the course of the fever. During 
the intervals of normal temperature the other objective symptoms of disease are 
usually absent, except an evident splenic tumor, and, not infrequently, the pecul- 
iar pale-yellow hue. 

Course of the Fever (see Fig. 2). — The beginning of the fever in the first 
attack is, as we have said, almost always sudden, so that it may even in a few 
hours reach a considerable height. The fever lasts, as a rule, five to seven days, 
but not infrequently as short a time as three or four days, or as long as ten or 
twelve days. During this time it may keep a tolerably uniform height, but 
oftener there are considerable remissions, which may even come to deserve the 
name of pseudo-crises. In such cases the temperature sinks in the morning to 
normal or even lower, so that we might believe the fever ended ; but in the even- 
ing the temperature rises again to its former height. These pseudo-crises are most 
frequent toward the end of the attack, but do occur sometimes in the very first 
days. The absolute height of the fever is, as a rule, very considerable. Tempera- 
tures between 105*5° and 106*5° (41° and 41*5° C.) are very often observed, and in 
themselves are not especially ominous in relapsing fever. The highest tempera- 
ture we have observed was 107*9° (42*2° C). Sometimes the temperature is more 
moderate (between 102° and 104°, 39° and 40° C). The fever almost always 
ends at the close of the attack by crisis, only rarely by a rapid, gradual decline. 
The crisis is often preceded by an especially great rise the evening before (pertur- 
batio critica) ; so that the subsequent fall of temperature is very considerable. It 
generally occurs at night, and is accompanied by profuse perspiration. The fall 



32 



ACUTE GENERAL INFECTIOUS DISEASES. 



may amount to 9° or 10° (5° to 6° C). The temperature sinks almost always 
below normal, often as low as 95° (35° C.) or thereabouts. Once we saw it fall to 
92-1° (33-4° C). 

To the first attack succeeds an interval during which there is no fever (apy- 
rexia), which lasts on the average about a week, sometimes a less time, and often 
a greater. The longest interval we have ever observed lasted seventeen days. 



1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 




Fig. 2.— Example of the temperature curve in relapsing fever. 



During this interval the temperature, which, as a rule, is at first subnormal, rises 
to normal, and then generally remains there. Exceptionally there are slight 
evening exacerbations to above 100 '5° (38° C). These may have no demonstrable 
cause, or may result from some complication, such as otitis, or a furuncle. Then 
comes another change, and generally a sudden one, ushered in with a chill, and a 
new rise of temperature, the beginning of the second attack or first relapse. 
During this attack the fever has the same general peculiarities as in the first at- 
tack. Generally the first relapse is briefer by a day or two than the first attack ; 
but the reverse is sometimes true. We will add that we have observed not in- 
frequently a rather high evening temperature (say 101*5°, 38'5° C.) for one or 
two days before the second attack began, as also before the third. 

Relapsing fever seems in many epidemics to have been made up of two attacks, 
so that not more than one tenth of the cases had a third attack. On the other 
hand, the majority of the cases in the last epidemic had two relapses. And in 
these cases the rule was for the interval between the second and third attacks to 
be one or two days longer than the first apyrexia ; but earlier epidemics seem to 
have had the second apyrexia, if there was one at all, briefer than the first. The 
third attack is set down in all reported cases as decidedly shorter than either of its 
predecessors. It lasts generally two or three days. Exceptionally we have seen 
it persist for four or even six days. 

A fourth and even a fifth attack may occur, but only exceptionally. If they 
do happen, they are usually imperfectly developed, and often are limited to a 
fever of one day's duration. The more accurately and persistently we take the 
temperature during convalescence, the oftener do we find slight rises of tempera- 
ture occurring at intervals late in the history of the case. These are probably to 
be interpreted as final, rudimentary attacks. 

The Spirilli. — The number of cases of relapsing fever in which no spirilli 
can be demonstrated in the blood, if the examination be accurate, has become so 



KELAPSINGr FEVEK. 



33 



small that it can be disregarded when we compare it with the much greater num- 
ber of cases where such demonstration is made with ease and certainty. The best 
way is to get a drop of blood by pricking the skin, and examine it as it is, without 
mixing anything with it. There is no need of an immersion lens. With a good 
Hartnack No. 8 [about 330 to 440 diameters, according to eyepiece] the spirilli 
are seen with perfect distinctness. We have often seen them plainly with a 
No. 7 [250 to 340 diameters]. It requires a little practice to make them out ; but 
this is easily obtained. Often the attention is first caught by little jogglings 
and motions of the red blood-corpuscles, and then we see the delicate, narrow 
threads. Their length equals about three to six times the diameter of the red 
globules (Fig. 3). They exhibit an active and almost continuous motion, like 
snakes. Often the whole thread bends upon itself, and then stretches out again. 
They are partly separate and partly tied up in knots composed of four to twenty 
individuals. The whole number visible in one field varies greatly in individual 
cases, and has no direct relation to the severity of the case. Often it requires 
long searching to find a few, while in other cases there may be twenty or more 
in the field at once. A very interesting fact is that their appearance in the 
blood depends upon the attacks of fever. On the first day of the attack we 
rarely find spirilli, and then only one or two. Upon succeeding days their num- 
ber increases. Shortly before the end of the attack — that is, before the crisis — 
they generally disappear entirely ; but even after the crisis they have been found, 
exceptionally and in very small numbers. 
They have very often been found by the 
author as well as other observers during the 
pseudo-crisis described above , so that, after 
the temperature has become normal, the 
presence of spirilli makes it very probable 
that another rise of temperature is impend- 
ing. The spirilli have thus far been found 
in the blood only, in the catamenia, in bloody 
urine, or in blood coughed up from the 
lungs, and never in the organs or secretions 
(urine, milk, sweat, contents of herpetic vesi- 
cles). There can hardly be any doubt that 
the spirilli which appear in the separate at- 
tacks are to be regarded as separate genera- 
tions. As to their manner and place of de- 
velopment we have as yet no knowledge. 
In the final, rudimentary attacks, we find few if any. If the patient dies during 
an attack, they are to be found in the blood after death. Artificial cultivations 
have not been very successful ; nor have pure cultures of them, to our knowledge, 
ever succeeded. Albrecht states that they will subsequently develop in blood taken 
from a patient during the interval when he has no fever. 

The blood is otherwise modified during relapsing fever. We very often find a 
slight increase in the white corpuscles. There is often a noticeable abundance of 
very small bodies, so-called granular elements (Kornchenbildungen). The signifi- 
cance of these (the remains of white corpuscles ?) is still doubtful. There are, 
finally, peculiar cells, rather large, with fat-granules. They were demonstrated 
by Ponfick in the venous blood, and are said to come from the spleen. We also 
find fatty-degenerated endothelium in the blood. 

Complications are on the whole rare, and mostly secondary. Important among 
these are troublesome ophthalmic disturbances, especially iritis and iridochoroid- 
itis. Sometimes parotitis, laryngitis, and pneumonia occur. Epistaxis is a not 
3 




Spirilli of relapsing fever in the blood. 



34: 



ACUTE GENERAL INFECTIOUS DISEASES. 



infrequent complication. It is usually profuse and persistent, and may even be 
dangerous. Sometimes there has been rather severe dysenteric trouble. In one 
case, which ended fatally, we observed a very peculiar intestinal lesion, consist- 
ing of haemorrhagic-necrotic foci in the colon and lower ileum. In severe cases 
acute hasmorrhagic nephritis occurs with comparative frequency. At the autopsy 
an important and characteristic phenomenon is the wedge-shaped white spots 
which occur in the spleen, like infarctions. They have a clinical interest, as the/ 
may become the starting-points of pyaemic conditions or of peritonitis. Splenic 
abscesses have been observed in a few cases. 

Variations in the course of the disease occur in this, as in all other acute infec- 
tious diseases. First there are mild, abortive cases, in which the attacks are few 
and brief. Then cases have been described resembling intermittent fever. Of 
chief importance is that severe variety of relapsing fever first observed in Egypt 
by Griesinger, and described as "bilious typhoid." There is no longer any doubt 
about the proper classification of this disease, for spirilli have been proved to ap- 
pear in it, and it has even been shown that its inoculation upon another person ( !) 
produces a common case of relapsing fever. Bilious typhoid fever occasions suc- 
cessive attacks, like those of relapsing fever. The type is much more severe. 
As a rule, there is marked icterus and often a fatal termination. 

The prognosis of ordinary relapsing fever is on the whole very favorable. In 
the last epidemics the usual mortality was only two to four per cent. The fatal 
cases could some of them be laid to wretched nursing. In the remaining por- 
tion death resulted from complications, such as pneumonia and nephritis. 

The treatment must as yet be purely symptomatic. Antipyretic treatment is 
generally needless, since the fever is relatively brief and often quite intermittent. 
Moreover, most patients can not well endure cold baths, because the muscles are so 
painful. As a rule, good nursing and proper food amply suffice. If the muscular 
pains are very violent, we may order chloroform liniment as an embrocation. 
Complications are to be treated on general principles. 

We are not acquainted with any remedy that can influence the disease itself or 
avert the relapses. Large doses of quinine, salicylic acid, etc., have been frequently 
employed for this purpose, but never with success. Lately there has been ascribed 
to calomel a favorable influence upon the general course of the disease, and its use 
is said to diminish the number of attacks. "We must await further evidence in 
support of this statement. 



CHAPTER IV. 

SCARLET FEVER. 

(Scarlatina.) 

We now begin the consideration of those acute infectious diseases which are 
usually embraced under the name of the " acute exanthemata." In this group are 
reckoned, beside scarlet fever, measles, rotheln, small-pox, varicella, and some 
times also facial erysipelas. The point which these diseases have in common is 
that in all of them is developed a characteristic eruption, of slight clinical signifi- 
cance in itself, in most cases, but of thoroughly characteristic appearance in each 
disease, and hence of essential importance jn diagnosis. A number of the acute 
exanthemata have this further point of mutual resemblance that they appear 
chiefly in children. These diseases are scarlet fever, measles, rotheln, and 
varicella. 



SCAELET FEVER. 



35 



iEtiology.— Infection with the specific scarlatinal poison occurs almost always 
by contagion, which takes place very readily. A single approach to a patient ill 
with scarlet fever may suffice to communicate the disease. There is no doubt that 
the disease may be transferred by objects which the patient has touched, such as 
linen, clothing, furniture, or toys. Persons who have been with the sick may be 
the means of transmitting the disease, although themselves unaffected. In Eng- 
land it has been thought that the contagium may be carried by milk. 

Numerous observations show that the scarlatinal poison is with great difficulty 
destroyed, and may keep its contagious powers for months (" tenacity "). We can 
thus see how difficult, how impossible, it may be in an individual case to point out 
the source of contagion. Scarlet-fever patients can communicate the disease cer- 
tainly as late as the end of the desquamative period. 

Details as to the manner of contagion, or as to the specific poison itself, are as 
yet unknown. There have been repeated statements about the presence of bacteria 
in the blood and in the tissues of scarlatinal patients ; but it is very improbable that 
the specific poison of scarlet fever has been observed. This poison must, however, 
be contained in the blood, and in the contents of the miliary vesicles, of scarlet- 
fever patients, for the disease has repeatedly been artificially produced in healthy 
persons by inoculation with these fluids. 

Predisposition to scarlet fever is far less universal than is predisposition to 
measles or small-pox. In families with several children often only one or two fall 
sick, while the rest escape, although equally exposed. As age increases, liability 
to the disease greatly diminishes, although there are cases of scarlet fever among 
adults. The majority of patients are between two and ten years of age. Scarlet 
fever is rare during the first year of life. It is an interesting fact that children 
with fresh wounds, either accidental or surgical, are especially liable to scarlet 
fever. An analogous and familiar fact is that women after delivery have a strong 
tendency to the disease.* With very few exceptions a person is attacked but once; 
so that, after the disease is over, an immunity from contagion is enjoyed ; but there 
are exceptions to this rule. 

Scarlet fever is now spread over the entire globe. Here in Germany there are 
almost always some sporadic cases in the larger towns, while from time to time, 
especially in autumn, there are more or less extensive epidemics in one place or 
another. There is considerable variation in the different epidemics of scarlet 
fever, as in many other infectious diseases, in the general character of the disease, 
and above all in the prevailing mildness or severity of the cases. 

Clinical History. — The period of incubation is about four to seven days, or is 
sometimes apparently shorter. There are hardly ever any decided prodromata. 
The disease begins rather suddenly, with fever, often introduced by chilliness, and 
sometimes by a well-marked rigor. There is almost invariably a painful, scar- 
latinal sore throat. A further symptom, in all cases of any severity, is cerebral 
disturbance, generally rather intense. There may be headache, dullness, uneasy 
sleep, delirium, and, in smaller children, sometimes even convulsions. A very 
frequent and characteristic early symptom is vomiting, which may be repeated. 

The characteristic rash usually appears as early as the close of the first day, or 
on the second, and begins on the neck and on the chest and face, soon becoming 
almost universal. The eruption consists at first of numberless small red points, 
crowded thickly together and soon united into a diffuse, intense, scarlet-colored 
erythema. The small and somewhat elevated points almost always correspond to 
the swollen hair-follicles. The diffuse redness is the result of an excessive hyperse- 

* la puerperal cases genuine scarlet fever and septic diseases were formerly often confounded. 
(See Chapter XVIII.) 



36 



ACUTE GENERAL INFECTIOUS DISEASES. 



mia of the skin, and vanishes completely on pressure. The back usually presents 
the most vivid tint. In the face there is generally pallor of the lips and chin, pre- 
senting a very striking and characteristic contrast to the bright-red cheeks. If 
some object like the end of a pen-holder be drawn over the red skin, there soon 
arise corresponding white lines, due to contraction of the blood-vessels. It is pos- 
sible thus to make letters or pictures upon the back of the patient. We should 
add, however, that this is not a peculiarity of the scarlatinal eruption, being seen 
in other erythematous eruptions. 

The rash persists for some three or four days, at first even increasing somewhat 
in vividness. It often appears more intense by artificial light than in the daytime. 
Meanwhile the severe general symptoms continue — the fever, the usually exces- 
sively rapid pulse, the cerebral symptoms, and the throat trouble. The spleen is 
often somewhat swollen, though seldom very large. Then the eruption begins to 
fade, the fever gradually ceases by lysis, the general condition and the difficulty 
in swallowing improve. With the end of the first week or the beginning of the 
second, the cases which run the typical course become fully convalescent. When 
the rash disappears, the epidermis usually begins to peel off, in a very characteristic 
way, in pieces of considerable size. The exfoliation upon the hands and feet is 
especially pronounced, and the little convalescents often amuse themselves by 
peeling off the epidermis in strips. Cases which are apparently the mildest and 
most benign may have their convalescence interrupted by the occurrence of a 
secondary scarlatinal nephritis. There is no certain prophylaxis against this. 

We will now pass on from this general summary to a more complete considera- 
tion in detail of general and local symptoms. And we shall see how manifold 
are the clinical phenomena presented by scarlet fever. 

1. Fever (see Fig. 4). — Although in a few undeveloped cases there is no fever 
or scarcely any, almost all cases of any importance have high fever. It is only 

exceptionally that severe cases are ob- 




served where the bodily temperature 
is little if at all elevated. As a rule, 
the fever rises rapidly upon the very 
first day, corresponding to the sudden 
onset of all the symptoms, to about 
104° or 105° (40°-40-5° C). The next 
day it often becomes a little higher 
still, and then persists with but slight 
variations, as a rule, so long as the 
eruption is at its height. During this 
period a temperature of 105° or more 
(40-5°-41° C.) is not infrequently ob- 
served. When the eruption fades, 
and the other symptoms decline, def er- 



Fig. 4.-Example of a normal scarlet fever curve. ^escence occurs. This happens but 

rarely by crisis, and that in the slight 
attacks. It is almost always by prolonged lysis, as in typhoid, only more irregu- 
larly and more rapidly. If the fever lasts into the second week of the disease, it 
is almost always (though not without exceptions) caused by demonstrable com- 
plications. The most frequent causes are the persistence of a severe sore throat, 
the occurrence of inflammatory changes in the cervical glands, or a purulent 
otitis media. In closing what we have to say about the fever in this disease, 
we would emphasize the fact that the pulse is often very rapid, even considering 
the height of the temperature. 

2. The Throat. — The throat presents the most constant local lesion of scarlet 



SCAELET FEVER. 



37 



fever. Sore throat is only in the rarest cases wholly absent ; but its form and 
intensity may vary extremely. The mildest variety is a simple, erythematous 
catarrh without much swelling-, but exhibiting a more or less intense reddening of 
the soft palate and tonsils, frequently associated with enlargement of the little 
mucous follicles. In addition to the redness there is often a variable degree of 
swelling. These latter cases form a connecting link between the ordinary variety 
and those cases of parenchymatous sore throat where the tonsils are intensely 
swollen and the soft palate and uvula are more or less cedematous. There may 
be small suppurating spots in the crypts of the tonsils, or these organs may suffer 
from larger abscesses, necrosis, or even gangrene. When the necrosed portions 
slough off, there may in rare cases occur a considerable haemorrhage from the 
tonsils. Often chronic hypertrophy of the tonsils remains after these severer 
forms of inflammation. 

These graver varieties are almost always accompanied by swelling of the sub- 
maxillary lymph-glands. The neighboring connective tissue will then often 
present diffuse infiltration and ©edematous swelling. This swelling may in severe 
cases involve the floor of the mouth and the entire neighborhood of the throat. 
The severity of the trouble in the throat does not always correspond to that in the 
lymph-glands. Very frequently the swelling of the lymph-glands and the neigh- 
boring structures ends in the formation of abscesses. 

The croupous and diphtheritic inflammations of the throat are the most impor- 
tant and justly the most feared. We believe that it is a mistake to speak of a 
" complication of scarlatina with diphtheria. " The diphtheria of scarlet fever has, 
from an setiological point of view, no relation to the common genuine diphtheria. 
It is a throat trouble having a direct connection with the scarlatinal process as 
such. It can, indeed, from its outward appearance,* be distinguished with diffi- 
culty, if at all, from the primary, genuine variety (q. v.) ; and therefore, from an 
anatomical point of view, it must be termed a croupous or diphtheritic inflam- 
mation. 

Scarlatinal diphtheria may be united with any of the above varieties of angina, 
either appearing at the very beginning of the illness, especially in very severe 
cases, or not till later, at the end of the first or even in the beginning of the second 
week. It is almost always the sign of a severe attack, and is therefore generally 
associated with high fever and grave general symptoms. The secondary swelling 
of the cervical lymphatic glands and the surrounding connective tissue generally 
attains a severe grade, and it is often very painful. Here, as in the other varieties 
of severe angina, there is almost always a simultaneous, intense stomatitis, and fre- 
quently a purulent coryza. There are often superficial ulcers on the alae nasi and 
at the corners of the mouth. This form of diphtheria has one peculiarity of great 
interest and clinical importance. Unlike primary diphtheria, it seldom extends 
to the larynx, so that it is only in rare cases of scarlet fever that there are symp- 
toms of laryngeal croup. A f urther important clinical difference between these 
two forms of diphtheria is that in scarlet fever there is scarcely ever any subse- 
quent paralysis of the soft palate or of the muscles of the eye. A dangerous, but 
fortunately a rare, complication is cedema of the glottis. This may quickly cause 
death from suffocation. We may finally mention that puerperal scarlatina is 
said to have in many cases extremely slight throat complications, or none what- 
ever. 

3. We proceed by a natural sequence to the consideration of the affections of 
certain parts adjacent to the throat, troubles which must be regarded as chiefly 



* In microscopic preparations, however, according to Heubner's investigations, there are evident 
differences between genuine primary diphtheria and that of scarlet fever. 



33 



ACUTE GENEEAL INFECTIOUS DISEASES. 



the result of direct extension, or of a conveyance of the inflammatory process from 
the throat. 

The stomatitis we have already mentioned, as well as the disturbance in the 
neighboring- lymph-glands * and the surrounding tissue. Parotitis is not rare in 
severe cases. Of especial importance is the scarlatinal inflammation of the middle 
ear, which often results in permanent deafness. 

This inflammation usually arises at the time of desquamation, but it may occur 
earlier. It is either a simple catarrh of the middle ear, or, in severe cases, an 
actual diphtheritic process. The deafness and earache are easily overlooked, as 
the other symptoms of the patient occupy the attention, so that the ear trouble is 
first recognized by the occurrence of perforation of the tympanum and subsequent 
purulent otorrhcea. After this declines there very often remains behind, as we 
have said, permanent deafness. Statistics have shown that four or five per cent, 
of all cases of deafness are referable to an attack of scarlet fever in childhood. 
The otitis is seldom immediately dangerous, but yet cases of purulent meningitis 
have been observed to follow it. 

We have already spoken of the purulent or even diphtheritic rhinitis which 
almost always accompanies the scarlatinal sore throat. In rare cases there may 
also occur a purulent conjunctivitis, which is most probably the result of a direct 
conveyance of inflam m atory secretions. 

The tongue in scarlet fever deserves special mention. The first coating cleans 
off, and then the tongue usually presents a very characteristic appearance. It is 
diffusely reddened and covered with little elevations corresponding to swollen 
papillse (strawberry tongue, scarlatinal tongue). 

4. The characteristic eruption, as developed in the great majority of cases, has 
been described above. It remains to describe certain variations from the usual 
appearances. 

First, the eruption may be rudimentary. It is then not pronounced, and visible 
only on a limited portion of the body (face, trunk, or extremities) . 

Variations from the type are not rare ; sometimes the papules are more strongly 
developed {scarlatina papulosa) ; very frequently there are little vesicles {scarla- 
tina miliaris). This latter form of the eruption appears by preference upon the 
trunk, but it also may come upon the extremities, and is often brought out by ex- 
cessive perspiration, or by wrapping up the patient too warmly. Many epidemics 
are noticeable from the frequent appearance of this miliary form. More rarely 
the rash has a spotted look, resembling the eruption of measles {scarlatina varie- 
gata). There may be minute ecchymoses, which are not ominous. Well-developed 
cases of hsemorrhagic scarlatina are, however, very dangerous, because here the 
general infection of the system is almost always exceedingly severe ; and there is 
besides, as a rule, a general hasmorrhagic diathesis. Other cutaneous lesions, 
especially herpes and urticaria, are not so very unusual in connection with the 
scarlatinal eruption. Furunculosis has been repeatedly observed after the rash 
fades. 

Desquamation generally begins as soon as the rash declines, but may not occur 
till a few days or even one or two weeks later. Its extent corresponds in general 
to the severity of the eruption, although extensive desquamation may follow a 
rudimentary eruption. It is seldom bran-like or furfuraceous, as in measles. The 
rule is for it to be in lamellae, so that, as we have stated, quite large strips of epi- 
dermis may be detached entire. 

In rare cases an oedema of the skin appears after scarlet fever, which can not 



* It should be remarked that not infrequently there is also in scarlet fever a slight universal swell- 
ing of the lymph-glands (back of the neck, axilla, groins, etc.). 



SCAELET FEVEK. 



30 



be shown to depend upon nephritis (vide infra), but may perhaps be due to an 
abnormal permeability of the walls of the cutaneous blood-vessels following the 
eruption (hydrops scarlatinosus sine nephritide). 

Kidneys. — Next to the severer forms of throat trouble, the most important and 
dangerous complications are located in the kidneys. They may appear as early 
as the acme of the disease, as in many other infectious diseases. The urine has a 
trace of albumen. In rare cases the amount of albumen may be considerable. 
The appearance of the urine is generally not much changed, and the microscope 
reveals but few abnormal constituents. There are some white and red blood- 
globules, a few hyaline casts, sometimes one or two renal epithelial cells. This 
initial albuminuria very rarely gives cause for alarm. 

The genuine scarlatinal nephritis scarcely ever develops much before the end 
of the second or the beginning of the third week. Sometimes it comes even later. 
In one case under our own observation it did not begin till the thirty-third day of 
the disease. It may, therefore, be regarded to a certain degree as a localized re- 
lapse. It may be so mild as to cause no subjective symptoms whatever, and 
would be unnoticed if the urine were not carefully examined. On the other 
hand, it may be accompanied by the gravest symptoms, and soon terminate fa- 
tally. It may follow either severe cases or the mildest, so that the rule should be 
to examine the urine in every case of convalescence from scarlet fever as often 
and as accurately as possible. No exact statement can be made as to the fre- 
quency of this complication, for it is much more common in some epidemics 
than in others. 

The development of nephritis is often marked by a fresh rise of tempera- 
ture. The elevation may be slight or it may reach 104° (40° C). According to 
our own experience, the fever often comes a day or two earlier than the changes 
in the urine. As the nephritis goes on, it is very often accompanied by a 
moderate fever with remissions. This fever may be almost wholly absent, es- 
pecially in mild cases. The pulse generally becomes harder, and is sometimes 
quickened ; but in many cases it will be slow, and it is sometimes irregular. 
Among other objective symptoms, the first to excite notice is generally a slight 
pufimess of the face, which is usually pale. The eyelids, particularly, present an 
evident oedema. In the milder cases this oedema remains limited, while in 
others it gradually increases in extent and degree, involving first, as a rule, the 
dependent parts of the trunk, and later the extremities. Severe cases develop a 
pronounced anasarca. There are then, usually, effusions into the serous cavities, 
especially ascites and hydrothorax. The hydrothorax is frequently combined 
with severe bronchitis, and then may occasion extreme dyspnoea. 

The urine exhibits the most important changes. These may be insignificant in 
the milder cases, but are very pronounced in the severe ones. The amount is 
much diminished. Sometimes there will be for several days almost complete 
anuria. In cases of any severity the urine is turbid, dark, often evidently bloody, 
with increased specific gravity (about 1015 to 1025), and containing a large 
amount of albumen. The sediment is generally abundant, and exhibits numerous 
hyaline casts of various lengths and diameters. To these may be attached red or 
white blood-corpuscles, detritus, granules of hsematoidin, or bacteria. In cases 
of some duration the casts are often moderately fatty. Very frequently there are 
found noticeably long and broad waxy casts, which are opaque and yellow. In 
many cases of scarlatinal nephritis the urine is peculiar in having very many 
white blood-corpuscles, either isolated or adhering to the casts. These un- 
doubtedly originate for the most part in the kidneys. Red globules, some of them 
in the form of colorless rings, are found. They are usually present in small 
numbers, but may become more abundant, especially for a day at a time. Renal 



40 



ACUTE GENERAL INFECTIOUS DISEASES. 



epithelium is frequently seen, but not invariably nor in very large amount. It 
must be mentioned, in conclusion, tbat in some rare instances the autopsy dis- 
closes quite a marked nephritis, although the urine was apparently normal during 
life, or at least was not very abnormal. 

Uraemic symptoms are not infrequent. They may be of all degrees of severity. 
They will be described in detail under diseases of the kidney (vide infra). The 
uraemia may be so severe as to cause convulsions, coma, and death ; but it is 
remarkable with what frequency children recover from what seems to be the 
most pronounced uraemia. 

The duration of scarlatinal nephritis varies greatly according to its severity. 
In cases which run a favorable course, the urine is generally abnormal for two to 
four weeks, or even longer. Death may be due either to ursemia or to dyspnoea. 
The latter cause is the more frequent one, and may depend upon the ascites and 
hydrothorax, or upon pneumonia (vide infra). Sometimes death comes from 
cardiac failure, which may now and then be very suddenly developed. The 
nephritis may go on into chronic renal disease, but this is rare. 

Pathologically, the kidneys present, in a more or less pronounced degree, the 
lesions of ordinary acute haemorrhagic nephritis (vide infra). It is sometimes 
astonishing to see how apparently insignificant the lesions are, in spite of the 
grave clinical symptoms. In such cases there is usually a so-called glomerulo- 
nephritis (Klebs), in which the lesions are chiefly confined to the walls of the 
capillaries and to the epithelium of the glomeruli. If the nephritis has been of 
some weeks' duration, we generally find that well-marked hypertrophy of the left 
ventricle has already developed, as was first pointed out by Friedlander. We 
have ourselves observed it, and have even been able to demonstrate it repeatedly 
during life. 

6. Joints. — When desquamation begins, or even earlier, pain and swelling 
may attack a certain number of the joints. This trouble was formerly called 
scarlatinal rheumatism, but now is usually known as scarlatinal synovitis. It is 
generally mild and quite temporary. The articular inflammation may, however, 
be severe and even purulent. 

We have seen a few instances of excessive pain in the muscles of the thighs, 
accompanied by a moderate, diffuse swelling. 

7. Another important complication of scarlet fever is pneumonia. In severe 
cases lobular pneumonia sometimes appears as early as the first stage of the dis- 
ease ; but it occurs more frequently in connection with the nephritis. The 
respiration may be very seriously interfered with by it. Inflammations of 
serous membranes in the chest — viz., endocarditis, pericarditis, and pleurisy — are 
more rare. They may or may not be accompanied by disturbances in the joints 
(vide supra). Quite severe intestinal symptoms, such as diarrhoea, may appear. 
These are generally the result of a catarrhal inflammation of the intestinal 
follicles. Dysentery is less frequent. The enlargement of the spleen has 
been already mentioned. The liver is also sometimes found to be considerably 
enlarged. 

Variations in the Course of the Disease.— The diversities of the clinical picture 
in different cases of scarlatina will be understood when we consider the variety 
and number of the disturbances thus far cited. It is to be added that the general 
course of the disease may exhibit numerous peculiarities, of which it is hardly 
possible to give an exhaustive presentation. We will content ourselves with a 
cursory statement of the most important deviations from the typical course. 

1. Rudimentary Forms. — To this class, in which the disease does not reach a 
perfect development at all, belong first the cases of simple sore throat with no 
eruption, or at most an extremely faint and partial one (scarlatina sine exanthe- 



SCARLET FEVER. 



41 



mate). Sometimes even the sore throat is hardly to be seen, and there is noth- 
ing but a brief and slight fever with mild symptoms of general disturbance. The 
recognition of these cases as scarlatinal is possible only when we consider their 
setiological relation to other undoubted cases of scarlet fever. We had an excel- 
lent opportunity to observe them when the disease broke out in the children's 
wards of the hospital at Leipsic. The diagnosis is sometimes confirmed by a slight 
though evident desquamation, affecting the hands, feet, legs, and back, or by an 
acute nephritis, which may follow the mildest attacks of this sort. Many cases 
of acute nephritis, though apparently wholly spontaneous and primary, must be 
regarded as aetiologically scarlatinal. 

2. Rudimentary but Pernicious Forms. — Under this head belong those attacks 
of scarlet fever where the eruption is scanty or absent, while from the very start the 
most violent general symptoms appear. There is a very high fever, enormously 
rapid pulse, and delirium. Such cases must be the result of an uncommonly severe 
general infection. They usually end in speedy death. Other cases, ending fatally 
in a few days, have a well-developed rash without other localized disturbances. 

3. Severe Forms with a more Protracted Course. — In these cases the long 
duration is not the exclusive result of especial complications, but is likewise due 
to the severity of the intoxication. One variety is the so-called typhoid form of 
scarlatina, with persistent high fever and severe constitutional symptoms. An- 
other variety is the hsemorrhagic form briefly mentioned above, in which there 
are extensive haemorrhages into the skin and into the mucous and serous mem- 
branes. This form may run an extremely acute course. Further, in all pernicious 
forms, there may be severe local complications, particularly diphtheritic or gan- 
grenous sore throat, inflammations of serous membranes, etc. Attacks of this 
sort are often not produced by the poison of scarlet fever alone, but by secondary 
complicating processes arising from the absorption of septic matter from diph- 
theritic ulcers in the throat or from the intestine. 

4. In extremely rare cases relapses do occur. After the first illness a fresh 
eruption breaks out with all the other symptoms of scarlet fever. In anomalous 
cases, running a severe course, there is sometimes, at an advanced stage, a fresh, 
imperfect eruption (generally in spots), which Thomas has termed a pseudo-relapse. 

Diagnosis. — The diagnosis of scarlet fever is made in most cases from the char- 
acteristic eruption taken in connection with the other symptoms. We should, 
however, bear in mind that exceptionally other eruptions appear which exhibit the 
closest resemblance to that of scarlet fever. 1. After the use of certain drugs, 
especially atropine (belladonna), quinine, copaiba, chloral ; and likewise after the 
ingestion of crabs, fish, etc. 2. As a symptom of other infectious diseases, such as 
typhoid fever, small-pox; and, above all, in septic diseases (vide infra). In an 
anomalous case factors of importance for diagnosis are the aetiology and the occur- 
rence of desquamation or of a secondary nephritis. 

The prognosis must in every case be guarded. From what has been said of the 
course of the disease, it is evident that, even in cases which are at first appar- 
ently the most favorable, dangerous complications may appear later, particularly 
nephritis. 

Treatment. — The majority of those cases of scarlet fever which take a typical 
course will recover completely without our aid. In these the task of the physi- 
cian, so far as treatment is concerned, consists in arranging the details of hygiene 
and the general care of the patient. The sick-room should be cool, and the diet 
rather strict, consisting mainly of milk or broths, to which an egg may be added. 
We should see that the skin and the mouth are kept clean. To change the linen 
frequently, if done with proper precaution, is not only permissible, but very desir- 
able. The favorite practice of rubbing the skin with fat pork has some merit, 



42 



ACUTE GENEEAL INFECTIOUS DISEASES. 



and is especially to be recommended if the skin be harsh and dry after the erup- 
tion has faded. 

[From the moment that the disease is declared the patient should be thoroughly 
anointed daily with carbolized vaseline, lard, or the like ; and this should be kept 
up until desquamation has ceased. Not only is the comfort of the patient pro- 
moted, but the danger of the spread of the infection is thereby greatly lessened.] 

A more vigorous treatment is demanded whenever there is considerable sore 
throat. Larger children may use a gargle (two-per-cent. solution of chlorate of 
potash, one- or two-per-cent. solution of carbolic acid). Inhalation of carbolic-acid 
spray is also to be recommended where practicable. If there is prostration, or if 
the child be young or willful, we must cleanse the mouth and throat at short inter- 
vals, by means of a spray-apparatus, with disinfectants, such as carbolic acid or 
permanganate of potash in solution. Sometimes it is a good plan to let the patient 
swallow slowly a half-teaspoonful of a solution of potassic chlorate (about 1 to 
40) every half -hour or oftener, with the object of contributing to the local disin- 
fection of the throat. Abscess of the tonsils may often be lanced. The diphtheria 
of scarlet fever is to be treated in the same way as is the genuine variety {vide 
infra). If the nose be likewise affected, the chief thing to do is frequent cleansing 
and syringing while the head is bent forward. We should be on the watch for 
the possible occurrence of otitis. In this particular the physician is often guilty 
of sins of omission. Much harm may be averted by a prompt cleansing of the 
ears, or, if need be, by insufflation of air into the middle ear, or paracentesis of the 
membrana tympani. 

Inflammation of the glands in the neck, if severe, is prone to pass on to sup- 
puration, and must then be treated surgically. When the swelling has just begun, 
or is still moderate, we may try to cure it by rubbing in iodoform ointment (1 to 
15) two or three times a day. Ice is generally not so well borne as warm applica- 
tions (poultices or warm bran-cushions). 

If there be continuous high fever, accompanied by rather severe constitutional 
symptoms, a moderate employment of the cold-water treatment is strongly to be 
recommended. The baths seldom need to be cooler than 81° to 88° (22°-25° R), 
and are to be employed two or three times daily, or oftener in severe cases. If the 
nervous disturbance be serious, or if the respiration be impaired, the patient should 
be douched with cold water during the bath. At the same time wine or strong 
coffee is to be given as a stimulant, or, if cardiac failure and signs of collapse 
appear, the best remedy is subcutaneous injections of camphor. We are convinced 
that internal antipyretics, such as quinine or antipyrine, may usually be dispensed 
with. If it is desirable to prescribe something, we can write for an acid mixture 
or for decoction of cinchona. 

If the pulse is abnormally rapid, and there is danger of cardiac failure, we can 
employ) beside stimulants, an ice-bag placed over the heart. Digitalis may also 
be tried cautiously. 

The scarlatinal inflammation of the joints is sometimes improved by salicylate 
of soda (forty-flve to sixty grains, grm. 3 to 4, in one dose [!]). Sometimes, how- 
ever, this remedy has failed us. 

We know of no means to avert the nephritis. In justice to himself, the physi- 
cian must always at the start point out the possibility of its occurrence, and must 
avoid as far as possible errors in diet or exposure to cold on the part of his patient. 
He may thus escape blame. For the treatment of the nephritis and its results see 
the section on renal diseases. We must likewise refer the reader to the appropri- 
ate chapters for the treatment of other possible complications of scarlet fever. 

The patient must, as a rule, keep his bed three to four weeks, even if convales- 
cence be uninterrupted. 



MEASLES. 



43 



[This injunction is rather extreme. Nephritis is as likely to follow a mild as a 
severe case, and occurs sometimes in spite of every precaution. The physician 
should use his discretion as to the length of time the patient is kept in bed, care- 
fully guarding against exposure to cold and imprudence in diet.] 

The disease is so dangerous that, whenever a case occurs in a family, isolation 
is absolutely demanded, and, if possible, all the other children should be sent away. 
If this advice be disregarded, we can reject all responsibility for any further cases 
and their results. 

[Scarlet fever is a disease at once so highly contagious and so common that it 
may be taken as the type of its class. Its hygienic treatment and the measures 
needful to prevent its spread consequently deserve more minute detail. 

The sick-room should be at the top of the house, if possible, and exposed to the 
south ; every unnecessary article of furniture and all ornaments should be re- 
moved beforehand, carpets, curtains, and stuffed or upholstered furniture being 
included. A window should be kept open constantly, top and bottom ; in cool 
weather a fire should be burning ; in warm weather ventilation is furthered by 
placing a gas-burner or large kerosene lamp near the throat of the chimney. 
Outside the door of the sick-room a sheet moistened with a disinfectant solution 
should be carefully hung. Only those whose presence is absolutely necessary are 
to be allowed in the sick-room, and the physician, when his visit is completed, 
should pass directly out of the house. 

A convalescent should be kept away from all who are liable to contract or con- 
vey the disease until desquamation has entirely ceased. Several warm soap-baths 
should be given before the child emerges into e very-day life, and it should finally 
be dressed in uncontaminated clothing. 

For further directions as to the disinfection of the room, the clothing, and the 
excreta, see pages 25, 26.] 



CHAPTER V. 

MEASLES. 

(Morbilli.) 

iEtiology. — In contrast with the malignancy of scarlet fever is the compara- 
tively benign nature of measles, a disease of childhood which is but little feared 
even by mothers. It is so widespread, and the susceptibility to it is so universal, 
that measles passes for an almost unavoidable but comparatively insignificant an- 
noyance. Indeed, few escape it ; and probably the reason that adults have mea- 
sles so much less frequently than children is simply that most adults have already 
suffered from it in childhood. A second attack of measles in the same individual 
may occur, but it is certainly extremely rare. 

[In highly civilized countries measles has prevailed so long that it would seem 
that a relative resistance against the poison has been acquired. The frightful rav- 
ages of the disease when it was planted in virgin soil, as among the Fiji Islanders, 
not many years ago, apparently bear out this view. The susceptibility to measles 
is greater and more widespread than is that to scarlet fever — that is to say, fewer 
individuals reach adult life without having experienced an attack of the former 
than of the latter.] 

Measles generally comes in epidemics. Sporadic cases are exceptional. In 
this respect measles differs decidedly from scarlet fever. The rapid spread of the 
disease when it has once broken out is a result of its great contagiousness. If one 



44 



ACUTE GENEEAL INFECTIOUS DISEASES. 



child in a family is attacked, the others almost always take the disease. The in- 
fection may be transferred even by well people and by means of articles with 
which the sick have come in contact. We are not yet acquainted with the spe- 
cific poison of measles, although its existence is to be taken for granted, nor with 
the details of its transmission. Still it seems most probable that the poison is 
inhaled through the mouth and nose, and that this is the reason why its effects 
are usually first developed in the respiratory passages {vide infra). The disease 
can be artificially produced by inoculation of healthy children with the blood or 
liquid secretions of those suffering from it. 

Clinical History. — The length of the stage of incubation is tolerably uniform. 
It is ten days to the beginning of the first symptoms, and thirteen or fourteen 
days to the breaking out of the eruption. These figures have been established by 
the observations of Panum, the opportunity having been afforded upon the first 
introduction of the disease into the Faroe Islands. As a rule, there are no espe- 
cial prodromata during the period of incubation except some slight elevations of 
temperature. At the end of ten days the initial stage * begins, generally suddenly, 
and with an abrupt rise of temperature to 102° or 104° (39°-40° C). At the same 
time the characteristic catarrhal symptoms appear ; nasal catarrh (coryza), to 
be recognized by the abundant nasal secretion, the frequent sneezing, sometimes 
also by nose-bleed ; more or less severe conjunctivitis, recognizable by the photo- 
phobia, the reddening of the eyes, and the increased flow of tears ; and, lastly, 
symptoms of a catarrh of the upper XDart of the respiratory tract, usually moderate, 
but nevertheless causing hoarseness and a slight cough. With all this the gen- 
eral condition is disturbed, the children are restless, have headache, and eat little. 
Symptoms of a mild sore throat are not infrequent, but are very far from being so 
prominent as in scarlet fever. 

These initial symptoms last, as we have said, three or four days. Then the 
eruption begins (stage of eruption). This is very often preceded for a day or 
two by a peculiar, usually spotted, reddening of the hard arid soft palates, termed 
"eruption upon the mucous membrane." The true eruption of measles begins 
almost always in the face, on the cheeks, forehead, and around the mouth (con- 
trasting with the characteristic pallor of the chin in scarlet fever), and spreads 
from there rapidly downward over all the rest of the body. The eruption con- 
sists at first of little papillae, corresponding to the follicles. These are soon sur- 
rounded by a pale-red, slightly elevated border, and in many cases become con- 
fluent. Perfectly flat elevations, of various sizes and of extremely irregular, den- 
tated, roundish, or angular shape, develop. These are often so thickly crowded 
together as to touch one another, but usually limited portions of normal skin 
intervene between them. Within each raised spot the little follicular papillae 
remain visible. 

With the beginning of the eruption the fever rises, having been, as a rule, 
slight during the last days of the initial stage. It attains about 104° or 105° (40°- 
40*5° C). In thirty-six to forty-eight hours the eruption reaches its full devel- 
opment and its greatest extent. The fever and the catarrhal symptoms also per- 
sist for the same length of time. Sometimes we find a slight swelling of all the 
lymph-glands. Then follows a decline of the fever, usually rapid, and indeed 
almost by crisis, while the eruption after a short period of full development begins 
gradually to fade during the two or three days following. At the same time the 

* We consider the term "initial stage" more correct than "prodromal stage." The "prodromal 
symptoms" are the first slight symptoms which occur during the time of incubation of an infectious 
disease, while the symptoms presented by measles before the breaking out of the eruption are a part 
of the already developed disease. 



MEASLES. 



45 



catarrhal symptoms diminish. A more or less extensive desquamation of the 
epidermis begins, scarcely ever in large pieces as in scarlet fever, but in little 
scales, "like bran." After eight or ten days, if the disease runs a normal course, 
the patient is fully convalescent. 

After this brief description of the usual course, we must consider more closely 
some of the symptoms and possible complications. 

The fever (see Fig. 5) of measles exhibits, as has been already implied, a tolera- 
bly typical course. It begins with a rather marked and rapid rise upon the com- 
mencement of the disease. On the morning of the second day there is usually a 
marked remission, often to normal. In the last two days of the initial stage the 
fever is moderate, very rarely being so high as at the beginning. With the erup- 
tion there is a new, rapid rise, usually higher than the initial one, so that we may 
well divide the fever into two periods — the prodromal fever and the eruptive 
fever. This latter is but brief and does not persist, as in scarlet fever, during the 
entire duration of the eruption. It falls by crisis when the rash has attained full 
development. There may, to be sure, 
be slight elevations of temperature dur- 
ing the next day or two ; but, if the 
fever is considerable and persistent, it is 
always a sign that complications have 
arisen, probably in the respiratory appa- 
ratus. 

The eruption usually assumes the 
form described above, but may present 
manifold varieties. Sometimes its de- 
velopment is rudimentary. Sometimes 
it does not begin in the face, but on 
some other part of the body. This is 
generally regarded as a sign that the 
case will be anomalous in other ways 
as well. The individual spots may be 
smaller than usual, and may remain en- 
tirely separate from each other {morbilli 
papulosi). In other cases the eruption 
is so confluent {morbilli confluentes) 
that it resembles the eruption of scarlatina. The formation of vesicles {morbilli 
vesiculosi) also occurs, but much more rarely than in scarlet fever. Hsemor- 
rhagic measles are also observed, but usually only in the form of small, capillary 
bleeding, and in cases that otherwise run a perfectly favorable course. Very 
rare cases have indeed been described, with a general hsemorrhagic diathesis and 
bad symptoms, resembling hsemorrhagic scarlatina. It is doubtful whether the 
" black measles " of the old writers was actually measles at all. In addition to 
the proper eruption of measles, other eruptions sometimes develop— among others, 
vesicles, wheals, and pustules. 

The complications of measles are for the most part exaggerations, or abnormal 
varieties and extensions, of those troubles which are observed during the usua] 
mild course of the fever. Compared with the great majority of mild attacks tak- 
ing the typical course, cases presenting complications of any severity are rare, and 
much less frequent than in scarlet fever. Epidemics are only now and then dis- 
tinguished by unusual severity. 

Often quite grave eye diseases are developed, particularly blennorrhagic con- 
junctivitis, keratitis, and iritis. 

Marked inflammation of the mucous membrane of the nose, throat, and lar- 



40-0° 



39-0 0 



38-0° 



37-0° 



1 2 3 4 5 6 7 8 

iHiiil 

ummm 
lllillH 



Initial Fever. Eruptive Fever. 

Eruption. 

Fig. 5. — Example of the temperature curve in 
measles. 



46 



ACUTE GENERAL INFECTIOUS DISEASES. 



ynx may prolong the course of the disease. These are often merely exaggera- 
tions of the usual catarrh. Otitis media likewise sometimes occurs. A laryngitis 
of marked intensity, with considerable swelling of the parts involved, may produce 
much discomfort, or even symptoms of stenosis (" false croup "). Actual croupous 
and diphtheritic lesions of the throat and larynx also occur (diphtheria of measles). 
This last is indeed much rarer than scarlatinal diphtheria, but may have the same 
unhappy termination. It is worth mentioning that sometimes genuine laryngeal 
croup is observed in measles, unaccompanied by lesions of the pharynx. 

It is, however, in the lungs that the most frequent and important of all compli- 
cations in measles occur. The usual mild bronchitis becomes very intense, ex- 
tends into the bronchioles (capillary bronchitis), and then results, for the most 
part, in a more or less extensive, lobular, catarrhal pneumonia (q. v.). This is 
almost always to be suspected when moist rales are heard in abundance over a 
large part of the chest, and there is at the same time persistent fever and pro- 
nounced difficulty in respiration, with cough or dyspnoea. We get decided dullness 
on percussion only when the separate centers of infiltration are more than usually 
confluent. Genuine lobar, croupous pneumonia appears much less often than the 
lobular variety. It attacks one lobe, or several, is attended by high fever, and 
may end with a well-marked crisis. 

The foregoing pulmonary symptoms usually appear at the height of the dis- 
ease, and persist after the eruption fades. They may delay convalescence for 
weeks. In other cases measles will seem at the start to run a normal course, the 
temperature will have already fallen, and then come new fever and the appear- 
ance of decided pulmonary disturbance. This is always to be regarded as a grave 
complication ; and especially in feeble children it may lead to death, with the 
symptoms of impaired respiration, or of constitutional exhaustion. 

Marked intestinal symptoms sometimes appear, particularly an excessive diar 
rhoea, due to intestinal catarrh. It is characteristic of measles that in severe cases 
such a diarrhoea may assume a pronounced dysenteric character, indicated by blood 
and slime in the dejections, symptoms which usually depend upon the develop- 
ment of follicular colitis with ulcerations. 

Now and then still other complications may present themselves, of which a 
full enumeration is impossible. Nephritis does occur, but far less often than in scar- 
let fever. A simple albuminuria during the acme of the disease is not infrequent, 
but as a rule has no especial clinical significance. We should mention gangrene 
of the cheek, the so-called noma, as a complication, which is very rare but appar- 
ently characteristic. 

Peculiarities in the course of the disease are much rarer in measles than in 
scarlet fever. Yet we see, on the one hand, unusually mild or rudimentary 
cases, in which either the rash or the other local symptoms are remarkably slight, 
and, on the other hand, abnormally severe cases. These latter are distinguished 
by the unusual height or persistence of the fever, by the severe constitutional 
and nervous symptoms, and further by the early appearance of complications. 
Such cases have been termed " typhoid measles." We have already mentioned the 
severe form of hemorrhagic measles. 

We should notice the clinical relation which measles bears to some other in- 
fectious diseases — to whooping-cough and tuberculosis. Measles and pertussis (q. v.) 
may follow each other in the same individual at a short interval, sometimes one 
and sometimes the other taking the initiative ; epidemics of the two diseases pre- 
vail with comparative frequency at the same time. Tuberculosis is likewise to be 
mentioned as an important sequela of measles. Its frequent appearance at the 
close of measles is of course to be explained by supposing either that, in children 
who are already the victims of tubercle, the further extension of the tuberculosis is 



MEASLES. 



favored by measles, or that the catarrhal inflammation due to measles leaves behind 
it an especial predisposition to infection with the tubercular poison. 

The diagnosis of measles, as of the other acute exanthematous diseases, is based 
chiefly upon the eruption. Personal experience does more to sharpen the percep- 
tion than can the fullest descriptions. We can merely suspect the disease during 
the initial stage unless an epidemic prevails. If, beside the characteristic catarrhal 
symptoms, the above-mentioned eruption on the mucous membrane of the palate 
exists, the diagnosis becomes tolerably certain. We should consider that erup- 
tions similar to that of measles appear in other diseases, more especially in rotheln, 
scarlet fever, typhus fever, in the beginning of small-pox, and in syphilis. In 
doubtful cases we shall be enabled to form a decided opinion by the other symp- 
toms and, above all, by the further course of the disease. 

Prognosis. — We have already remarked how favorable in general the prognosis 
is, but we must here repeat that all epidemics do not exhibit the same benign 
character, and that in every case the physician must bear in mind the possibility 
of complications, and particularly the danger of severe pulmonary disturbances. 

Treatment. — The patient should in general be kept somewhat warmer than 
in scarlet fever. Even in what seem to be the mildest cases the child should 
be kept in bed till desquamation is over. The sick-chamber is to be somewhat 
darkened, on account of the photophobia which usually exists at first. In this 
way normal cases run on favorably without any especial therapeutic interposition. 
The catarrhal symptoms, however, should always be heeded, since to disregard 
them may lead to their becoming aggravated. The chief requisite is cleanliness. 
At regular intervals the eyes, the nasal cavity, and the mouth should be washed 
out with lukewarm water. 

If, despite all this, certain disturbances appear in a worse form than usual, or 
if complications develop, these must receive especial attention. Severe eye 
troubles should be treated according to the usual ophthalmological practice ; and 
here unguentum hydrargyri oxidi flavi (1 to 100) [U. S. P. is 40 to 420] and atropine 
are chiefly employed. The treatment of croupous trouble in the throat or larynx 
will be fully described in a later chapter. For the pulmonary troubles, lukewarm 
baths, combined if need be with rather cool douches, constitute the most effectual 
remedy, which we should employ if it is in any way possible. We thus evoke 
deeper inspirations and promote expectoration, and thereby contribute largely to 
preventing the development, or the aggravation, of severe lung trouble. Inhala- 
tions of steam or of medicated fluids are often advantageously combined with the 
baths. To substitute the cold pack for the baths is in general justifiable only 
when the baths are not practicable. The pack is in many respects less efficient 
than the baths, and is, besides, often less agreeable to the patient. We are not 
acquainted with any internal remedies for the lung troubles which are at all 
reliable. In rare instances the excessive accumulation of mucus in the bronchi 
requires the administration of an emetic. As expectorants we may try ipecac, 
liquor ammonii anisatus, or benzoin. If considerable intestinal disturbance arises, 
we must employ small doses of opium, or calomel, or subnitrate of bismuth. We 
hardly need to say that, whatever else is done, the strength of the patient should be 
kept up as much as possible by giving wine, broths, milk, eggs, etc. For at least 
two or three weeks after the disease has ended, the child must be very carefully 
watched. 

As the disease is usually so mild, prophylaxis is not very strenuously attempted. 
If one child in a family is attacked, it is probably already too late to isolate the 
others, and it is even an advantage to the family to have all the children finish at 
once what they will hardly be able eventually to avoid. We would make an 
exception in favor of isolation if the disease prevailed in a severe form. 



48 



ACUTE GENERAL INFECTIOUS DISEASES. 



[It is not customary with us to insist so strongly upon isolation and thorough 
disinfection as in scarlet fever. But the tendency of the present day is toward a 
wide application of the principles of preventive medicine. It is certainly of no 
advantage to a child to contract the measles. Delicate children, especially those 
with tubercular predisposition, should be carefully guarded against it ; and, even 
if it is decided that it is not worth while to attempt to confine the disease to one 
member of a family, every precaution should be taken against infecting other 
families. Under suspicious circumstances, consequently, children are to be kept 
away from school and from contact with others. 

The liability to scrofulous and tubercular affections after recovery from the 
disease is to be borne in mind, and often demands in mothers special attention to 
general hygiene in order that full vigor may be regained.] 



CHAPTER VI. 

ROTHELN. 

( German Measles.) 

Rotheln is a disease similar to measles, but distinct from it, although formerly 
often confounded with it, and perhaps with scarlet fever as well. The observations 
of Steiner, Thomas, and others leave now no room to doubt that these diseases are 
distinct, for epidemics occur in which all cases present the characteristic peculiari- 
ties ascribed to rotheln. But the best proof is that children who have had rotheln 
are not infrequently attacked by genuine measles later. It may indeed be very 
difficult in an individual case to decide which disease is present ; but that rotheln 
does exist, as an independent form of disease, can be denied by those alone who 
have never seen it. 

After an incubation of about two or three weeks the disease begins with the 
appearance of the eruption. Initial symptoms preceding the eruption are either 
wholly absent or at most last for half a day. The eruption is decidedly like that 
of measles, but its individual spots are smaller. They are seldom larger than 
small peas and circular, being only exceptionally as dentated and irregular in 
outline as are the maculae of measles. They appear on the whole face, the head, 
the trunk, and the extremities, are pale red, but slightly elevated, and are not apt 
to become confluent. The soft palate sometimes exhibits, as in measles, a faint 
macular eruption at the beginning of the disease. After two to four days the 
eruption fades. There is usually no decided desquamation. 

Other symptoms of disease than this eruption are slight. Fever in many cases 
appears to be entirely absent. As a rule, there is for a day or two a slight eleva- 
tion of temperature, reaching 102° (39° C.)'at most. Tokens of a moderate catarrh 
of the conjunctiva, the nasal mucous membrane, the throat, and the larynx are 
also observed — viz., photophobia, nasal discharge, and cough. Sometimes the 
cervical lymph-glands are a little swollen. The constitutional disturbance is 
generally so slight that the child can hardly be kept in bed. Important complica- 
tions hardly ever occur. 

The prognosis of rotheln is therefore perfectly favorable, and the employment 
of any special treatment is needless. 



SMALI^POX. 



49 



CHAPTER Vn. 

SMALL-POX. 

( Variola. Varioloid.) 

etiology. — Small-pox has been known for centuries, although formerly often 
confounded with other diseases.* It is one of the most dreaded acute infectious 
diseases, and in earlier times it has destroyed thousands in its pestilential progress. 
It was the discovery of the possibility of prophylactic inoculation, and the ever- 
increasing spread of this precautionary measure, which first robbed the disease of 
some portion of its terrors. 

Numerous statements have been made about the occurrence of micro-organisms 
in the variolous eruptions on the skin and mucous membranes, but we are com- 
pelled to say that we are not yet acquainted with the specific, organized poison of 
small-pox, however strongly justified we may be in assuming its existence. Bac- 
teria can in fact easily be demonstrated in the eruption of variola, but most of 
them come from the surrounding atmosphere, and have no relation to the specific 
variolous processes. Likewise the colonies of bacteria found in internal organs 
(liver, spleen, kidneys) are regarded by their discoverer (W eigert) himself as due 
to septic processes complicating the small-pox, and not peculiar to it. 

Predisposition to variola, except as diminished by vaccination (vide infra), is 
universal. The disease may appear at any age, even in utero. It is said that 
persons ill with another acute infectious disease, such as scarlet fever, measles, or 
typhoid fever, are, for the time being, tolerably secure from infection with small- 
pox. The same individual rarely takes the disease a second time. 

A case of variola is always the result of transmission of the poison to a healthy 
person from one who is already ill with it. In many cases we can not, however, 
determine with exactness the mode of transmission, since the contagion may either 
be direct or by means of objects and utensils with which a patient has come in 
contact ; for example, the soiled linen. The dead body is capable also of transmit- 
ting the disease. In general, numerous instances point to a considerable "tenaci- 
ty " in the poison. It has been demonstrated that the disease can be transmitted 
to healthy persons by direct inoculation of the contents of the variolous pustules. 
It is stated that monkeys may be successfully inoculated in the same way. 

Course of the Disease. Variola and Varioloid.— The stage of incubation lasts 
some ten to fourteen days, often a somewhat shorter time, seldom longer. During 
this period prodromal symptoms are absent or insignificant. 

The disease itself begins suddenly with what are usually very characteristic 
initial symptoms — rigor, fever, headache, and intense pain in the loins. It is only 
in comparatively few cases that one or another of these symptoms is slight or 
wanting. The constitutional symptoms may be very severe — a dry tongue, stupor, 
wakefulness, delirium. The fever continues intense for some days. The pulse is 
much quickened. There is almost total anorexia, and often there is vomiting. 
There is constipation, or, more rarely, diarrhoea. Frequently there is a slight sore 
throat, and sometimes a slight bronchitis. The spleen is enlarged in most of the 
severe cases, and the urine often has a trace of albumen. In women, menstruation 
occurs in a remarkably large number of cases. The proper variolous eruption 
does not at once appear, but from the second day other characteristic efflores- 
cences are not rare. These are termed the initial rash of small-pox. We may 

* The very name small-pox {petite verole) is significant of its confusion with syphilis, which was 
termed the "great pox." 
4 



50 



ACUTE GENEKAL INFECTIOUS DISEASES. 



find either a diffuse or macular erythema, extending in varying degree over the 
trunk and extremities, or a haemorrhagic eruption with small spots appearing by 
preference upon the hypogastrium and the inner surface of the thighs (in the so- 
called femoral triangle of Simon). It is noticeable that this particular region usu- 
ally remains free from the proper variolous eruption. The erythema soon van- 
ishes, but the petechias remain visible for some time. 

The initial stage, just pictured, lasts usually three days. Severe symptoms 
occurring at this time do not exclude the possibility that the further course of the 
disease may prove favorable, while mild symptoms are of good omen. 

At the end of the third or on the fourth day the temperature makes a decided 
fall, and the regular variolous eruption begins to be developed upon the skin — the 
stadium eruptionis. During this period an evident difference among the separate 
cases becomes manifest. This distinction can not indeed be always drawn with a 
narrow line, but it is noticeable enough to justify the establishment of two types 
of variolous disease. We refer to the division into a severe form (variola vera), and 
another, mild form (varioloid). The variola proper has a well-developed eruption 
with many pustules, and, as a result of this, a second stage of fever {stadium sup- 
purationis). Varioloid has a much more scanty eruption, and little or no suppura- 
tive fever. We must now discuss these two forms separately. 

Variola. Vera. 

The eruption almost always begins in the face and upon the hairy scalp, ap- 
pearing somewhat later on the trunk and arms, and last of all upon the legs. 
It begins in the form of little red dots and spots, which develop in about two days 
to small papules (stadium floritionis) . If the hand be passed over thickly set and 
well- developed papules of variola, a peculiar soft, satin-like feeling is perceived. 
On the points of these papillae a little vesicle forms. This keeps growing larger 
and larger, its contents become turbid and purulent, till at last, on the sixth day 
of the eruption and the ninth of the disease, the development of the genuine pus- 
tule of variola is complete (stadium suppurationis). The pustule usually presents 
upon its summit a little dimple (" Pocken-nabel "), and is surrounded by a red 
border or "halo." Where the pocks are especially close together, as in the face, 
the skin between them is diffusely swollen, and the consequent burning and pain 
are excessive. The countenance becomes much disfigured. Often the eyes can not 
be opened because of the oedema. The hands also are apt to be intensely affected, 
especially the back of the hands, and also all parts which have previously been 
injured in any way (pressure or friction of clothing, etc.). The immunity of the 
skin in the so-called femoral triangle has been already mentioned. 

At the same time with the eruption upon the skin, or even somewhat earlier, a 
perfectly analogous efflorescence develops upon the mucous membranes. The 
chief places for its appearance are the mouth and throat, the tongue, the soft pal- 
ate, the nasal cavity, also the larynx, the trachea, and the upper part of the oesopha- 
gus. In the vagina and rectum it is rare and scanty. In this mucous efflores- 
cence, however, there are no proper pustules, but small, superficial ulcers. These 
result from the maceration of the uppermost layers of the mucous membrane. 
They sometimes become confluent. The annoyance produced by this eruption in 
the mouth and throat is, of course, very great. The pocks in the larynx manifest 
themselves by hoarseness, and occasionally by symptoms of stenosis. 

As we have said, the beginning of the eruption is the signal for a noticeable 
fall in the temperature. But in true variola the fall does not reach the normal, 
or only temporarily. The other symptoms likewise remit, especially the head- 
ache and lumbar pain. When, however, the suppuration begins, the fever rises 



SMALL-POX. 



51 



once more, and there are fresh symptoms of constitutional disturbance. This is 
the time for the dreaded attacks of delirium, during which the patient must be 
vigilantly watched, lest some untoward event happen. Now, too, complications 
may arise {vide infra). 

On the twelfth or thirteenth day of the disease the pustules begin to dry up 
{stadium exsiccationis) . The purulent contents of the pustules, part of which 
have burst, form yellow crusts, the swelling of the skin subsides, and, a few 
days later, the crusts and scabs begin to fall off . With the beginning of desic- 
cation, the fever declines ; the local as well as the constitutional symptoms 
become daily slighter, and convalescence follows. The healing of the pustules is 
frequently accompanied by an extremely troublesome itching. After the scabs 
have been cast off, the skin presents pigmented spots, which persist for months. 
Wherever the cutis vera has itself been destroyed by the suppuration, a scar is 
inevitable. Thus arise the familiar scars of small-pox, which continue visible 
through life. Very often, after the end of the disease, there is almost complete 
alopecia. The hair often grows again, but not always. 

Varioloid. 

The distinction between varioloid and variola vera is not in land, but in de- 
gree. Varioloid is only a milder form of variola. There is, as we have already 
said, no sharp boundary-line between the two. Varioloid is most often observed 
in those whose susceptibility to the variolous poison has been diminished by 
vaccination {vide infra). 

As above mentioned, the behavior of the disease during its initial stage will 
not permit us to decide positively whether variola or varioloid will be developed. 
It is true that if the symptoms be especially mild, we may guess that it will be 
varioloid ; and, likewise, the appearance of the initial erythema already spoken of 
is regarded as a favorable omen. 

Shortly after the pocks begin to appear, the decision can almost always be 
made with certainty. In varioloid the eruption is rather scanty. It is often 
irregular, and does not by any means always begin, like variola, in the face, but 
often on the trunk. The individual pocks are in no way different from those of 
variola ; but it often happens that they do not pass through all the regular stages 
to full suppuration, but undergo resolution before this occurs. Such cases, where 
there is nothing beyond papillae or vesicles, are sometimes spoken of as variolois 
verrucosa seu miliaris. The scantiness of the eruption and the limited amount 
of suppuration have for their corollary an absence, or at least a very slight 
development, of the suppurative fever. 

When the eruption appears, the temperature usually falls by crisis to the 
normal level and remains there. The desiccation may begin as early as the 
eighth or tenth day of the disease, so that the whole duration of varioloid is con- 
siderably shorter than that of variola. Grave complications are very exceptional. 
The pocks may develop upon the mucous membranes, but here, too, they are 
scanty and not very vigorous. 

Course of the Fever, Symptoms presented by Separate Organs, and Com- 
plications. 

1. Fever {vide Fig. 6).— In the initial stage, as we have said, the temperature 
rises rapidly as a rule, with a pronounced rigor ; and during the first days it very 
often reaches 104° to 106° (40°-4l° C). It sinks on the third to the sixth day, 
when the first papillae develop, and now, in the case of varioloid, falls rapidly to 
normal, and remains there. In variola the decline is slower and less complete ; 



52 



ACUTE GENERAL INFECTIOUS DISEASES. 



and with the beginning of suppuration the temperature begins to rise again. The 
violence of this suppurative fever is usually in direct proportion to the severity of 
the eruption. It has manifold fluctuations, but seldom lasts, in severe cases, less 



2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 




Initial Fever. Suppurative Fever. 

Eruption. 

Fig. 6.— Example of the temperature curve in true small-pox. 



than a week. Temperatures of 104° (40° C.) and higher are common. The fever 
declines by lysis. In case of approaching death, the temperature may be ex- 
tremely high, even reaching 108° or 109° (42°-43° C). 

2. Skin. — We have already described the macroscopic appearance of the erup- 
tion. It remains to mention briefly the histological phenomena. The first de- 
monstrable changes are in the cells of the deeper layers of the rete Malpighi. As 
a result of the variolous infection, the cells perish, are swollen by the lymph 
which escapes from the papillary blood-vessels, and are transformed into flaky, 
homogeneous masses without nuclei (" coagulation necrosis " of Weigert). The 
lymph becomes more and more abundant, and crowds the cells farther and far- 
ther apart. These are thereby finally changed into threads and membranes, 
forming a distinct net-work in the vesicle. This explains why, if such a vesicle 
be pricked, its entire contents are never discharged at once. Great numbers of 
white corpuscles escape, along with the lymph from the blood-vessels, and finally 
render the contents of the original vesicle purulent. Proliferative processes occur 
in the surrounding epithelial cells, which are still intact, and thus the margin of 
the vesicle becomes elevated, while the dead portion in the center sinks in. Thus 
the pock becomes umbilicated. If a portion of the papilla itself suppurates, a scar 
must be left on healing. If the process remain limited to the epithelium, complete 
regeneration takes place, and the skin reassumes its normal appearance. 

Certain secondary complications, which sometimes attack the skin, remain to 
be mentioned : abscess, phlegmon, erysipelas, gangrene, and bed-sores. None of 
these are directly due to the specific variolous intoxication. 

3. Respiratory Organs. — The disturbances here are in part symptoms of the 
specific process of the disease, and in part secondary. The frequent occurrence of 
secondary symptoms in small-pox is easy to understand (compare the chapter on 
lobular pneumonia). Of the primary symptoms, we should mention genuine pocks 
in the larynx, the trachea, and the larger bronchi. As sequels to these, more or less 
severe secondary disorders are very frequent : laryngeal ulcerations, which may 
even lead to laryngeal perichondritis and oedema of the glottis ; diffuse bron- 
chitis ; lobular pneumonia, often of great extent, due to the inhalation of solid 
matter into the lungs, and frequently accompanied by pleurisy. It should be 



SMALL-POX. 



53 



especially noticed that lobar, croupous pneumonia is not rare. Whether this he 
likewise secondary or a direct result of the variolous poison is not yet known. 

4. Digestive System. — The genuine pocks often develop, as stated, in the 
mouth and pharynx, and likewise in the upper part of the oesophagus. They are 
not observed in the mucous membrane of the stomach or intestines. The active 
diarrhoea sometimes seen depends upon catarrh of the intestine. Dysentery is 
rare. The eruption in the mouth and throat may result in severe secondary trou- 
bles, purulent otitis, parotitis, pharyngeal diphtheria, etc. The spleen is almost 
always considerably enlarged, and often the liver, but in a less degree. 

5. Circulatory System. — Pathological changes in the heart are rare, ♦ if we 
except the slight parenchymatous degeneration of its muscular fibers, common to 
almost all severe infectious diseases. Sometimes there is a slight endocarditis 
(q. v.), which is probably secondary. Pericarditis is rather more frequent. 

6. Organs of Special Sense. — Genuine variolous pustules occur upon the eye- 
lids and the conjunctiva. Later in the disease there may be keratitis, iritis, or 
choroiditis. 

We have already mentioned the relative frequency of aural disturbances, par- 
ticularly purulent otitis media. 

7. Articular swelling may appear in the suppurative stage. The shoulders and 
knees are most apt to be attacked. Periostitis also occurs. 

8. Nervous System. — We find no pathological changes corresponding to the 
severe nervous derangements manifested during the disease. After the small-pox 
is over, spinal diseases sometimes occur, with either paralysis or ataxia. Westphal 
has demonstrated as their cause, in some cases, numerous disseminated centers of 
inflammation in the spinal cord. 

9. Albuminuria is quite frequent in severe attacks, but genuine nephritis is a 
very rare complication. 

Anomalies in the course of the disease are manifold. We do not speak of 
the two typical forms already considered. There are abnormally mild cases, with 
scarcely any initial symptoms, or with an obscure eruption, or with no eruption at 
all (febris variolosa sine exanthemate) . In such cases a correct diagnosis is pos- 
sible only at the time an epidemic prevails, and by the aid of the attendant setio- 
logical circumstances. There are also abortive cases in which the first symptoms 
are severe, but which recover with remarkable rapidity. 

The abnormally severe cases are more important. First, there is the confluent 
variety. This is merely the typical process in its completest development. The 
initial symptoms are themselves generally very severe, and are followed, without 
any considerable remission of the fever, by the eruption of hundreds of pustules. 
The skin of the face and hands is one continuous area of suppuration. The local 
discomfort is extreme, as is also the intensity of the fever and of the constitutional 
symptoms. The nervous system suffers most. There is at the same time an un- 
usually abundant eruption upon the mucous membranes. The occurrence of the 
above-mentioned complications affecting the various organs of the body is fre- 
quent. Death is a common result ; or, if recovery takes place, it may be delayed 
by tedious sequelae. 

Hsemorrhagic small-pox is the worst anomalous form. The name is applied 
to several different varieties. In the first place, any variolous eruption may 
become more or less hsemorrhagic, and yet the general course of the disease not 
be essentially altered. Such cases are more common among elderly people, cachec- 
tic persons, and drunkards. Secondly, there is a very severe form of small-pox, 
which is generally quickly fatal. The initial stage is marked by the unusual 
severity of the symptoms. The abundant eruption soon becomes hsemorrhagic, 
and there are also ecchymoses in the mucous membranes and the internal organs. 



ACUTE GENEEAL INFECTIOUS DISEASES. 



This has heen called black small-pox, and by Curschmann variola hcemorrhagica 
pustulosa. 

There is another form of hemorrhagic variola, different from these but linked 
to them by transitional varieties. In it the acute haemorrhagic diathesis develops 
during the initial stage. Death almost always occurs before the regular variolous 
eruption. This most frightful form is usually termed purpura variolosa. That it 
is small-pox is proved by its ^etiological relations alone. Otherwise it would be 
impossible to distinguish it from certain other acute septic disorders. It is prone 
to attack the youthful and vigorous. Chills, headache, and pain in the loins are 
the first symptoms, just as in ordinary cases. Cutaneous ecchymoses appear as 
early as the second or third day. They increase in area so rapidly that one can 
almost see them grow. They are most extensive in the hypogastric region. There 
are also ecchymoses in the eyelids, the conjunctiva, the mouth and pharynx, and, 
as the autopsy discloses, many in the internal viscera. The constitutional symp- 
toms are most severe, and the patient seldom survives the fifth or sixth day of the 
disease. 

Diagnosis. — The certainty with which we can make the diagnosis of small-pox in 
any well-developed case is equaled by the difficulty of deciding about it during the 
beginning of the disease, or even during the beginning of the eruption. At this 
period diagnosis may be impossible. When the variolous eruption is in process 
of development, it may be confounded with typhus fever, with that form of mea- 
sles in which the papillae are prominent, with syphilitic eruptions, and with cer- 
tain forms of erythema exsudativum, just breaking out. We can not here fully 
discuss all the factors which should be considered in making this diagnosis. It is 
important not to regard the cutaneous appearances alone, but to note all the other 
symptoms besides. But it is often necessary to watch a doubtful case for some 
time before a diagnosis can be established. 

Prognosis. — The facts which are of greatest weight in prognosis have already 
been emphasized. We may repeat that during the initial stage the prognosis of 
any individual case can seldom be determined. If the first symptoms are mild, 
or if the initial erythema appears," the case is regarded hopefully. The abundance 
of the eruption has an influence upon the severity of the disease. Circumstances 
peculiar to the individual are also important — e. g., age, constitution, or alcoholic 
habits. We have already called attention to the danger of confluent small-pox, 
and to the almost absolutely fatal prognosis in the genuine haemorrhagic variety. 
The mortality varies greatly in different epidemics ; on the average it may be taken 
at about fifteen to thirty per cent. Beyond doubt, the introduction of vaccination 
has decidedly lessened the fatality of the disease by diminishing the frequency of 
the severe forms. 

Treatment.— 1. Prophylaxis— Vaccination. — As in all contagious diseases, 
isolation is of little avail unless complete. This fact has led to the erection in late 
years of small-pox hospitals. All utensils used by the patient, and his clothing, 
bedding, and the like, should be most carefully disinfected. The best method is to 
employ a high degree of heat— viz., 240° to 250° (115°-120° C). 

These precautionary measures are employed in many other diseases as well, but 
for small-pox we are acquainted with a peculiar method of prophylaxis. It is 
founded upon a fact which is at once the most remarkable and inexplicable, and 
the most beneficent, within the domain of the infectious diseases. We refer to 
vaccination. It must long ago have been remarked that a person who lias had the 
disease once, enjoys, to a large degree, immunity from any fresh infection. This 
suggested the idea of exposing children purposely to contagion, so as to insure 
them from small-pox for the rest of their lives. The actual inoculation of small- 
pox is said to have been long practiced in India and China. In the year 1717 it 



SMALL-POX. 



55 



was employed by Lady Montague, of England, upon her own son, and with suc- 
cess. Unfortunately, however, the inoculated small-pox proved fatal in many 
instances ; and, being itself contagious, it served to spread the disease still further. 
Then appeared an article written by the English surgeon, Edward Jenner, in 1798. 
This informed the medical profession of a fact already known to the rural popu- 
lation of his native place, but which Jenner first established scientifically, and 
recognized in all its importance. There sometimes occurs a disease similar to 
small-pox upon the teats and udder of the cow, called variola vaccina. It is appar- 
ently a local trouble, and can easily be inoculated upon the skin of human beings. 
Vaccine pustules will be developed upon the spot inoculated. These almost invari- 
ably heal without any great constitutional disturbance ; but the person vaccinated 
possesses the same immunity from small-pox as if he had had small-pox itself. 
This statement of Jenner's was soon confirmed upon every side. The result is 
the continually spreading custom of prophylactic vaccination. In some coun- 
tries it is enforced by law, and it can be opposed only by ignorance or by lament- 
able prejudice. 

To explain how vaccination can protect against small-pox in this way is still 
utterly beyond our powers. We have lately gained this much help in understand- 
ing it, that it is no longer an isolated fact ; for analogies have been discovered in 
the case of other acute infectious diseases (cf . the chapters on hydrophobia and 
malignant pustule). We are likewise in the dark as to the relation between small- 
pox and vaccinia. Many authors regard the virus of vaccinia as merely a modifi- 
cation of the variolous poison, while others assume that there is a specific differ- 
ence between the two. As yet, the infectious material of neither has been exhib- 
ited in a pure state ; and we must for the present therefore leave this question 
undecided. A statement in support of the essential unity of the two infectious 
agents can be adduced. The inoculation of cows with small-pox is said to produce 
vaccinia, which, inoculated in its turn upon children, will result in vaccinia and 
not in small-pox. This demands further investigation. 

We can mention only the most important of the details relating to vaccination 
and the method of its performance. The inoculation is made either with animal 
virus, direct from the cow, or with humanized virus, obtained from persons previ- 
ously vaccinated. The lymph taken from a vaccine-pustule can be kept a long 
time, either pure or mixed with glycerine, without deteriorating. It is kept in 
small glass tubes, hermetically sealed, or in a dried form upon little " points " 
made of bone. The most common mode of vaccination now in use is to make 
three shallow incisions, not too close together, in the skin of the upper arm, and to 
introduce the vaccine-lymph into them. The surrounding tissue becomes swollen 
in three or four days. In seven or eight days the vaccine vesicles are well devel- 
oped, if the disease takes its normal course. Next they become purulent, and then 
dry up, and finally, on healing, leave the familiar scar behind. The whole process 
occupies about three weeks. If the vaccination fails, or is but partially successful, 
it must be repeated after a few months. The protective power of vaccination does 
not last indefinitely, and therefore re-vaccination is necessary every five or six 
years. The first vaccination of children usually takes place when they are three 
or four months old. If they are feeble we wait longer, unless small-pox is prevalent. 

It must be confessed that vaccination is not without its dangers. The little 
cutaneous wound made by it may lead, like any other, to sepsis or to erysipelas. 
The latter has been called vaccination-erysipelas. But such misfortunes are 
extremely rare. The "vaccine roseola" deserves especial mention. It appears 
first upon the arm vaccinated, and spreads over the rest of the body ; but it is not 
a serious matter. It is of course possible that other diseases, among which syphilis 
is of chief importance, may be inoculated along with vaccinia ; but this is a very 



56 



ACUTE GENERAL INFECTIOUS DISEASES. 



rare occurrence — much more so than the enemies of vaccination pretend. If 
the physician exercise proper care, it can be entirely avoided. The exclusive 
employment of animal virus in vaccination does away with a number of danger- 
ous possibilities, and for this reason it is constantly growing in popularity. 

[The incubation stage of vaccinia being shorter than that of small-pox, the 
prompt vaccination of an unprotected individual who has been exposed to infec- 
tion should always be practiced, if possible ; oftentimes the severe disease may 
thus be prevented.] 

2. The treatment of small-pox is purely symptomatic. When the disease has 
once begun it is too late for vaccination to have any influence upon its further 
course. During the initial period we may advantageously employ cool baths to 
diminish the fever and alleviate the constitutional symptoms. An ice-bag will 
relieve the headache. We must not let the lumbar pains lead us to any but a 
cautious use of local irritants, for the pocks come out in greater abundance upon 
such portions of the skin as have been in any way irritated. If the disease proves, 
during the stage of eruption, to be varioloid, there will be no further need of special 
treatment. Good nursing and proper food will suffice. 

The true small-pox, on the other hand, demands the interposition of the physi- 
cian. He must strive to guard the regular course of the disease in the skin and in 
those portions of the mucous membrane which are accessible from being disturbed 
by secondary inflammations. For we have no doubt that the ruptured pustules 
furnish a most easy ingress to septic impurities from the surrounding atmosphere, 
so that later, when there is extensive suppuration of the skin, or analogous and 
severe disturbance in the mucous membrane, it is impossible to discriminate 
between the effects of the small-pox itself and those due to the secondary suppura- 
tion. If we were able to have the whole process go on " antiseptically " we 
should certainly have made an important advance in therapeutics. Indeed, the 
methods of treatment which have been up to this time recommended fulfill this 
indication up to a certain point, e. g., painting the skin with tincture of iodine, or 
with a strong solution of nitrate of silver — methods formerly much in vogue. 
Schwimmer's suggestion seems still better. He recommends, from the beginning of 
the eruption, the use of a paste made as follows : Acid, carbol., parts 4 to 10 ; ol. olivae, 
40 ; cretse prseparat., 60. M. et ft. pasta mollis. This is spread on pieces of old linen 
and laid upon those parts where the eruption is apt to be worst — viz., the forearm, 
hand, and leg. The face is covered with a mask, having holes corresponding to 
the mouth, nose, and eyes. The applications are changed every twelve hours. 
Under this treatment the local distress is said to be diminished, suppuration slight, 
and healing comparatively rapid. The pain and sense of tension in the skin are 
often relieved by cold applications, or by simple ointment or oil. Under Hebra, in 
Vienna, continuous warm baths were employed in severe cases with great success. 

The treatment of the affected mucous membrane in small-pox must also meet 
the indication above-mentioned. The most thorough disinfection of the mouth 
and pharynx must be aimed at. The means to be used are careful washing and 
gargling with solutions of chlorate of potash (1 to 30), carbolic acid, borax, per- 
manganate of potash, or liquor f erri chloridi. The eyes, if they need it, must also 
be appropriately treated. As to all other complications, cool baths are relatively 
the most useful remedy. They can be given without difficulty. The chief indica- 
tions for them are severe pulmonary or nervous symptoms, or continuous high 
fever. Internal antipyretics, such as quinine or antipyrine, are also employed. 
Violent nervous disturbances, such as delirium, sometimes require the cautious use 
of narcotics. There is nothing to add as to the treatment of malignant hsemor- 
rhagic small-pox, for, as we have said, such cases are unfortunately almost 
hopeless. 



VARICELLA.— ERYSIPELAS. 



57 



CHAPTER VIII. 

VARICELLA. 

(Chicken-pox.) 

Varicella is truly one of the children's diseases. Adults very rarely have it. 
It is contagious, and often comes in epidemics. 

The stage of incubation does not last over thirteen to seventeen days. The 
disease begins with the appearance of vesicles, the size of a pea or a little larger, 
usually having a small red areola, and varying in number from ten to one hun- 
dred or more. The trunk usually bears the greater part of the vesicles, while the 
extremities have few. The face is frequently the seat of a considerable number, 
and sometimes there are a few upon the hairy scalp. There may be a vesicle here 
and there upon the mucous membrane of the mouth or palate. There are seldom 
any prodromata. Slight symptoms of fever may attend the eruption itself. The 
eruption is usually over in a few days, although there may be repeated crops, so 
that we often see fresh vesicles by the side of others which are drying up. Each 
separate vesicle heals quickly, and the pustulation seen in small-pox is here excep- 
tional. The course of the disease is completed in a week or ten days. Most chil- 
dren feel perfectly well the whole time, although there may be in rare cases pain 
in the limbs, anorexia, and a slight coryza. A severe complication is hardly ever 
seen. 

Exceptionally, the disease may be rudimentary, with a varicelloid roseola and 
no formation of vesicles. On the other hand, some cases present quite severe con- 
stitutional symptoms and a high fever, even reaching 105° (41° C.) temporarily. 
In most cases, however, as we have said, the child is so slightly disturbed that a 
physician is hardly thought necessary. 

The diagnosis is almost always easy. Formerly varicella was often con- 
founded with small-pox, and to this day the followers of Hebra, in Vienna, for 
some inconceivable reason, maintain the identity of the two. That they are essen- 
tially distinct is shown (1) by the epidemics of the two appearing entirely separate 
from each other, (2) by the fact that having one does not give immunity from the 
other, and (3) by the uniform failure of attempts to produce variola by inoculating 
varicella, or vice versa. Still, we must bear in mind, in order to avoid mistakes, 
that many dermatologists class the mildest cases of small-pox as varicella. Those 
who devote themselves to general diseases are probably all now convinced that 
varicella is a separate disease. 

The prognosis is perfectly good. There is no special treatment necessary, but 
young children should be kept in bed till the eruption has dried up. 



CHAPTER IX. 

ERYSIPELAS. 

(St. Anthony's Fire.) 

iEtiology. — Erysipelas is an inflammation of the skin, excited by the presence 
of a specific, pathogenetic micrococcus (vide infra), and recognized by redness, 
swelling, and pain. It has the peculiarity of spreading gradually, by direct exten- 
sion, from its point of origin over a larger or smaller portion of the skin. There 
are two varieties commonly recognized — an idiopathic, or exanthematic, and a trau- 



53 



ACUTE GENEEAL INFECTIOUS DISEASES. 



matic. The latter may follow any cutaneous wound if it be infected with the spe- 
cific virus of erysipelas. Traumatic erysipelas is therefore a surgical disease, and 
will not be further considered here ; nor shall we treat of puerperal erysipelas, a 
possible sequence to injuries inflicted upon the female genital organs during par- 
turition ; nor of the erysipelas of the new-born, which usually has its origin in 
the navel or in small fissures of the anus. 

The so-called idiopathic erysipelas appears almost exclusively in the face, or at 
least it starts there. As it goes on it very frequently spreads to the hairy scalp, 
and not infrequently it also extends down upon the trunk. The clinical manifes- 
tations are perfectly characteristic. It is, however, a question whether idiopathic 
erysipelas is essentially different from the traumatic variety. There is good reason 
to suppose that facial erysipelas is really traumatic in every case, having its origin 
in injuries of the skin or mucous membrane, which are so small as to be over- 
looked. This view not only seems a priori very probable, but is supported by nu- 
merous cases. We see, for example, erysipelas taking its origin in excoriations of 
the nose or the borders of the nostrils, or in excoriations or fissures of the lobe of the 
ear. Quite often coryza precedes the erysipelas, and, in that case, the first inflam- 
matory swelling of the skin is at the nose. The probable explanation of this fact 
is that the nasal catarrh is apt to cause slight erosions of the mucous membrane, 
and that these furnish an opportunity for infection with erysipelas. On the other 
hand, it can not be denied that there are cases of facial erysipelas where it is abso- 
lutely impossible to make out any cutaneous excoriation, and where there is an 
initial stage with feverish symptoms preceding the localized trouble in the skin 
(vide infra). Such cases suggest the thought that erysipelas is like the acute 
eruptive diseases, and that it is at least possible that infection may take place in 
some other way than the one mentioned. 

The specific virus of erysipelas has been brought to our knowledge chiefly 
through the researches of Fehleisen. He has demonstrated a characteristic " chain- 
forming micrococcus " in the lymphatic vessels and serous canaliculi of the dis- 
eased skin. This micrococcus is distinguished by its peculiar behavior in pure 
gelatine cultures, and invariably causes erysipelas in the rabbits and the human 
beings that are inoculated with it. 

Facial erysipelas is most apt to attack the young, and seems to be somewhat 
more frequent in women than in men. The laity erroneously regard catching cold 
as one of the chief causes of the disease. If we except the predisposing causes 
above mentioned — viz., coryza, slight scratches, cuts, etc. — we usually find no cause 
of which we can feel certain. Often endemic influences are important. It has 
been long known that traumatic erysipelas can get so secure a footing in particular 
hospitals or wards that every wounded person treated in them is in danger of this 
disease. But the apparently idiopathic variety is sometimes remarkably frequent 
in particular places. Likewise several members of one family may have facial 
erysipelas simultaneously. In nearly all such cases the sufferers are infected from 
some common source, for direct contagion is certainly exceptional. Direct inocu- 
lation can, however, as has been proved, convey the disease from a patient to other 
persons or to animals. 

In contrast with the behavior of the acute eruptive diseases, erysipelas is pecul- 
iarly apt to attack the same person over and over again. There are people who 
have facial erysipelas about every one or two years. Often the explanation of this 
apparently lies in some chronic disease — e. g., chronic ozsena — which makes infec- 
tion easy, but in other cases no cause can be discovered. Marasmus seems to pre- 
dispose to erysipelas. At least we have observed that erysipelas occurred with 
relative frequency, in the Leipsic hospital, in patients suffering from the last 
stages of phthisis or cancer, or similar diseases. 



EEYSIPELAS. 



59 



Clinical History. — In many cases the first subjective symptoms are simultane- 
ous with the cutaneous swelling, and these are chiefly local. There is pain and a 
sense of tension in the skin. Soon subjective symptoms of fever also appear, such 
as general malaise, anorexia, and headache. In other cases the disease starts with 
more violent constitutional symptoms : there is an initial rigor, with violent head- 
ache and great languor. Almost at the same time, or sometimes two or three days 
later, the patient notices that the face is swollen. In rare instances the disease 
begins with sore throat. We saw three almost simultaneous cases of facial ery- 
sipelas in one family, where a severe sore throat lasted for four or five days pre- 
ceding the appearance of the cutaneous disorder. 

The erysipelatous process in the skin is almost always circumscribed at first. 
It usually starts on the nose, less often upon the cheek, the ears, or the hairy scalp. 
The skin becomes considerably swollen, grows red, smooth, and shiny, and feels 
hot. The redness and swelling keep spreading. There is usually a sharp, elevated 
ridge, perceptible to sight and touch, separating the diseased from the still healthy 
portion of the skin. As long as the erysipelas is spreading, we see stretching out 
from its border, or somewhat removed from it, small red streaks and spots which 
gradually increase in area and intensity, and finally coalesce. Any decided fold in 
the skin may hinder for a time the extension of the disease. The naso-labial folds 
are particularly apt to limit it. The border of the hairy scalp frequently forms a 
terminal line ; but the whole scalp may be attacked, the inflammation stopping 
only when it reaches the nape of the neck. It is only in a relatively small num- 
ber of cases that it spreads farther yet, attacking the back, the arms, and the an- 
terior surface of the trunk, or even extending to the feet. This is known as ery- 
sipelas migrans. The facial erysipelas may be healed long before the disease 
ceases to extend over other parts of the body. When the spreading process is 
about to cease, the inflammation usually becomes decidedly milder, appears only 
in isolated spots, and finally stops completely. In most cases, only the face, the 
ears, and a part of the scalp are attacked. 

It is not a rare thing for vesicles or bullae to form in the portions of skin at- 
tacked. Such cases are called erysipelas vesiculosum or erysipelas bullosum. The 
serum may change to pus in these blisters, and then we have erysipelas pustulo- 
sum. Exceptionally the infiltration of the skin becomes so intense as to result in 
a localized necrosis or gangrene — erysipelas gangrenosum. The parts most apt 
to be attacked by this are the eyelids. 

Microscopic examination of the skin shows a marked hyperemia of all the 
blood-vessels and a very considerable infiltration of both the skin and the subcu- 
taneous connective tissue with serum and cells. In those parts where vesicles are 
formed there are many dead and disintegrated epithelial cells in the rete Malpighii. 
The presence of great numbers of the specific chains of micrococci has been already 
mentioned. 

The inflammation in any one spot usually ends four or five days after it has 
made its appearance there. There is usually much attendant desquamation. The 
face is often left with a finer complexion than it had before. 

The other symptoms, of which the constitutional disturbance and the fever are 
chief, correspond pretty closely to the severity and extent of the cutaneous lesion. 
It is comparatively seldom that this correspondence does not exist. 

The fever in facial erysipelas usually rises rapidly at first, and to a considerable 
height. We have seen but few cases where the high fever was delayed till a day 
or two after the skin was attacked. The temperatures observed in erysipelas are 
often extreme : 106° (41° C.) is not at all rare. The highest we ever saw was 
107*2° (41 "8° C). While the erysipelas continues or is spreading, the fever is sel- 
dom continuous, nor are the remissions insignificant. Pronounced intermissions, 



60 



ACUTE GENEKAL INFECTIOUS DISEASES. 



even down to normal, are very frequent, but are followed again by a rapid and 
great rise of temperature. The fever may terminate with a genuine crisis. In in- 
tense cases of considerable extent, or in erysipelas migrans, the termination is 
more apt to be by a more or less gradual lysis. We have seen the cutaneous in- 
flammation in erysipelas migrans still extend itself a little, in a rudimentary 
form, after the fever had completely ceased. 

The headache is often intense, and seems to result not merely from the inflam- 
mation of the scalp, but from disturbances of the circulation in the underlying 
parts. Other severe cerebral symptoms are also relatively frequent. The patient 
may be very restless, excited, and wakeful. At night there may be mild or even 
violent delirium ; or there may be decided stupor. All these symptoms are in 
part due to the constitutional infection, but also justify a surmise, as we have said, 
that there is circulatory derangement in the meninges and the brain itself, result- 
ing from the inflammation in the scalp. In drunkards, delirium tremens is not 
infrequent. 

One of the most constant symptoms in facial erysipelas is gastric and intestinal 
disturbance. There is usually complete anorexia. The tongue is thickly coated. 
Vomiting is frequent, not only at the beginning but during the course of the dis- 
ease. There is constipation ; or there may be quite severe diarrhoea. There is no 
pathological lesion known corresponding to these clinical symptoms. 

The entire duration of the disease varies greatly in different cases. A very 
light case may get well in a few days. Most cases of average severity last a week 
or ten days. Erysipelas migrans may continue for many weeks. We have sev- 
eral times seen a relapse come on after a number of days of complete apyrexia. 
Either the face would be once more attacked, or some portion of the skin which 
had previously escaped. 

Local complications are comparatively rare in erysipelas. The lymphatic 
glands of the throat and back of the neck are very frequently somewhat swollen, 
but seldom attain great size. Bronchitis and lobular pneumonia may develop in 
severe cases, but are not at all characteristic. Some observers call attention to the 
occurrence of pleurisy, endocarditis, and pericarditis ; but these complications also 
are probably secondary. The spleen is usually slightly swollen. Sometimes there 
is an icteroid hue. The urine frequently contains a small amount of albumen, 
although genuine nephritis is exceptional. Swelling of the joints has been re- 
peatedly observed. It is more frequent in the severe surgical forms of erysipelas, 
which are combined with universal septic and pysemic conditions of the system. 
Purulent meningitis may complicate an erysipelas located in the head, but it is 
very rare. We should be exceedingly cautious about asserting its existence even 
when the cerebral symptoms are very pronounced. 

Cutaneous complications are relatively frequent. We have seen herpes labialis 
quite often, and a number of cases of urticaria. Of much greater importance are 
the cutaneous abscesses which occur in severe cases. These are due to a phleg- 
monous or even gangrenous inflammation of the connective tissue. Then most 
frequent seat in the face is the eyelids, as already stated ; and in that case the eye 
may itself be endangered. At the close of severe cases of erysipelas migrans, 
numerous abscesses may develop in the skin of the trunk and extremities, delay- 
ing convalescence. 

The diagnosis of erysipelas is almost always easy when once the cutaneous 
lesion has developed. Phlegmonous inflammation of the skin and lymphangitis 
are to be eliminated ; but this is always possible, with proper care. After a single 
examination, we may confound it with acute facial eczema of great severity, or 
even with a marked urticaria. Chief attention should be paid to the characteristic 
border of erysipelas and to its manner of extension. 



DIPHTHERIA. 



61 



The prognosis of facial erysipelas, when it attacks a healthy person, is very 
favorable. In drunkards a severe case may be complicated by delirium tremens, 
and the issue be unfavorable. We saw one case end fatally because of gangrene 
in the eyelids, followed by purulent inflammation of the orbital connective tissue. 
Erysipelas migrans may so exhaust the powers of feeble patients as to become 
dangerous. The prognosis of surgical erysipelas is relatively more unfavorable, 
but can not be considered here. 

Treatment. — In a case of not more than average severity no special treatment 
is needed. To lessen the local discomfort, we usually cover the skin with pow- 
dered starch, or anoint it with olive-oil, carbolized oil, or vaseline. An ice-bag 
on the head is agreeable to most patients. If we wish to prescribe something, we 
may choose an acid mixture, as follows : Acid, muriat. dil., parts 8 ; syrup, 15 ; 
aquae, 120. M. 

In a severe case, however, the high fever and the nervous symptoms may 
demand our interference. The remedy to be chiefly recommended is cold baths, 
of which two or three may be given in a day, and which most patients bear very 
well. The exhibition of quinine is seldom called for, as there is a tendency to 
great spontaneous intermissions in the fever. If the facial inflammation proves 
to be part of an erysipelas migrans, the chief indication for treatment would be to 
check the unceasing advance of the disease ; but, unfortunately, the means recom- 
mended for this purpose too often fail. It used to be customary to cauterize the 
skin along the border of the erysipelas with nitrate of silver, but this has been 
almost entirely abandoned as useless. Hueter recommends the injection of a two- 
per-cent. solution of carbolic acid beneath the skin at a little distance from the 
border of the inflammation. Although this is certainly a rational method of treat- 
ment, we have seldom seen any brilliant results from it. We have repeatedly em- 
ployed Pirogoff's camphor treatment. The patient takes every hour or two three 
grains (0*15 grm.) of powdered camphor and drinks large quantities of hot tea, to 
promote perspiration. In severe cases this method deserves a trial. Numerous 
other internal remedies have been recommended ; but we need not enumerate 
them. We have not seen any influence upon the extension of the disease exerted 
by large doses of salicylic acid or benzoate of soda. In England a prominent 
remedy is liquor ferri chloridi (in the form of tr. ferri chlorid.), given to the 
amount of drachms jss.-ijss. in the course of the day (6-10 grm.). In the severe 
cases the main point, after all, is to maintain the patient's strength by nursing and 
food. If cutaneous abscesses form, they should be opened promptly, when they 
usually soon heal. 



CHAPTER X. 

DIPHTHERIA. 

(Dip7ithe7'itis. Croup. Cynanche contagiosa^) 

JEtiology and General Pathology— Clinically, " diphtheria " means a certain 
well-characterized, specific, acute, infectious disease, the chief visible lesion of 
which is a croupous-diphtheritic inflammation of the pharynx and upper air-pas- 
sages. In a purely pathological sense, however, the terms " croupous " and " diph- 
theritic " have a broader meaning. They denote a certain form of inflammation 
which may occur in the mucous membrane of almost any part of the body. It is 
frequent in the intestine and bladder. There is great diversity in the causes which 
may produce it. 



62 



ACUTE GENERAL INFECTIOUS DISEASES. 



The pathological characteristic of croupous-diphtheritic inflammation consists 
in the formation of a fibrinous exudation. This may either be a croupous mem- 
brane, which is grayish white, rather firm, elastic, and can be lifted off with com- 
parative ease from the mucous membrane upon which it rests, or it may be a 
diphtheritic infiltration with necrosis of the tissues. Here the exudation is more 
or less deeply imbedded within the proper structure of the mucous membrane 
itself. There is no essential difference between croup and diphtheria ; diphtheritic 
inflammation is the severer form of the disease, croupous inflammation the milder. 
In diphtheria the fibrinous exudation is preceded by a necrosis of the epithelium 
and of the underlying tissues of the mucous membrane as well, while in the case 
of croupous exudation the necrosis is limited to the epithelium. The croupous 
membrane never rests upon an intact mucous surface, but replaces the epithelium, 
which has already been totally or in very large part destroyed. Flaky remnants 
of the epithelium, no longer nucleated, are sometimes found in the meshes of the 
fibrin. The preceding destruction of the epithelium is essential to the occurrence 
of fibrinous, croupous inflammation. The fibrinous exudation can be formed in 
those places only where the cause which excites the inflammation kills the epithe- 
lium at the same time. Apparently the epithelial cells have little if any share in 
the formation of the exudation. It is more probable that the material for the 
fibrin comes from the fibrinogen of the inflammatory matter which transudes 
through the walls of the vessels, and also from the disintegrated migratory white 
blood-globules. These last are abundant throughout the deposit itself, and still 
more numerous in the entire tissue of the mucous membrane beneath the croupous 
or diphtheritic exudation. If recovery takes place in croup, all that is needed 
after the exudation has been cast off is the renewal of the epithelium, which can 
be accomplished through the exclusive agency of the remnants of epithelium left 
along the borders of the diseased spot. In diphtheria, however, the entire necrotic 
portion of mucous membrane must slough off, a line of demarkation being formed, 
and cicatricial tissue replaces the necrosed portion. 

The above is a bare outline of the present views about croupous and diph- 
theritic inflammations. They have been reached gradually through the labors of 
E. Wagner, Weigert, and others. We have not yet touched upon the astiological 
factors ; but what precedes renders it evident how manifold they may be, for 
any cause which destroys the epithelial layer of the mucous membrane, and at 
the same time promotes inflammation, may excite croup. We have mechanical 
causes, such as impacted faeces, gall-stones, renal calculi ; chemical irritants, caus- 
tics, like ammonia and the acids ; and, finally, a number of specific, infectious, dis- 
ease-producing poisons. Among these is the specific poison of diphtheria proper. 

Beyond a doubt the diphtheritic poison is organized. To demonstrate this, 
however, has been thus far extremely difficult, for there are in the diseased spots 
a great number of diverse micro-organisms, originating in the mouth and throat, 
and really secondary to the diphtheritic process ; but, although they of course are 
entirely different from the specific " diphtheritic bacteria," it is very hard to sepa- 
rate them. The latest systematic investigations of Loffler have made us acquainted 
with a bacillus which can be found in most cases of diphtheria, while at other 
times it is very rarely found in the mouth. Loffler's bacilli are little cylinders 
with a peculiar club-like swelling at their ends. In croupous membranes they are 
found in colonies. Inoculated upon animals, they have a decidedly pathogenetic 
power, and produce a disease similar to diphtheria. That they constitute the long- 
sought diphtheritic poison is therefore probable, but it is by no means conclu- 
sively proved. 

Diphtheria is chiefly a disease of childhood. It is much less frequent in those 
over ten years of age than in earlier life. In the larger towns sporadic cases are 



DIPHTHEKIA. 



63 



occurring all the time, but now and then the cases become so numerous as to be 
endemic or epidemic. As to the precise way in which a human being becomes 
infected the opinions of physicians differ. We think it most probable that the 
poison reaches the pharynx along with the inspired air or in some other way, and 
here penetrates into the mucous membrane. It is very rare for the larynx to be 
the point of entrance {vide infra). It first excites a local disturbance, to which 
the general infection of the system {vide infra) is only a sequel. The original 
source of the infectious material is probably always some other case of diph- 
theria. Sometimes a direct, immediate transmission of the poison (contagion) is 
extremely probable — e. g., due to coughing, or to sucking out bits of membrane 
after tracheotomy. The latter is a comparatively frequent cause of the disease in 
physicians and nurses. The infection is often spread by some person who may 
himself escape the disease, or by fomites, playthings and other objects, to which 
the poison is adherent. The potency of the inf ectious matter is not easily de- 
stroyed. As to what extent the diphtheritic poison may have a power of inde- 
pendent reproduction outside the body — e. g., in the ground, or in the floor of 
dwellings — we remain in complete ignorance. Finally, we should notice that of 
late attention has been called to the possibility of catching diphtheria from dis- 
eased animals. Poultry, doves, and calves have diseases that are at least similar 
to diphtheria. 

[While it can not be denied that there is strong evidence in favor of the view 
that the poison often is confined to a limited area at the start, and thence infects 
the system, it seems equally probable that in other cases a constitutional infection 
through the pulmonary blood-vessels precedes the formation of membranes. 
Clinical observation as well as analogy point to this double line of invasion. 
Infection through the alimentary canal is not probable, though it can not be posi- 
tively denied. 

There are still points in the aetiology and pathology of this affection which are 
involved in obscurity. Much has been said and written in this country and in 
England about the relations of filth and diphtheria. That filthy surroundings 
contribute a soil favorable to the development of the poison, and at the same time 
dimiriish the resisting power of the human organism, can not be doubted ; but, as 
long as the parasitic theory of infectious diseases prevails, sewer-gas and the like 
must be classed among the predisposing or accessory causes. 

Some of the frightfully virulent epidemics of diphtheria in sparsely settled 
country districts and on the Western plains are difficult to explain under the theory 
that each case is mediately or immediately the result of a previous case ; these 
difficulties will, however, doubtless be cleared away in time.] 

Clinical History. — The incubation is rather brief, seldom exceeding two to five 
days. The disease itself almost always begins with general malaise, headache, 
fever, and pain on swallowing. Little children, however, often do not complain 
of this last symptom, and in older children the sore throat may not be very 
troublesome at first. It is therefore a very important rule for the physician to 
examine the throat carefully in every child who presents ill-defined general symp- 
toms. If diphtheria is beginning, we find redness of the soft palate, and more or 
less swelling of the tonsils. Upon the inner surface of the latter, and perhaps 
upon the arch of the palate and the uvula also, are spots covered with a grayish- 
white coating, which is quite firmly adherent to the mucous membrane. They are 
less frequent upon the posterior wall of the pharynx and the hard palate. Their 
extent varies greatly in different cases. In the mildest they are chiefly confined 
to the tonsils, attacking the soft palate or the tonsillar surface of the uvula but lit- 
tle if at all. In severer attacks the spread of the false membrane during the first 
days of illness is rapid. Almost invariably there is a very early and consider- 



64 ACUTE GENERAL INFECTIOUS DISEASES. 



able swelling of the lymph-glands at the angle of the jaw. The constitutional 
symptoms persist. The children are restless. There is complete anorexia, and 
frequently vomiting. The temperature-curve is not typical. It is irregular, but 
is often rather elevated, reaching 104° (40° C.) or more. On the other hand, fever 
may be slight or almost absent, even in the worst cases. The pulse is very rapid. 
The urine may have a trace of albumen. 

In mild cases the local and constitutional symptoms remain moderate ; and at 
the end of a week or ten days there is decided improvement, with rapid convales- 
cence. In severe cases, however, dangerous symptoms appear, perhaps early ; the 
croupous inflammation involves neighboring organs, or a severe constitutional 
infection is developed. 

The diphtheria very frequently extends into the nose. This "diphtheritic 
coryza," though not in itself dangerous, is usually a sign that the case is a severe 
one. The inflammation of the nasal mucous membrane may be simply muco- 
purulent, but it may also be croupous. It is betrayed by the abundant purulent 
discharge. Excoriations and superficial ulcers are usually soon produced at the 
edge of the nostrils. There may be nose-bleed. 

A much more dangerous complication is the extension of the process into the 
larynx. This creates a mechanical hindrance to respiration, which proves fatal in 
a great many cases, as the child's larynx is so small. Formerly "croup" — i. e., 
croupous inflammation of the larynx — was regarded as a different disease from 
diphtheria. Many specialists in children's diseases still maintain this view ; but 
it is in direct opposition to the teachings of pathological anatomy as well as of the 
clinical symptoms. We grant that there are cases where the pharynx is slightly 
affected, while the croupous inflammation of the larynx is extreme ; and once in 
a great while the diphtheritic infection results in croupous laryngitis and trache- 
itis alone, the pharynx escaping disease. Still the proposition that there are two 
distinct diseases, " croup " and " diphtheria," is absolutely untenable. In the over- 
whelming majority of cases the throat is first affected and then the larynx. We 
should also consider how easily slight lesions in the pharynx might be over- 
looked, especially if located upon the posterior surface of the soft palate or upon 
the epiglottis. Cases of what is called " ascending croup," in which the laryngeal 
affection precedes the appearance of the disease in the pharynx, are, to say the 
least, very exceptional. 

Usually hoarseness is the first indication that the diphtheria has attacked the 
larynx. Then follows the peculiar, harsh, ringing, " croupy cough," so dreaded by 
the parents, and, finally, there are signs of beginning laryngeal stenosis. Respira- 
tion is not much accelerated, but is labored, and the accessory muscles of respira- 
tion are called more and more into action. The child becomes more restless and 
anxious. Its face grows pale and livid. The chief cause of the dyspnoea is un- 
doubtedly the mechanical stenosis due to the croupous deposit. Paralysis of the 
laryngeal muscles may perhaps be a factor. If portions of the false membrane 
become partially detached, they may act like valves, being sucked in at each 
inspiration, and pushed aside by the current of expired air. If stenosis occurs, 
respiration becomes noisy, resembling snoring. Inspiration, particularly, is pro- 
longed and " sawing," and is attended by marked depression of the larynx toward 
the sternum. An important diagnostic point is the drawing in during inspiration 
of the supra-sternal region, the epigastrium, and the lower part of the sides of the 
thorax. This is the direct result of the obstructed flow of air into the lungs. As 
the lungs do not expand enough to correspond to the inspiratory dilatation of the 
thorax, the parts mentioned are forced in by atmospheric pressure. The degree of 
dyspnoea may vary at different times. The false membrane may be loosened and 
coughed up, rendering respiration easier for a time, till fresh exudations or dis- 



DIPHTHERIA. 



65 



placements of membrane cause renewed distress. Recovery is still possible. The 
membrane may be expectorated and no more be formed. Unfortunately, this 
happy termination rarely occurs. In most cases the symptoms of suffocation in- 
crease more and more, respiration grows quicker and more superficial, and the 
child becomes more and more stupefied by the excess of carbonic dioxide in the 
blood. The pulse gets very small, rapid, and irregular. There are mild convul- 
sions and then death. 

The autopsy in these cases discloses usually that the croupous inflammation 
has extended into the larger bronchi or even into the smaller. The lumen of the 
bronchioles may be almost completely occluded by false membrane. There is 
also sometimes a genuine croupous inflammation of the pulmonary parenchyma. 
Lobular pneumonia in the lower lobes is much more frequent, however. It is 
probably secondary and to be regarded as a pneumonia from inhalation. During 
life the pulmonary complications may be suspected, but can hardly be diagnosti- 
cated. If we hear abundant moist rales over the lower lobes we are usually justi- 
fied in supposing that lobular infiltration exists, even if there be no dullness on 
percussion. The croupous bronchitis as such gives rise to no especial auscultatory 
signs. If it is very extensive and reaches into the smaller bronchi, it may prove 
fatal, even if there be no laryngeal stenosis. This is more apt to occur in adults. 

Another danger from diphtheria is through the general infection of the system, 
which may cause a fatal result. Although diphtheria does seem to start as a local 
disease, yet infectious matter (or poisonous substances) are certainly absorbed from 
the primary lesion into the general system. These exert their deleterious influ- 
ences mainly upon the nervous system. In such cases we see the child sink into 
somnolence, and finally into complete sopor ; its pulse becomes weaker and 
weaker, and more and more rapid, reaching 200 or more, and at last there is 
"paralysis of the heart" and death. All this occurs without any great degree 
of laryngeal stenosis. Such cases of severe constitutional infection, or "septic 
diphtheria," are most frequent when the local disorder in the pharynx is of un- 
usual intensity, and the croupous exudation is replaced by deeper-reaching, 
necrotic, or even gangrenous inflammation within the mucous membrane. This 
has been called " gangrenous diphtheria." In such cases, also, the cervical lymph- 
glands are usually intensely inflamed. It must be noted that, exceptionally, a 
comparatively mild local disorder may co-exist with the worst general symptoms. 
A question of great interest, but which can not yet be answered, here presents 
itself. It is whether the constitutional symptoms are in every case directly de- 
pendent upon the diphtheria, or whether the diphtheria is not re-enforced by a 
peculiar, secondary, septic infection, proceeding from the diphtheritic ulcerations. 
We regard the latter view as probable. In adults the constitutional infection is a 
prime factor of danger, for in them laryngeal stenosis is less apt to occur, as the 
parts are so much larger than in children. 

As to the part which the other organs play in diphtheria, we should mention 
that the process may extend not only into the nose and larynx, but into the Eu- 
stachian tube and the middle ear. It may also attack the anterior portion of the 
mouth, the gums, and the lips, or it may travel through the nose and the nasal 
ducts to the conjunctivae. Very exceptionally the croupous process extends into 
the oesophagus. The infectious matter may be transferred, by the finger or in 
some similar way, to excoriations or accidental lesions of the skin, and excite diph- 
theritic exudations upon them. The frequent cases of inflammation of the eyes 
probably originate in the same manner, and also the diphtheria of the external 
genitals seen in children. The heart and kidneys deserve especial mention. It 
has already been stated that in severe cases of diphtheria the pulse becomes re- 
markably small and rapid. It is also often irregular. Further, even in cases that 
5 



66 



ACUTE GENERAL INFECTIOUS DISEASES. 



otherwise seem mild, sudden cardiac failure may occur, ushered in by excessive 
rapidity of the pulse, and often proving quickly fatal. This misfortune often 
happens at a time when convalescence seems to be fully established. Small islets 
of myocarditis are frequently found in diphtheria, but it is probable that the col- 
lapse is not so much due to them as to derangement of the cardiac nerves, par- 
ticularly the vagus {vide infra). Renal disturbance betrays itself through the 
greater or less degree of albuminuria existing in most of the severe cases. It 
usually appears when the disease is at its height, less often at a later period. We 
often find a few casts in the urine, but seldom much blood. (Edema is rare. At 
the autopsy there is generally little macroscopic alteration of the kidneys. The 
microscope reveals the ordinary degenerative changes of acute nephritis {vide 
infra). 

Diphtheritic Paralysis. — The convalescent from diphtheria is liable to be at- 
tacked by certain nervous sequelae. Of these, diphtheritic paralysis is the most 
frequent. It appears about one or two weeks after the throat trouble ceases, or 
perhaps earlier, and it is quite as likely to follow mild cases as severe ones. It 
attacks the soft palate by preference. The tone becomes nasal and deglutition 
diflicult. The naso-pharynx is imperfectly cut off during the act of swallowing, 
and with each attempt liquid regurgitates through the nose. Usually the pharyn- 
geal mucous membrane is anaesthetic at the same time, and deprived of its reflex 
excitability. There may also be paralysis of the vocal cords upon one or both 
sides, and this again is frequently combined with anaesthesia of the mucous mem- 
brane of the throat. There may be paralysis of the ocular muscles, of which those 
controlling accommodation are most apt to be affected, rendering the vision for 
near objects imperfect. Paralysis of the muscles of the trunk and extremities is 
least frequent, but it may be very extensive. In some cases there is well-marked 
ataxia of the lower limbs without paralysis. This renders the gait very uncertain 
and tottering, the tendon reflex is almost always abolished, while sensation is 
affected slightly if at all . Very rarely diphtheria is followed by contracture of 
the hands or other parts, by difficulty in articulation and paresis of the bladder. 
The objective lesions corresponding to all these conditions have not yet been satis- 
factorily investigated. In most of them, and particularly in the common forms of 
diphtheritic paralysis, there is certainly degeneration of the corresponding pe- 
ripheral nerves. This fact harmonizes with the usually favorable termination of 
the nervous sequelae of diphtheria. But there is one paralysis which is highly 
dangerous — that of the heart, as already mentioned. It may occur suddenly during 
convalescence. Probably it is analogous to the other nervous derangements, and 
the result of degeneration in the fibers of the pneumogastric. 

Diagnosis. — The physician will seldom mistake a case of actual diphtheria if 
he pays proper attention. The characteristic deposit and the severe general and 
local symptoms make the diagnosis certain. It is much more common to take 
other forms of sore throat, particularly in adults, for diphtheria. The most decep- 
tive are follicular and necrotic tonsillitis {vide infra). We must not suppose that 
every white spot upon the tonsils is diphtheritic. The above-mentioned forms of 
sore throat are, however, frequent during epidemics of diphtheria, and even, as 
we have often observed of late years, in families where there are simultaneously 
cases of genuine diphtheria ; so that the thought is suggested that they may 
aetiologicalry have some relation to true diphtheria. It is at any rate advisable 
not to omit proper precautionary measures, especially if there are children about. 

[When the membranes are confined to the nose, the diagnosis may be more or 
less difficult ; but it is especially in cases in which the nasal mucous membrane is 
involved that we encounter great swelling of the glands at the angles of the jaw. 
There is also apt to be a thin, acrid, bloody, or sero-purulent discharge. 



DIPHTHERIA. 



67 



Jacobi states that while diffuse pharyngeal injection may or may not point to 
imminent diphtheria, marked local congestion is either traumatic or diphtheritic. 
An examination of the urine should never be neglected in doubtful cases ; in diph- 
theria a trace of albumen is very common; in simple or follicular sore throat 
albumen is very rare, if indeed it occurs at all.] 

Prognosis. — The unfavorable prognosis of the disease is universally known, 
even by the laity. The very fact that the best-developed and healthiest children 
so often fall victims to it associates the name diphtheria with the saddest memories. 
There are indeed many mild cases which recover in a week or two, and severer 
ones which end happily in three or four weeks ; but in most cases, where the pro- 
cess extends into the larynx, or the symptoms of a severe constitutional infection 
occur, medical interference has, unfortunately, no power to control the unfavor- 
able issue. What the dangers are, and how recognized, can be well enough in- 
ferred from the preceding description of the symptoms. We will only remind the 
reader how carefully the physician should watch the behavior of the heart, since 
danger is apt to arise from this source, even when the case seems otherwise to be 
taking a favorable course. 

Treatment. — If we take the ground that diphtheria begins as a merely local pro- 
cess, then local treatment of it certainly seems rational, at least at first. Unfor- 
tunately, the practical result bears out the theory very imperfectly. An actual 
and complete destruction of the croupous exudation is but seldom possible ; and 
the attempt to accomplish this in a struggling child is so difficult and disagreeable 
that to-day most physicians have entirely abandoned the application of caustics or 
other substances to the throat. If it does, nevertheless, seem desirable to try ener- 
getic local treatment at the commencement of the disease, the best agents to choose 
are a concentrated solution of argentic nitrate (1-10), or a solution of corrosive 
sublimate (1-1000), or a mixture containing equal parts of carbolic acid and alco- 
hol. If the disease has already made some progress, we may well spare the patient 
needless torture, and consider that, by destroying the mucous membrane and by 
wiping off the exudation, we are likely to contribute to a further extension of the 
diphtheritic process. 

We do not, therefore, regard actual local treatment as justifiable except at the 
very beginning of the disease ; but we do believe that both then and at a later 
period it is extremely desirable to disinfect the mouth and throat as thoroughly as 
possible. Although this has little effect upon the diphtheria itself, it is at least 
a factor in preventing secondary septic infection. Adults and older children 
should rinse the mouth and gargle frequently, using disinfectant solutions, e. g., 
of potassic chlorate or carbolic acid. Inhalations and the cautious syringing of 
the pharynx are still better. A spray apparatus for inhalation may be employed 
with such patients as are not too young. If the child be young or very weak, we 
may at least keep up a constant spray at the bedside, so as to load the inspired air 
with the vapor. A five-per-cent. solution of carbolic acid is most frequently em- 
ployed for this purpose ; but, considering the possibility of carbolic-acid poisoning, 
it is a good way to substitute now and then the following solution : Acid, salicyl. , 
parts 4 ; acid, boracic, 20 ; aq. destil., 1200, or a two-per-cent. solution of hyposulphite 
of sodium.* The best substances for direct inhalation are a one- or two-per-cent. 
carbolic solution, liq. calcis mixed with an equal amount of aq. destil. , and a two- 
per-cent. solution of potassic chlorate. It is not so very difficult to syringe out the 
nose, mouth, and throat in almost any child by the exercise of a certain amount of 

* In the Leipsic surgical clinique it was formerly the custom to add to every §iijss. (100 c. c.) of 
this solution a teaspoonful of a twenty-per-cent. solution of lactic acid. This caused the precipitation 
Dt sulphur in extremely minute particles. 



68 



ACUTE GENEEAL INFECTIOUS DISEASES. 



dexterity. The child is to be brought to a sitting posture for this purpose, with its 
head bent sharply forward. A common surgical syringe is employed, with a short 
piece of rubber tubing on the end, and a weak solution of salicylic acid is injected 
(1-400), or a one-per-cent. solution of carbolic acid. It has also been recommended 
to pour a few teaspoonfuls of cold water at short intervals into the nose, giving 
what is called a "cold nasal douche." And, finally, we may try to contribute to 
the disinfection of the mouth by dusting the diphtheritic ulcers with iodoform. 

We shall mention only a few of the numerous other remedies which have been 
recommended. There is another local remedy, papayotin, which is obtained from 
the milky juice of a certain plant, and has the property of digesting albumen. If 
a diphtheritic exudation be frequently touched with a five-per-cent. solution of this, 
it will sometimes disappear rapidly ; but the drug can not be shown to have an 
active influence upon the disease itself. Of internal remedies, we should mention 
potassic chlorate, which has been much vaunted as a specific, when given inter- 
nally in rather large doses. We recommend it, but it should be used as follows : 
a half-teaspoonful of a two- or three-per-cent. solution should be slowly swallowed 
about every half -hour. The aim is to obtain, not a constitutional, but a local 
antiseptic action. It should not be given in larger amounts than drachm j-jss. 
(grm. 5-6) in twenty-four hours, lest it cause hsemoglobinuria or other toxic symp- 
toms. Several physicians have lately recommended spirits of turpentine very 
highly, one half to one teaspoonful being given several times a day. It has not 
become popular. Injections of pilocarpine have also been praised. They are said 
to promote the detachment of the false membrane ; but their efficacy is doubtful. 

[The tincture of the chloride of iron is much used in this country in the treat- 
ment of diphtheria, and appears to be of real service ; but it must be given in large 
doses. The following prescription is recommended by Jacobi, whose experience has 
been very large, for a child of two years : 



M. S. : Teaspoonful every fiftsen, twenty, or thirty minutes. 

Turpentine is better as an inhalation than by the stomach ; a teaspoonful or two 
of the oil can be poured in water kept at the boiling point by an alcohol-lamp. 
The whole air of the room is thus charged with the remedy. No drug should be 
used which disorders the stomach.] 

If the larynx is attacked, and the consequent laryngeal stenosis threatens to 
cause suffocation, tracheotomy is our only resort. It is never indicated by the dis- 
ease itself nor by the severity of the case, but only by persistent obstruction of the 
larynx. It is therefore not invariably easy to decide whether tracheotomy is 
called for in any particular case. If the general condition be bad and respiration 
already impaired, it may be very difficult to determine whether laryngeal stenosis 
exists. Tracheotomy will be of no avail if the croup has already extended to 
the bronchi, or if the dangerous condition of the patient is due to the severity of 
the constitutional infection or to incipient paralysis of the heart. This explains 
why the results of tracheotomy are not remarkably brilliant. On an average, 
only about one third or one fourth of the cases operated upon get well ; but even 
this number is enough to make us prize the operation very highly. How' it is per- 
formed, and in what the after-treatment consists, must be learned in the text-books 
on surgery. 

The attempt to expel the false membrane from the larynx by inducing vomit- 



^ Tinct. ferri chloridi 

Potas. chlorat 

Glycerin, pur 

Aquae 



3 ij ; 



gr. xx ;. 

I j ; 

It. 



DYSENTERY. 



69 



ing is still often made, but seldom succeeds, and tortures and exhausts the child. 
Warm baths with cold douches may prove very beneficial. They excite deep 
respiration and more vigorous coughing, and also tone up the whole nervous 
system. The wet pack is also often employed, and sometimes with great benefit. 
Outward applications upon the throat are of little use. In general, we prefer the 
cold, wet compress to the ice-bag and ice-poultice, which are likewise often em- 
ployed. 

[Dr. Geo. W. Gay says (" Phila. Med. Times," 1884) : " Not a single case of 
pseudo-membranous laryngitis has ever recovered in the Boston City Hospital 
without operation." In twenty years tracheotomy has been done one hundred 
and eighteen times with thirty-nine recoveries. 

Four, if not five, successful cases were practically moribund at the time of 
operation.] 

In the severe cases of septic diphtheria, treatment usually proves completely 
futile. We must seek to avert cardiac paralysis as well as we can by stimulants, 
such as wine and camphor, and endeavor to improve respiration and the condition 
of the nervous system by lukewarm baths combined with douches. Finally, we 
repeat that the physician should never neglect to maintain the patient's strength, 
as far as possible, by proper nourishment. 

The nervous sequelae of diphtheria are best treated with the constant current. 
As an internal remedy, iron is good, and also nux vomica or strychnine. The last 
may be given subcutaneously, if desired, in doses of gr. -gV^sV (grm. 0 "001-0 - 002). 

[Diphtheria is a disease which involves commonly much exhaustion, and too 
much stress can hardly be laid on the importance of administering the maximum 
amount of nourishment in the most assimilable and easily swallowed forms from 
the start. 

It is also important to give stimulants early in most cases, not waiting for 
signs of exhaustion. Enormous quantities of brandy can often be given to small 
children without the slightest toxic effect. No general rule can be laid down ; 
the requirements of each case must be studied and. met. 

When painful deglutition interferes with nutrition, peptonized milk, eggs, 
brandy, and the like, must be given by the rectum. Rectal alimentation and 
stimulation are also to be resorted to in cases of post-diphtheritic paralysis of the 
oesophagus.] 



CHAPTER XI. 
DYSENTERY. 

JEtiology. — By " dysentery " is meant a disease of the colon, which appears 
sporadically, but more often in epidemics ; it is excited by infection with an 
organized pathogenetic poison, about which we have as yet no further knowl- 
edge ; and the infection is probably at first a local one. The true home of 
dysentery is in warmer and tropical countries, where the disease is much more 
violent and wide-spread than here. For example, the mortality among the soldiers 
of the Anglo-Indian army due to dysentery is said to be thirty per cent, of the 
entire number of deaths. In our climate most of the epidemics occur at the end 
of summer and in autumn. Endemic influences are certainly important. The 
condition of the soil in some places is evidently very favorable for the develop- 
ment and dissemination of dysenteric germs, and that of other places is equally 



TO 



ACUTE GENERAL INFECTIOUS DISEASES. 



unfavorable. There can be no other explanation of the immunity of some 
localities contrasting with the great prevalence of the disease in others. How 
infection occurs we do not yet know. Dysentery does not seem to be directly 
contagious ; but that it can be spread through the medium of the faecal dejections 
of the sick — e. g., from privies, chamber- vessels, and bed-linen— is very probable. 
Many cases were formerly referred to catching cold or to some error in diet ; but 
we must, of course, regard these merely as predisposing influences. 

The objective pathological lesion of the colon, in all severe cases, consists in 
a pronounced croupous-diphtheritic inflammation. The remarks as to the general 
pathology of such inflammations made in the preceding chapter are equally ap- 
plicable to the analogous dysenteric inflammation. In this case, too, there is first 
a destruction of the epithelium and then the formation of a fibrinous exudation 
occupying its place, and penetrating down into the tissue of the mucous mem- 
brane itself. At the same time there is an intense purulent infiltration of the 
mucous and submucous tissue, accompanied by extensive ecchymoses. In the 
most virulent cases the macroscopic appearances are marked thickening of the 
whole wall of the intestine, congestion of the serous layer, and the conversion of 
the inner surface into a mottled, dark-red, irregularly roughened area of ulcera- 
tion. The disease may be confined to the rectum and the sigmoid flexure, but in 
severer cases it involves the entire colon as far as the ileo-caecal valve, or even 
extends to the lower portion of the ileum. Beside this severe form of diph- 
theritic or even gangrenous dysentery, there is a milder variety, termed catarrhal 
dysentery. In this the mucous membrane is found in a state of intense purulent 
inflammation, with ecchymoses. Even here little masses of croupous exudation, 
which can be torn off, have replaced the epithelium ; but they never form con- 
tinuous layers of great extent. There is no sharp boundary-line between the two 
forms, the milder catarrhal-croupous, and the severer diphtheritic dysentery. 
Numerous transitional and combined varieties exist. 

We must remark, in conclusion, that precisely the same anatomical changes 
as are presented in true dysentery may result from other causes. Important 
among these is persistent faecal impaction in the rectum, which, by a purely me- 
chanical effect upon the epithelium, may excite a diphtheritic inflammation in the 
mucous membrane. And any severe constitutional disease whatsoever, such as 
typhoid fever, measles, small-pox, septicaemia, or phthisis, may be attended by a 
so-called " secondary dysentery." This is most frequent in hospitals. Whether 
it has the same aetiology as genuine dysentery is doubtful. 

Clinical History. — Throughout the entire Illness the most prominent symptoms 
are intestinal. There may be first of all some slight irregularity of the bowels for 
a time ; and then appears a moderate diarrhoea. The stools are at first feculent, 
although thin, and number two to six daily. After a few days the discharges in- 
crease in frequency, and become extremely characteristic. 

The stools are very frequent, occurring ten to twenty, and even sixty or more, 
times in twenty-four hours. In severe cases there may be a distressing and almost 
constant desire to evacuate the bowels. After every operation, and to some extent 
during it, there is tenesmus attended by intense burning pain in the anus. The 
stools soon lose their usual feculent character in great part if not entirely. They 
become scanty, so that not more than about half an ounce is evacuated each 
time. For the most part, they usually consist of a sero-mucous fluid, in which 
are suspended numerous shreds and particles of varying size. These are blood- 
. stained bits of mucus, little coagula of blood, and necrosed pieces of mucous mem- 
brane. One or another of these constituent parts may predominate, so that there 
may be slimy, purulent, or bloody stools, or all sorts of combinations of these 
varieties. We often find, besides, a few small masses of faeces, usually covered 



DYSENTERY. 



71 



with mucus. We sometimes see numerous clumps of mucus, resembling sago or 
frog's spawn ; they are probably mucous casts of the follicles. Under the micro- 
scope the greater part of the dysenteric discharge is seen to consist of pus-corpus- 
cles and blood. There are also cylinder epithelium and an enormous amount of 
detritus, and the bacteria of putrefaction. A purely dysenteric stool has no bad 
odor, except that in the worst cases of gangrenous dysentery the discharges become 
blackish and extremely offensive. 

The rectal tenesmus may be accompanied by a cramp-like pain during micturi- 
tion. There are often violent attacks of colic. The abdomen is usually rather 
tense, and tender on pressure along the line of the colon, but without tympanites. 
The anus may be red, inflamed, and excoriated. Gastric symptoms are on the 
whole infrequent, if we except the complete anorexia which exists in all severe 
cases. Sometimes there is repeated vomiting. Occasionally hiccoughs prove dis- 
tressing. The tongue usually has a dry, greasy coating. 

The symptoms just depicted last about a week or ten days. If the case is of 
much intensity, the general condition is also greatly affected. The patient seems 
very much collapsed, and is very languid and feeble, with a small and rapid pulse. 
The skin becomes cool and rough, the voice weak and hoarse. There is pain in 
the muscles. The patient wastes away. The temperature has little that is charac- 
teristic or typical. In many cases there is no fever at all ; and the temperature 
may even be subnormal. In most cases, however, there is an irregular fever, 
seldom exceeding 104° (40° C), and having remissions. 

In the worst cases the general weakness may increase more and more, and 
death occur ; but with us a favorable termination is much more frequent. The 
distress gradually diminishes, the stools assume more and more of a feculent char- 
acter, the patient becomes stronger, and after one and a half to three weeks con- 
valescence is established. It may be a long while, however, before a patient com- 
pletely recovers from a severe attack. A third possibility is the transition of the 
acute into a chronic dysentery. In this the symptoms of a chronic colitis, 
usually attended with cachexia, may persist for months and years. 

Mild, rudimentary forms of dysentery also occur, presenting less violent intes- 
tinal symptoms, and recovering at the end of a few days. In these cases, too, great 
sensitiveness of the intestine to disturbing influences frequently persists for quite 
a long time after the illness. There may be exacerbations of the disease, and re- 
lapses. 

Complications of dysentery, localized in other organs, are rare, at least in epidem- 
ics here. Abscess of the liver is mentioned oftenest by physicians in warm climates, 
and probably is best explained as the result of metastasis by way of the portal sys- 
tem. Articular disturbances also occur, and inflammation in the serous mem- 
branes. A few cases of peritonitis due to perforation have been observed, and a 
combination of dysentery and a " general scorbutic diathesis " has been described. 

The diagnosis is rarely very difficult. It is based exclusively upon the intesti- 
nal symptoms and the character of the stools. It is only the cases of secondary 
dysentery which occur in the course of other severe diseases that can easily escape 
observation. 

The prognosis is mainly influenced by the character of the epidemic, which, as 
we have said, is in our climate usually benign. There may be danger, particularly 
to elderly people, from bodily weakness and collapse. 

Treatment. — Prophylaxis demands that the isolation of the patient and the dis- 
infection of the stools be as complete as possible. The healthy must be very care- 
ful during an epidemic not to catch cold, and to avoid errors in diet, for expe- 
rience shows that an opposite course predisposes to the disease. 

The patient must be kept warm, and must not leave his bed, even if the attack 



72 



ACUTE GENEKAL INFECTIOUS DISEASES. 



be mild. The diet must be rigorous. If the strength is fair, thin porridge, milk, 
and broths suffice for some days. To a feebler person we should give somewhat 
stronger nourishment from the start, e. g., eggs, peptonized meat, and wine. 
Most patients bear liquids that are lukewarm better than those which are cold. 

As to drugs, the habit of almost all experienced physicians is to give at first a 
mild laxative. Although opium does not usually control the diarrhoea and tenes- 
mus at all, it is the rule for decided improvement to follow the exhibition of the 
laxative. During the first days, or, if need be, later, we give two to four table- 
spoonfuls of castor-oil daily. If this medicine is very disagreeable to the patient, 
we can replace it by a strong infusion of rhubarb (10-100). In southern countries 
large doses of calomel (gr. x to xv, grm. 0*5-1) are customary, and are highly 
praised by the physicians there. Further on in the disease we may content our- 
selves with giving mistura amygdalae. Or we may administer the following mixt- 
ure : bismuthi subnit., parts 5 ; mucilaginis acaciae, syrupi simpl., aa 15 ; aquae 
destil., 120 — to be shaken before taking. But if the disease should get worse again, 
we should always try a laxative. 

Emetics at the beginning of the disease are often employed in the tropics, but 
seldom with us. Ipecacuanha {radix antidy 'sent erica), given in large doses of fif- 
teen to thirty grains (1-2 grm.), is even regarded by many as a specific. Numer- 
ous attempts have been made, at local treatment by enemata. Yet no brilliant 
results can be claimed for any of these methods or medicines. A decidedly pallia- 
tive effect can be obtained from the injection of thin starch to which twenty or 
thirty drops of laudanum have been added. Suppositories of cocoa butter con- 
taining extract of opium often mitigate the tenesmus. Other injections are recom- 
mended, each to measure § ij to iijss. (grm. 60-100), and to contain either argenti 
nitrat., gr. j to vj (grm. 0*05-0*30), or plumbi acetat., gr. ij to viij (grm. 0*1-0*5), 
or potassii chlorat., gr. xv to xx (grm. 1-1*5). Many other solutions are used. 
The success of this treatment is, however, dubious. In all cases the margins of 
the anus must be protected from inflammation by frequently washing and anoint- 
ing the skin. 

The treatment of weakness and collapse is by the usual stimulants — wine, 
ether, camphor, and the like. In chronic dysentery the main point is to persevere 
in a strict control of the diet. We may exhibit astringents, such as tannin and 
columbo. Subnitrate of bismuth is also given, and nitrate of silver and acetate of 
lead. And in these chronic cases a long-continued and thorough use of rectal 
irrigation with fluids containing some mild astringent or disinfectant may have a 
good effect. 

[Sporadic dysentery is a self -limited disease, and, as has been shown by Flint, 
runs its course within ten days without medication. Treatment, however, adds to 
the comfort of the patient and shortens the course. It is not customary with us 
to use daily laxatives. If there is any doubt as to whether the intestines have been 
emptied, a saline should be given, the action of which should be followed by 
opium in sufficient doses to allay pain and tenesmus. Subsequent action on the 
bowels is best obtained by simple large enemata. In weak persons castor-oil is to 
be preferred to salines. 

In epidemic dysentery active treatment is much more important. Laxatives 
are contra-indicated by sero-sanguinolent dejections or by asthenia, but enemata 
can be freely used. Stimulation is often required ; nutrition must be carefully 
looked after, such articles being chosen as are digested and absorbed by the upper 
portions of the intestinal tract, leaving as little residue as possible to pass on to 
the inflamed colon. Opium is often demanded and tolerated in large doses, and 
astringents, such as the acetate of lead, gallic acid, and the pernitrate of iron, are 
of service. 



CHOLERA. 



73 



In chronic dysentery, oftentimes a very persistent disease, change of climate is 
desirable, and very large injections of a solution of nitrate of silver — gr. j-ij to 
the ounce of water, the patient being placed on the left side with the hips raised — 
yield very gratifying results in some cases. 

The chronic disease not infrequently taxes the resources of the physician to 
the utmost.] 



CHAPTER XII. 

CHOLERA. 

(Asiatic Cholera.) 

Historical Remarks. — The home of genuine Asiatic cholera is India. The first 
epidemic with which we are accurately acquainted, and which was very wide- 
spread, occurred in 1817. The disease was probably endemic there at an earlier 
period. In the next few years the cholera spread in all directions, and reached 
Astrakhan by way of Persia. Between 1830 and 1832 the disease made its first 
great epidemic progress over Europe. Invading all European Russia, it reached 
Germany in 1831, and Prance and England in 1832. Then came many smaller 
epidemics up to 1838, when there was a complete cessation till 1846, in which year 
the disease, again starting from Asia, overspread Europe. There have since then 
been epidemics in many places, but we can not here enter into the particulars 
of them. The last time that cholera occurred to any extent in Germany was 
in 1866, during the German- Austrian war. No one has forgotten the somewhat 
violent epidemic which has prevailed for the last year or two (1883 and 1884) in 
France and Italy. 

iEtiology. — Some time ago it had become evident that the real cause of cholera 
consists in the infection of the system by a specific micro-organism. Koch was, 
however, the first to succeed in the search for the poisonous agent. He was in 
charge of the scientific expedition sent out by the German Government in 1883 to 
Egypt and India for the purpose of investigating the disease. Koch found in th3 
intestines of all the victims of cholera whose bodies he examined a certain kind 
of micro-organism which he named the comma bacillus. It is shorter than the 
bacillus of tuberculosis, but somewhat thicker, and it is usually bent in the shape 
of a comma, or even like a semicircle (see Fig. 7). In the culture-preparations, 
the special peculiarities of which we can not give in detail, the comma bacilli 
grow into long spiral threads, resembling the spirilli of recurrent fever. Exam- 
ined in a liquid, the individual bacilli are seen to make vigorous movements. 
They flourish best at a temperature between 86° and 104° (30° and 40° C). Below 
61° (16° C.) they cease to grow, but they are not killed even by a greater degree of 
cold. The free access of oxygen is absolutely indispensable to their growth. They 
multiply very rapidly in liquids — e. g., broth or milk — while they can be readily 
destroyed by desiccation. In this again they resemble the genuine spirilli, which 
can maintain their existence only in fluids. In spite of every effort, Koch has 
failed to find a permanent form of the comma bacillus, or a permanent spore ; 
and probably there are none. 

These statements have been since confirmed by all competent investigators, 
while the various alleged refutations of Koch's results have all proved erroneous. 
It has been shown that in every case of genuine Asiatic cholera the comma ba- 
cilli are present in the intestine, and that they are never found under any other 
circumstances. Even the last postulate which was needed to show their patho- 



74: 



ACUTE GENERAL INFECTIOUS DISEASES. 



genetic significance has been fulfilled. Rietsch and Nicati, followed by Koch 
himself, have succeeded in producing cholera in a guinea-pig by introducing into 
its duodenum pure comma bacilli. 

Investigation as to the origin of cholera must, therefore, now meet this culmi- 
nating question : Under what circumstances and through what channel do the 
comma bacilli penetrate into the human system, and in what manner do they 
there excite the characteristic processes of the disease ? There can be no doubt 
that among us Europeans, and probably everywhere except in India, the cholera 
is invariably imported. It is equally certain that the dejections of cholera patients, 
which are rich in comma bacilli, are the chief if not the only agent by which the 
disease is spread. The bacilli which escape into the outer world with the stools 
find abundant means to prolong their existence. They continue their growth upon 
moistened bed-clothes, or in water which contains a sufficient amount of organic 
substances, or in food, such as fruit or milk, or in moist earth. And the ways by 
which they can in turn enter the system of a healthy human being are infinite in 

number. It is easy to understand why cer- 
tain persons — e. g., laundresses and nurses 
— are more liable to infection than others ; 
and it is equally intelligible that the 
spread of the disease should often bear a 
relation to certain outward circumstances. 
The fact has long been a familiar one that 
the cholera almost always progresses along 
the world's most frequented highways, and 
'i \ that it never travels faster than the means 

of human intercommunication render pos- 
sible. This is important, because it shows 
plainly that the germs of the disease are 




W \'*" it" ) / / 



" >'<*" 



{ ' P i "V // C ) f \ not disseminated by currents of air. It is 



^ { I easy to understand that the distribution of 

// iV^/'// ' ' the disease should sometimes correspond 

/ ' i J J J 1 1 with that of water destined for personal 

_ „ ' ^ tt \ t. mi- * "use. Apparently in every case the disease- 

Fig. 7.— (From Koch.) Comma bacilli from a , . . J . 

cholera dejection which has lain for two days producing poison enters the intestinal 
on a wet cloth. The S-shaped bacilli are at -, £ , . ir . - n 

a. 600 diameters. canal, tor the comma bacilli are round ex- 

clusively in the intestine, never in the 
other internal viscera ; and this is true, not only in the early, but also in the later 
stages of the disease. We must, therefore, suppose that the bacilli are swallowed, 
and, if not destroyed in the stomach, develop their pathogenetic functions in the 
intestine. In apparent agreement with this is the frequently observed fact that 
every gastric catarrh, however acquired, existing at the time of an epidemic, pre- 
disposes to the disease. 

The views thus far expressed are opposed by Pettenkofer. He ascribes to the 
condition of the soil, varying with time and place, the chief role in the spread of 
cholera. He doubts whether the poison as'contained in the stools is as yet efficient. 
It must, he thinks, undergo further development in an appropriate soil before it 
can acquire fresh pathogenetic potency. His main argument is drawn from the 
fact that certain places, particularly those on rocky soil, enjoy immunity ; the 
rarity of attacks upon shipboard is analogous. He points out that in cholera as 
well as in typhoid (q. v.) there is an evident harmony between the frequency of 
the disease and the varying stand of the water which underlies the surface of the 
ground. Further investigations, which will now for the first time have a firm 
foundation, afforded by the discovery of the comma bacillus, must decide how 



CHOLERA. 



T5 



much influence the condition of the soil does exert upon the dissemination of 
the pathogenetic poison. As it is, we feel certain that to give exclusive promi- 
nence to the condition of the soil, and to deny the possibility of infection in any 
other way, is to put a violent interpretation upon the observed facts. 

Most cholera epidemics happen in the months of summer. Liability to the dis- 
ease is very wide-spread, although some remarkable exceptions are seen. Sex is 
unimportant. Age has more influence. The disease occurs in sucklings, but, 
as a rule, is more rare among children than among adults. Elderly people are 
very apt to take the disease, while of typhoid fever the opposite is true. Most 
authors lay great stress upon predisposing causes. Among these, taking cold 
is not so important as are errors in diet and mild attacks of gastro-intestinal 
catarrh, which are shown by numerous observations to predispose strongly to 
the disease (vide supra). The stage of incubation seldom lasts over one to three 
days. 

Clinical History. — As is the case in most acute infectious diseases, the intensity of 
the illness varies between the extremes of mildness and severity, so that usually a 
correct interpretation of the mildest cases is rendered possible only by the fact that 
an epidemic exists. These insignificant cases are called simple choleraic diarrhoea. 
The symptoms are those of a violent acute intestinal catarrh ; the dejections are 
watery, rather large, painless, and number about three to eight in twenty-four hours. 
There is considerable malaise, complete anorexia, and thirst, and there may already 
be indications of severer choleraic symptoms : vomiting, slight pains in the calves 
of the legs, and diminished secretion of urine. Many cases recover after a few 
days or a week, but in others the first mild diarrhoea is succeeded, at the end of 
about one to three days, or rarely later still, by a severe attack of cholera. In 
such cases we speak of a "premonitory diarrhoea of cholera." 

The mild form is succeeded in a gradual transition by the cases designated as 
"cholerine." Cholerine exhibits the symptoms of a violent, rather sudden cholera 
morbus. It often begins at night. To the diarrhoea, which now and then displays 
even at this time the characteristics of pronounced cholera, vomiting is soon added. 
The accompanying constitutional symptoms are rather severe. There is great 
languor and depression. The voice grows weak, the extremities are cool, the pulse 
is small and accelerated, painful cramps occur in the calves of the legs, the urine 
grows scanty and perhaps albuminous. The whole attack lasts about a week or 
two, till recovery is complete. The course of the disease is not infrequently varied 
by repeated improvements and relapses. 

From these cases of medium severity there is again a continuous line of transi- 
tion to the pronounced severe form of cholera proper. Statistics as to the fre- 
quency of the separate forms can not be given, since many of the milder cases 
escape observation. 

The true attack of cholera may begin suddenly with the severest symptoms. 
As a rule, however, it is preceded, as already stated, by a first stage of brief pre- 
monitory diarrhoea. This, after one to three days, is replaced with equal sudden- 
ness by the severe symptoms of the second or " algid stage," or " cholera asphyxia." 
Its first symptoms are the abrupt appearance of great bodily weakness, chilliness, 
and vertigo. The characteristic gastro-intestinal symptoms soon declare them- 
selves. 

The diarrhoea grows very violent. At short intervals there are copious painless 
dejections, which at first retain somewhat of a feculent character, but very soon 
present a characteristic resemblance to "rice-water" or "whey." A single stool 
will measure a little less than half a pint (grm. 200). The stools have no color and 
almost no odor. They are watery, and usually deposit a finely granular, grayish- 
white sediment upon standing. Their reaction is neutral or alkaline. Only one 



76 



ACUTE GENERAL INFECTIOUS DISEASES. 



or two per cent, is solid matter, with a little albumen and a relatively large amount 
of sodic chloride. In many severe cases the dejections contain more or less blood. 
The microscope reveals epithelium, triple phosphate, and numerous micro-organ- 
isms. Of these last a part are the comma bacilli, and a part are bacteria of putrefac- 
tion, etc. If the comma bacilli be demonstrated, of course the diagnosis is absolute. 
To accomplish this we take a coagulum of mucus from the stool, and, spreading it 
upon a cover-glass in as thin a layer as possible, carefully warm the glass by pass- 
ing it repeatedly through a flame, in order to dry the mucus and fix it in its place. 
The preparation is then stained with an aqueous solution of methyl blue. If the 
bacilli be very abundant, the microscopic examination suffices for their demon- 
stration, although complete certainty about their identity depends upon their 
behavior in pure culture-preparations. These must therefore be instituted in all 
doubtful cases ; but it would lead us too far if we entered upon the particulars 
relating to such cultures. 

These excessive evacuations are but very rarely absent or nearly absent. 
They are more apt to fail if death occurs at the end of a few hours — cholera 
sicca. 

[In cholera sicca the intestines after death contain the characteristic rice-water 
material which, perhaps owing to paralysis of the muscular coat, was not expelled 
during life.] 

The appearance of the diarrhoea is soon followed by frequent though rarely 
distressing vomiting. The vomitus consists in part of ingested liquids and in part 
of an actual transudation through the mucous membrane of the stomach and intes- 
tine. Hiccoughs may accompany and follow the emesis. 

In addition to these prominent digestive symptoms of vomiting and profuse 
diarrhoea there are complete anorexia and excessive thirst. The tongue has a thick, 
dry coat. The abdomen is usually flat and soft, or it may be concave and hard. 
Sometimes we may feel fluctuation in the intestines, due to their being filled with 
fluid. There is not much real abdominal pain ; what there is, is described as a 
" feeling of heat and pressure " around the umbilicus. 

At the same time very severe symptoms develop in other organs. The circu- 
latory system is chiefly affected. 

The action of the heart may be stimulated at the beginning of the attack. The 
patient complains of palpitation and great precordial anxiety. After a brief time, 
however, cardiac weakness appears, and continually increases. The action of the 
heart becomes very weak, and the heart-sounds feebler and feebler. The pulse at 
the wrist grows very small, and is usually somewhat accelerated. In a severe case 
the pulse vanishes completely after a few hours. 

This collapse of circulation makes itself quickly evident in the appearance of 
the patient. The face and extremities grow cool, and then ice-cold ; the complex- 
ion becomes partly livid and partly a bluish gray ; the lips are almost black. The 
surface temperature may fall below 95° (35° C), while in the rectum febrile 
temperatures may often be observed, reaching 102° (39° C.) and higher. The 
eye and cheek grow very hollow, the sldn becomes wrinkled, and loses all its elas- 
ticity. The voice grows hoarse and feeble (voice of cholera). Respiration is 
laborious and superficial. The mind may remain unclouded to the end, but usu- 
ally there is great apathy, and all acuteness of perception is impaired. But few 
patients are restless and excited. Reflex action is much impaired. 

One characteristic symptom is the cramps in the muscles. These are usually 
very painful, and consist in tonic contractions of the muscles, particularly those 
of the calf of the leg, but also those of the toes, thighs, arms, and hands. The 
cramps occur spontaneously or upon the least provocation, last a few minutes, and 
recur at short intervals. The precise reason of their occurrence is not yet known. 



CHOLERA. 



77 



They can be observed in other severe acute diseases, although most marked in 
cholera. They sometimes occur in cholera morbus. 

In a well-developed attack of cholera there is almost invariably oliguria or 
anuria. The urine, if any be secreted, is concentrated, with abundant sediment, 
and very often contains albumen. In many cases not one drop of urine reaches 
the bladder for days, and this condition persists till death or recovery. 

The symptoms thus far depicted, if taken as a whole, represent the algid stage, 
which seldom lasts more than one or two days. In many cases death occurs 
during this period. It is ushered in by the tokens of extreme general prostration, 
and may take place after a few hours, or more frequently in the second half of the 
-first day. But in other cases the " stage of reaction " succeeds. This may be a 
true compensatory period, leading directly to convalescence. The evacuations 
become less frequent and more feculent, and the vomiting ceases. The pulse 
becomes stronger, the cyanosis and coolness of the extremities diminish, and an 
abundant perspiration is not infrequent. After a few days urine is again excreted, 
which is almost invariably quite albuminous, and usually contains casts and red 
blood - globules. If convalescence be uninterrupted, however, the urine very 
soon becomes perfectly normal, and after a week or two the patient is to be 
regarded as completely recovered. 

Departures from this favorable course of the stage of reaction are frequent. 
Recovery may be interrupted by repeated relapses into the previous condition, and 
sometimes with a fatal result. Or, instead of convalescence, there is developed a 
severe third stage, usually with fever. This stage usually bears the generic name 
of cholera typhoid, although it is subject to manifold variations in its clinical 
symptoms as well as its exciting causes. 

Cholera typhoid may present an actually typhoidal general condition with 
severe fever. There is a considerable elevation of temperature, headache, and 
dullness. The pulse is full and rapid, the face flushed. The skin, particularly 
that of the extremities, sometimes presents the so-called choleraic eruption, in the 
form of an erythema, roseola, urticaria, or the like. This variety of cholera 
typhoid ends after a few days in recovery, or else passes into one of the following 
conditions. 

A second form of cholera typhoid is distinguished by the development of the 
most diverse local inflammations. Thus, there may be a severe dysenteric or diph- 
theritic inflammation of the small and large intestine, attended by offensive puru- 
lent and bloody stools. Pneumonia is also possible, as well as purulent bronchitis, 
diphtheritic inflammation of the larynx, pharynx, bladder, and female genitals, 
parotitis, and sometimes erysipelas and pyaemia. And when we consider that, 
beside all these conditions, the intestinal symptoms, or those of choleraic nephri- 
tis, may exist also, it is evident how varied the clinical picture may be. The 
development of these local affections frequently lays the foundation for numerous 
sequelae. 

Choleraic nephritis gives rise to the third or uraemic variety of cholera typhoid. 
The secretion of urine is almost suspended. The little that is still passed contains 
numerous casts, albumen, and frequently renal epithelium and white and red 
blood-globules. Somewhere toward the end of the first week, or possibly earlier, 
there are grave nervous symptoms, to be regarded as uraemic ; first there is head- 
ache and vomiting, then sopor and coma, or delirium and convulsions. Most of 
these cases are fatal. 

Pathology. — We are now acquainted with the manifold symptoms and varieties 
of the disease. If we seek for the pathological changes which control the process 
and endeavor to find some correspondence between them and the symptoms, we 
shall be disappointed. At least, in its early stages, cholera is merely a severe local 



73 



ACUTE GENERAL INFECTIOUS DISEASES. 



disease of the intestine. We find the serous layer of the coils of the small intes- 
tine rose-red from congestion. The mucous membrane is in a state of catarrhal 
inflammation : it is swollen, reddened, and at first covered with a layer of tough, 
transparent mucus. But very soon an abundant transudation flows into the canal, 
so that the intestinal coils are filled with a large amount of clear fluid, looking like 
" rice-water " or " gruel," and so devoid of bile as to indicate the suspension of its 
secretion. The signs of inflammation of the mucous membrane now grow more 
pronounced. The solitary follicles and Peyer's patches become swollen, with 
edges of a vivid red, and frequently there are many small ecchymoses in the 
mucous membrane. The extensive desquamation of the epithelial lining of the 
intestine has also been regarded as important, because it was regarded as in part 
the cause of the copious transudation.* Still it may be questioned whether the 
desquamation is not, at least to some extent, a post-mortem change. In yet later 
stages of the disease the intestinal trouble very frequently assumes a croupous- 
diphtheritic character. The surface is necrosed and ulcerated in many places, 
and the contents of the intestine are no longer colorless, but sanious and bloody, 
with a foul odor. 

Otherwise most of the post-mortem lesions correspond to what was obvious 
at the bedside. The muscles exhibit an early and persistent rigor mortis, and fre- 
quently contract in such a way as to throw the corpse into some unusual posture. 
All the internal organs are remarkably dry, pale, and anaemic. The left ventricle 
is contracted. The blood lies mostly in the large veins, the right side of the 
heart, and the cerebral sinuses. It is thickened, is but little clotted, and is said to 
resemble the juice of bilberries or huckleberries. The spleen is not enlarged — an 
exception to the rule in infectious diseases. The kidneys present marked passive 
congestion, most pronounced in the cortex. The microscope reveals a greater or 
less degree of parenchymatous nephritis, with great destruction of the epithelium. 
If death takes place at a rather advanced stage of the disease, the tissues have lost 
their characteristic dryness, and the most diverse local lesions, including nephri- 
tis, may be found to have occasioned death. 

If we search for the connection between the pathological changes just de- 
scribed and the cause of the disease, or again between these lesions and the clini- 
cal symptoms, the first point to guide us is that the comma bacilli are found 
only hi the wall of the intestine, and never in the blood or in other parts of 
the body. The intestinal symptoms are satisfactorily explained by this abnor- 
mal state of the intestine, but for all the other grave symptoms we have to 
seek some special cause. The desiccation which the body undergoes as a result 
of the excessive liquid dejections can not fail to affect the tissues, but can not 
fully explain the symptoms, for at least the circulatory disturbances and the 
cardiac failure may develop before large evacuations have occurred. It is possi- 
ble that the result is due to the well-known sympathy between the abdominal 
organs and the heart. Nor should we overlook the suggestion made by Koch 
himself, that perhaps the vital processes of the comma bacillus create a toxic 
substance, the absorption of which causes a part of the severe constitutional 
symptoms of cholera. As to the complications which occur in the later stages 
of the disease, and are embraced under the generic name of cholera typhoid, we 
regard them as mainly secondary. The choleraic process itself does not cause 
them, but is merely the occasion for their appearance. The examination of the 
intestine in such cases shows that numerous other varieties of bacteria follow 



* We should add that a few authors, and among them Cohnheim, do not regard the fluid which 
tills the intestine in cholera as the result of transudation at all, but as an extraordinarily profuse 
secretion of the glands of the small intestine, due to the choleraic poison. 



CHOLERA. 



79 



closely upon the comma bacillus, gaining entrance to the system by treading in 
its footsteps. 

The diagnosis of a pronounced case of cholera has no difficulties at the time of 
an epidemic. We must always be somewhat cautious about sporadic cases, for 
violent intestinal disturbance, simulating perfectly the milder forms of cholera, 
may be excited by other causes. In this connection we should mention the 
cholera morbus common among us ; and poisoning, particularly acute arsenical 
poisoning, may give rise to symptoms wonderfully like cholera. But now that 
Koch's discovery has been made, the diagnosis of all such doubtful cases becomes 
perfectly certain if we can demonstrate the presence of comma bacilli in the 
stools {vide supra). We have no doubt that this demonstration will also lead 
us to a decisive conclusion as to the setiological importance of mild choleraic 
attacks. 

The prognosis should always be guarded at the beginning, even if the symptoms 
be mild, for, as already mentioned, a simple diarrhoea may prove to be " premon- 
itory " of a severe attack of cholera. During the real attack the prognosis grows 
graver in proportion as the case presents the characteristics of asphyxia and 
cyanosis. The mortality in many epidemics is frightful. All the inhabitants of a 
house or street may in a brief period be swept away. Minute statistics are diffi- 
cult to give. If we count the typical cases alone, the mortality is not infrequently 
fifty to seventy per cent. In about two thirds of the fatal cases death occurs during 
the first days of the stage of asphyxia, and in about one third during the second 
period, known as "cholera typhoid." The influence of the diet and the hygienic 
surroundings of the patient before his illness is important. A greater proportion 
of children and old people perish than of the middle-aged. 

Treatment. — The measures to be taken to prevent the spread of the disease, 
when it has once started in a place, we can not here discuss. We can merely say 
that the further extension of the disease may be hindered simply by isolating the 
localities attacked as completely as possible, or at least regulating intercourse with 
them very strictly. We must try to prevent the communication of the disease by 
isolating individuals attacked and by disinfecting the dejections with five-per- 
cent, carbolic solution, and likewise disinfecting everything that may have been 
contaminated by the excreta, such as linen and bed-clothes, for which dry heat is 
the agent. We must content ourselves with a brief mention of these facts. In- 
dividual prophylaxis is of the greatest importance. It has been proved again and 
again that a mild intestinal catarrh will predispose to cholera, and will aggravate 
the attack if cholera does occur. So that the slightest gastric or intestinal dis- 
turbance at the time of an epidemic of cholera demands the greatest attention 
both as to diet and medicine. We may well quote from the last proclamation of 
the Prussian Department of Public Improvement (Cultusministerium) that, " by 
exercising and promoting cleanliness and moderation, each person will not only 
best protect himself, but also most efficiently support the efforts of the authorities 
in behalf of the common weal." 

[The vital importance of the serious treatment of a beginning diarrhoea during 
a cholera epidemic can not be too strongly insisted on. Rest, simple diet, and a 
little medication will, in the vast majority of instances, entirely prevent serious 
consequences. The apparently trifling character of the symptoms is apt to lead 
people into a false security. Those who can leave an infected district should do 
so without delay. 

With reference to the prevention of an epidemic, a pure water supply and 
strict cleanliness in its broad sense possess far more virtue than cordons of troops 
or measures of quarantine. It is more practicable to destroy the soil than to keep 
out the seed in these days of constant and rapid international communication. The 



80 



ACUTE GENEKAL INFECTIOUS DISEASES. 



systematic disinfection of all cholera discharges or articles soiled by them should 
be a matter of course.] 

The drug chiefly used at the beginning of cholera is opium, Avhich forms the 
chief constituent of the various " cholera drops." The best form is the tincture, in 
doses of ten to twenty drops, or gr. § to j (0*03-0 "05 grm.) of powdered opium, 
repeated every two or three hours. A more complicated formula is : Tr. opii, 1 
grm. ; vin. ipecac, 3 ; tr. valerian, seth. [P. G. : valer., part 1 ; sps. setheris, 5], 10 ; 
ol. menth. pip., gtt. v. M. S. : Twenty to thirty drops. Or we may give tinctura 
opii benzoica [an elixir of which two hundred parts contain one part of opium, 
four of benzoic acid, and two parts each of camphor and oil of anise]. 

The opium treatment approved itself in the last epidemic, although a few 
physicians regard it as irrational and prefer to give at the beginning of the disease 
one or two good-sized doses of calomel (gr. v to viij, grm. 0*3 to 0*5) . Cantani and 
other Italian physicians praise highly enemata of a solution of tannin or some 
disinfectant. 

When the attack is fully developed, we usually continue the use of opium. 
The patient is wrapped up in warm blankets and subjected to friction ; or warm 
oil may be rubbed into the skin. Hot tea may be given, or strong coffee, or broth, 
or mulled wine. Hot baths have proved beneficial in repeated instances. Vomit- 
ing is to be controlled by morphine or ice. The painful cramps in the calf of the 
leg require subcutaneous injections of morphine. The feebler the action of the 
heart becomes, the more energetic must be the stimulants employed. We can 
give champagne, or inject camphor or ether. The attempt has been made again 
and again to make good the loss of fluid by injecting a solution of common salt 
beneath the skin or into the veins. Samuel recommends for this purpose a solu- 
tion containing six parts of sodic chloride and one part of sodic carbonate in one 
thousand parts of water, at a temperature of about 100° (38° C). 

Great caution must be exercised about the diet, not merely during the attack 
itself, but for a considerable time afterward. At first we can allow only thin por- 
ridge, milk broths, and possibly a soda biscuit. It is advisable to administer dilute 
hydrochloric acid with the food. 

The treatment of cholera typhoid varies greatly, of course, according to the kind 
of attack. The separate affections should receive their customary treatment. 

[In the first stage absolute rest, opium, and lumps of ice by the mouth ad libi- 
tum are the chief measures on which reliance is to be placed. It should be remem- 
bered that the entire function of the intestinal tract is reversed ; thus, instead of 
an absorbing, it has become an excreting surface. 

In the stage of collapse the nervous system is more or less paralyzed, the blood 
is damaged by the loss of its watery constituents, and the circulation of that fluid 
is greatly impeded. The subcutaneous or gastric absorption of drugs is conse- 
quently delayed or suspended. The utility of any active internal treatment dur- 
ing this stage is very questionable. Certainly narcotism by opium is highly un- 
desirable. Mild external stimulation and the tentative administration of ice and 
small quanties of champagne or food are, at all events, not likely to do harm. 
Nature sometimes reasserts herself when the conditions are seemingly desperate, 
and the third stage, or that of reaction, comes on. In this stage careful nursing 
and a sensible symptomatic, but in no way meddlesome, treatment are most like- 
ly to be followed by good results. ] 



MALABIAL DISEASES. 



81 



CHAPTER XIII. 

MALARIAL DISEASES. 

{Intermittent Fever. Fever and Ague. Swamp Fever.) 

iEtiology. — Malarial poisoning is the best example of a purely "miasmatic" 
affection. The poison which produces the disease is without doubt localized in 
certain places, in which every human being is liable to become its victim. But if 
an infected person comes to a place free from malaria and not naturally disposed 
toward it, there is no danger that* he will cause the disease in others. The disease 
is never caught through contact with the patient. It is not at all contagious ; 
the malarial poison, after it has once penetrated into the body, has practically no 
opportunity to escape again in an efficient form from the diseased system into the 
outer world. 

If we except the polar zones, there are few regions where malaria is not endem- 
ic in certain parts, at least from time to time, if not constantly. There is, how- 
ever, great variation in the virulence as well as in the number of cases. While the 
common forms of intermittent fever are very frequent in Germany, in numerous 
places, yet. the grave forms of the disease are very rare. Other lands are notorious 
for the severe malarial diseases, e. g., Hungary, the lands lying on the lower 
Danube, the Roman Campagna, the Pontine marshes, Sicily, and numerous dis- 
tricts in other parts of the world, chiefly tropical. Numerous observations have 
only served to confirm the statement that the soil is the true home and cradle of 
the malarial poison, and that the virus, escaping thence into the lower strata of 
the atmosxmere, may be taken into the system, probably during inspiration. Per- 
manent dampness of the soil is essential to the development of the malarial poison. 
This explains why marshy districts are so often malarial. The ground must not 
be covered by a great amount of water, but must during the dry season lie ex- 
posed to the atmospheric air. The access of air to the moist soil seems to be a 
second essential condition for the development of the malarial germs. A third 
influential factor is the temperature of the air, as proved by the great prevalence 
of the disease in southern countries and in the summer season. 

[Periodical fever is very widely distributed in the United States, and in the 
southern portions occurs in severe though not in the severest forms. Some regions 
which were formerly free from it are no longer so, and, vice versa, some regions 
which were greatly subject to it are now exempt ; these changes are closely con- 
nected with the clearing and upturning of virgin soil largely impregnated with 
decaying vegetable matter and with the subsequent cultivation of the same for 
considerable periods of time. The poison does not extend far above the surface of 
the ground, as is shown by the relative safety of sleeping in the upper as compared 
with the lower story of a house ; during the night the poison seems to exist in 
greater intensity than during the day. Attacks are more liable to occur during 
the spring and autumn than at other seasons. 

The hopes which have been entertained in some quarters that malarial regions 
might be rendered healthy by large plantations of the Australian eucalyptus globu- 
lus, a rapidly growing tree which absorbs immense quantities of water, do not 
seem likely to be realized in the light of French experience in Africa, and in that 
of the Trappist monks in Italy.] 

Klebs and Tommasi-Crudeli have made extensive investigations as to the nature 
of the malarial poison. We must regard it as organic. The authorities just 
named state that the true cause of malaria is a specific variety of bacillus. They 
6 



32 



ACUTE GENERAL INFECTIOUS DISEASES. 



found peculiar bacilli and their spores both in the earth of malarial regions and 
in the adjacent strata of the atmosphere ; and, by infecting rabbits with these, 
they were able to induce attacks of fever, swelling of the spleen, and the charac- 
teristic formation of pigment matter {vide infra). Before this, bacilli and spores 
had been found in the blood and spleen of patients suffering from malaria. It can 
not yet be said just how much significance these discoveries have. 

[Marchiafava and Celli have found, in the red blood-corpuscles of those suffer- 
ing from acute malarial poisoning, organisms composed of protoplasm which are 
endowed with active amoeboid movements and can be stained by various agents. 
They have failed to find these organisms in other conditions. The bodies often 
contain reddish or black pigment, derived from a transformation of haemoglobin 
into melanin, perhaps through the agency of the parasite. Melanaemia is present 
or absent according as this production of pigment takes place or fails to do so, and 
depends in no way on the pernicious or simple character of the infection. 

The malarial poison can be transmitted in the human subject by intra-venous 
injection of blood derived from a person with acute malaria, a fact which is 
proved not only by the clinical course of the resulting affection, but also by finding 
the characteristic organisms in the blood of the inoculated individual until the 
symptoms are relieved by treatment. The organisms have not yet been found 
outside of the human body.] 

Liability to the disease is very wide-spread. No race, no age, no sex, enjoys 
immunity. It is a noticeable fact that those who have had the disease once are 
all the more apt to have it again. Former patients, although they feel perfectly 
well in a non-malarious region, are very liable to fresh attacks, or at least much 
discomfort, as soon as they re-enter an infected district. The time of incubation 
does not seem to be constant. It is put at from six to twenty days, but may be 
shorter. We shall consider below chiefly the common forms of intermittent, such 
as occur among us in Germany, contenting ourselves with a very brief descrip- 
tion of the severer forms. 

Varieties op Malarial Disease. 

1. Intermittent Fever. — This is the sinrplest form, and has for its especial char- 
acteristic the relative brevity of the febrile attacks, which almost always exhibit a 
remarkably uniform type. A febrile attack of this kind is frequently the very 
first symptom of the disease. In other cases the paroxysm of fever is preceded by 
a prodromal stage lasting several days, during which the patient feels languid, 
has no real appetite, complains of headache and pain in the back of the neck and 
in the limbs, and often even thus early presents a slightly yellowish complexion 
and an enlarged spleen. 

In the typical attack of intermittent fever there are three stages. The attack 
begins with a chill. There is pronounced malaise, attended by intense chilliness 
and more or less shivering. The skin is cool and pale, the face may be somewhat 
livid. The temperature of the interior of the body is elevated, and rapidly rises 
higher. In by far the greater number of cases the attack occurs in the morn- 
ing, or at least before noon, and but seldom later in the day. This cold stage 
varies greatly in length, usually lasting an hour or two. 

The chilliness gradually ceases and is followed by the hot stage. The skin 
grows burning hot, the face flushes, the pulse, which was before small, becomes 
full, and the action of the heart is excited. At first the temperature continues to 
increase, reaching its maximum for the attack. It is exceptional for it to remain 
under 104° (40° C), and by no means rare for it to touch 106°, or even 107° (41°- 
41 "5° C). This stage almost always lasts longer than the preceding, generally 



MALAEIAL DISEASES. 



S3 



about three to five hours. The temperature may begin to fall as early as the latter 
part of the hot stage, but may persist till the beginning of the third stage. 

In this sweating stage the skin grows moist, and there is soon a profuse gen- 
eral perspiration. The patient begins to feel much better. In a few hours the 
temperature usually becomes normal, and, after lasting in all about eight to twelve 
hours, the attack is over. It may be shorter or rarely longer. Usually, however, 
the temperature keeps on sinking slowly, so as to be still subnormal even on the 
next morning, perhaps not above 97° (36° C). 

There are certain peculiarities in the temperature-curve. The elevation of 
temperature is almost invariably more rapid than its decline. The rise is most 
rapid during the first hours of the cold stage, and slower during the first portion 
of the hot stage. The ascent is but very seldom interrupted. During the hot 
stage, when the fever is highest, in the neighborhood of 106° F. (41° C), there 
are not infrequently two little summits to the fever-curve, if the temperature be 
taken at short intervals. But the temperature may for hours remain the same. 
The temperature generally begins to fall some little time before the perspiration 
is evident. The decline is slow. It may be perfectly continuous, or it may be 
interrupted by fresh elevations, which are sometimes slight and sometimes con- 
siderable. In many cases the descent is by steps, the temperature remaining the 
same for half an hour or an hour, and then abruptly falling a couple of degrees 
and remaining for a time at this new level. 

The chief characteristic is not, however, the nature of the single attacks, but 
the peculiar manner of their repetition. If the case is not under treatment, the 
single attacks keep recurring for a time, either daily as in the quotidian variety, 
or every second day. This latter type of tertian intermittent fever (cf. Figs. 8 
and 9) is probably the most frequent. There may exceptionally be still longer 



4i-o° 



40-0° 



37-0° 



36-0° 




mm 

mm 



41 0° 



400° 



39 0° 



mm 

ii 
i 



IBUli 

a 

nnir 






Fig. 8.— Quotidian intermit- 
tent fever. 



Fig. 9.— Tertian intermittent fever. 
[Chinin 20 = Quinine, 30 grains.] 



afebrile intervals. Thus we have quartans, quintans, etc. If there are two 
attacks in one day, a rare event among us, we have a double quotidian. If there 
is a violent attack every second day, and on the intervening days there are milder 
attacks, it is a case of double tertian. Very often the attacks do not recur at just 
the same time of day, but a few hours earlier each time. Less frequently they 



84 



ACUTE GENEKAL INFECTIOUS DISEASES. 



are later. This peculiarity is expressed by the term "anticipating" or "retard- 
ing," as the case may be — e. g., a retarding tertian ague. In cases of long stand- 
ing, the paroxysms may finally lose all regularity, so that the fever is described 
as "erratic." 

Next to the febrile attacks, the swelling of the spleen is the most constant and 
important symptom. It is usually considerable and capable of demonstration by 
percussion and palpation. At first the tumor increases with every fresh attack, 
and diminishes but little during the intervals. After the patient is freed from his 
attacks of fever the spleen may continue enlarged for some time. It is tender on 
pressure. The liver may likewise be swollen, but this is less constant and also 
less important. 

Certain changes in the skin are very characteristic, chief among which is a 
peculiar yellowish-brown discoloration. This is due to an abnormal deposition of 
pigment in the skin. Genuine jaundice occurs but seldom in the milder cases of 
malarial poisoning. 

Herpes on the lips or nose is seen very frequently during the attacks. We 
have seen one case of herpes on the cornea. Mention has also been made of urti- 
caria, purpura, and other eruptions. 

Other internal organs than those already spoken of are rarely much disturbed. 
One should be mentioned, which we have ourselves seen several times, viz., a 
quite marked acute dilatation of the heart during the attack. There were no bad 
results, and the normal condition was soon re-established. We may hear during 
the attack functional cardiac murmurs of a blowing character. Thoracic exam- 
ination, particularly if made during the attack, may afford the signs of a dry 
bronchitis. Sometimes there is considerable diarrhoea, or other symptoms of intes- 
tinal derangement. Catarrhal jaundice is confined to the severer cases. Some- 
times the urine has a moderate amount of albumen. Genuine nephritis is met 
with only in the graver varieties of the disease. The increased excretion of urea 
on the days of the fever results, as in any fever, from the increased destruction 
of albumen. Severe pain in the cervical and upper dorsal vertebras is regarded 
as characteristic of intermittent. 

Besides the typical attacks, rudimentary and modified ones are not rare, in 
which the separate stages are ill denned, or in part wanting. We are most apt to 
see this in cases which have been already treated with quinine. Children do not 
have a true rigor. They merely become pale or livid. They may present marked 
nervous symptoms. 

2. Pernicious Intermittent Fever.— This dangerous form occurs only in the 
true malarial districts, and is often preceded by a few attacks of a milder charac- 
ter. Then appear, in addition to the more or less perfectly marked stages of the 
febrile attack, other graver symptoms which not infrequently end in death. Severe 
nervous symptoms are most frequent. There may be unconsciousness, coma, 
delirium, or epileptiform or tetanic convulsions. None of these symptoms persist 
longer, as a rule, than does the common sort of an attack, and in a favorable case 
vanish completely when the sweating, which is usually profuse, begins. The 
great danger comes from the recurrence of the attacks. A second form of perni- 
cious intermittent fever causes violent gastro-intestinal symptoms, which may 
almost exactly imitate the algid stage of cholera, with vomiting, diarrhoea, and col- 
lapse ; or there may be severe cardialgia, dysentery, and the like. In the so-called 
pernicious intermittent with jaundice, intense jaundice appears during the attack, 
with vomiting and diarrhoea, and sometimes the gravest nervous symptoms. 
There are certain very peculiar forms, in which local diseases, such as pleurisy or 
pneumonia, can be demonstrated during every attack, but vanish wholly or in 
part when the temperature declines, only to appear again during the next attack. 



MALARIAL DISEASES. 



85 



[The pernicious form occurs in isolated cases wherever the ordinary variety of 
the disease prevails, but is much more common in the Southern and Western 
States, and there varies in frequency in different years. Periodicity in the attack 
is not always observed. The pernicious character is not always manifested in the 
first attack, one or more mild paroxysms being often precedent. In this country 
the algid form of pernicious periodic fever is often called " congestive chills," and 
this form is more common than the comatose or another form not mentioned 
by the author — the hemorrhagic. In the latter the blood escapes from the kidneys, 
and less constantly from the mucous membrane. During the late civil war the 
mortality in the white soldiers of the United States army from pernicious malarial 
fever was 23 - 91 per cent.] 

3. Remittent and Continuous Forms of Malarial Fever.— These are generally 
severe, and are seen, like the preceding, only in the worst haunts of malaria. The 
proof that they have the same aetiology as intermittent fever lies in the fact that 
they are sometimes developed out of the milder forms ; but it is to be noticed that 
many types of disease which physicians in the tropics describe as malarial affections 
have not yet been proved to our satisfaction to have an actual identity of origin 
with the common intermittent fever. The symptoms of this variety are likewise 
those of a severe constitutional infection. Gi-astro-intestinal symptoms may pre- 
dominate ; or there may be such grave nervous symptoms as coma, delirium, and 
convulsions ; or there may be jaundice, haematuria, and even a general haemor- 
rhagic diathesis ; or various local disorders may exist, such as pneumonia, nephri- 
tis, and hepatic and splenic abscesses. The fever is high, but without any sort of 
regular intermissions, maintaining for one or two weeks a remittent or a tolerably 
continuous type. Milder forms may end in recovery after eight to fourteen days, 
but often death ensues at this time, or even earlier. 

[The remittent form apparently shows a greater intensity of the poison or a 
greater susceptibility of the individual. In the United States army, from 1861 to 
1866, its mortality was twelve times as great as that from the intermittent form.] 

In all severe varieties of malarial disease, including the pernicious intermit- 
tent, the remittent, and the continued fevers, there is one very constant and 
remarkable symptom. It is also observed in the malarial cachexia, of which we 
shall speak below. This symptom is an abnormal and abundant formation of 
pigment matter. During life the pigment can be readily demonstrated in the 
patient's fclood — i. e., " melanaemia " exists. We find minute rounded granules or 
flakes, either free or in the interior of white blood-globules. After death the pig- 
ment is found in the greatest abundance in the spleen. This organ is enlarged, 
resistant, and of a dark grayish-brown color. The matter lies in part along the 
blood-vessels, in part within the cells. Pigment is also found in the liver, the 
lymph-glands, the marrow of bones, the kidneys, lungs, brain, and other organs. 
As to the process of its formation we have no accurate knowledge. Marchiaf ava 
and Celli teach that the transformation of haemoglobin into melanin takes place 
within the red blood-globules themselves, and, it is affirmed, under the influence 
of micro-organisms which have penetrated into the interior of the globules. Some 
authors ascribe great clinical importance to the formation of pigment. They refer 
the grave cerebral disturbances, as well as other symptoms, to the occlusion of 
minute cerebral vessels by emboli of pigment matter. 

4. Chronic Malarial Cachexia. — This occurs in the true malarial regions, and 
affects not only people who have had frequent attacks of pronounced intermittent 
or remittent fever, but also those who have never had acute attacks. The condi- 
tion is chronic. It may exhibit a genuine intermittent character. The patient 
usually has a decidedly yellowish, malarial complexion, and almost always the 
spleen is evidently enlarged. There are no regular febrile attacks, but merely 



86 ACUTE GENEKAL INFECTIOUS DISEASES. 

symptoms of general debility, anorexia, tendency to diarrhoea, or, more rarely, 
constipation, vertigo, wakefulness, frequent perspiration, pains in the muscles and 
joints, dyspnoea, and palpitation. There may be such nervous symptoms as trem- 
bling, paralysis, and mental disturbance ; or we may see intestinal symptoms and 
jaundice. Dropsy occurs ; also epistaxis, cutaneous ecchymoses, and other signs 
of a scorbutic condition. The spleen and liver gradually become greatly hyper- 
trophied and melanotic. At the same time there may be an irregular fever, 
approaching either an intermittent or a remittent in type. Finally, secondary 
diseases are possible — e. g., tuberculosis, amyloid, or dysentery — and these may 
prove the immediate cause of death. The milder forms may be cured, but seldom 
unless the patient abandons for ever the malarial district. 

5. Masked Intermittent. — This is the designation of cases where, although 
there is no fever, certain other disturbances arise in regular intermittent attacks. 
Chief among these is neuralgia. Its favorite seat is the supra-orbital branch of 
the trigeminus. It may occur in the other branches of the same nerve, or in the 
sciatic, the anterior crural, the nerves of the brachial plexus, and elsewhere. Car- 
dialgia may occur in the same way. These attacks last from thirty minutes to 
several hours, and are frequently associated with all sorts of constitutional symp- 
toms, but, as we have said, are afebrile. There may be a splenic tumor, which 
aids diagnosis ; but this sign may be wanting. 

Numerous other intermittent disorders besides neuralgia have been described 
as masked intermittent. The list includes anaesthesia, convulsions, and paralysis ; 
also intermittent haemorrhage, oedema, cutaneous affections, and intestinal symp- 
toms. We must add, however, that those who have described diseases of this sort 
some of which seem strange enough, have not always been as critical as they 
ought, and have omitted to prove satisfactorily that such cases should be referred 
to malarial poisoning. 

Diagnosis. — It is often very difficult to diagnosticate a case of intermittent fever 
at the first visit, particularly in a place where malarial poisoning is infrequent. 
The history of the case is by no means always enough to put one on the right 
track ; and a single examination of the patient may prove equally negative in its 
practical results, whether it is made during the febrile stage or in the interval. 
Continued observation, however, will almost always disclose the regularity of the 
febrile attacks, the splenic tumor, the characteristic complexion, and the herpes ; 
and our diagnosis becomes evident. Still it is not very exceptional for an inter- 
mitting fever to be taken at first for an intermittent malarial one, while event- 
ually some quite different disease is found to produce the symptom. Pyaemia 
may give rise to mistakes of this kind ; also purulent phlebitis, acute ulcerative 
endocarditis, and even tuberculosis. We should be very cautious in making a 
hasty diagnosis of " irregular intermittent fever." Our own experience has taught 
us that almost invariably the case turns out to be something else. Where there is 
doubt we may, in addition to a careful consideration of all the symptoms and a 
thorough physical examination, be aided by the therapeutic action of quinine 
{vide infra). If a high fever of intermitting type is affected by large doses of 
quinine but temporarily if at all, then a diagnosis of malarial intermittent fever 
is rendered doubtful. 

Treatment. — Malarial poisoning is one of the few diseases upon which we can 
make a direct attack with assured success. In quinine we possess a remedy which 
probably acts upon the very cause of the disease, and the therapeutic efficiency of 
which is undisputed. Quinine is, therefore, the sovereign remedy in all forms of 
malarial poisoning, and is often the only drug employed. In the mild cases, which 
are the only kind that occur among us, we do not usually give the remedy upon 
the instant that the patient comes under treatment. It is best to wait for one or 



MALAEIAL DISEASES. 



87 



two attacks, partly to make sure of our diagnosis, and partly to learn what the 
type of the fever is, whether quotidian, tertian, anticipating, or recurring at the 
same hour. And in most cases this delay works no harm to the patient. Dur- 
ing the attack itself there is seldom any use in special treatment. Of course 
the patient must stay in bed and be kept warm during the cold stage, and have 
lighter coverings during the hot stage. During the afebrile interval the patient 
may be up if he feels strong enough and is careful. Quinine is given about five 
or six hours before the next attack is due. It is best to administer one large 
dose of twenty to thirty grains (1*5-2 grm.), either in solution or in capsules of 
seven grains (0*50 grm.) each. If the quinine be given in powder or capsules, it 
is a good way to follow it with a few drops of muriatic acid, to promote its solu- 
tion in the stomach. Often one large dose prevents the next attack. In other 
cases it does occur, but with less subjective disturbance, no chill, and more mod- 
erate fever. We must then give another large dose before the second attack is 
expected. If the attack does not take place, then we may give for several days 
quinine to the amount of eight grains (0*5 grm.) per diem. After all, relapses 
are possible, even at the end of several weeks ; but they yield readily to quinine. 

Judging from our own experience, conchinine is the only one of the other 
preparations of cinchona which is as efficient as quinine. It costs only half as 
much, and is prescribed in just the same way. A disadvantage is that it is more 
apt than quinine to excite vomiting. All the other preparations of Peruvian bark, 
such as chinoidine and cinchonine, are much more uncertain in their action. 

In the treatment of pernicious intermittent fever, of the masked forms, of the 
remittent and continued fevers, and of malarial cachexia, the chief remedy is like- 
wise quinine, given in sufficient doses. In all cases of considerable duration it is 
also of the greatest importance to remove the patient from the malarial region, 
if it can possibly be done. This often proves to be the only way to avoid relapses 
and attain a perfect cure. 

In cases of longer standing, quinine sometimes loses its power. Then we re- 
sort to arsenic. It is frequently employed in malarial cachexia and in inter- 
mittent neuralgia, either alone or combined with iron. We give gtt. v to viij of 
Fowler's solution two or three times a day in water. It may be added that arsenic 
is also said to have a prophylactic virtue : a long-continued use of it is stated 
to render a person proof against malarial poisoning. We will not speak of the 
numerous other remedies recommended, such as eucalyptus, piperine, pilocarpine, 
and many others, for they can be entirely dispensed with. 

The management of the severe varieties of malarial disease involves sympto- 
matic treatment as well as the administration of quinine. We can not enter into 
the particulars. In combating the grave, nervous, intestinal, pulmonary, and 
renal symptoms, the dropsy and the anaemia, the physician must conform to the 
general rules of treatment. 

[There is nothing to be gained by allowing a patient to have an unnecessary 
chill. If there is a reasonable probability that his paroxysms are due to malaria, 
a prompt effort should be made to cut them short. Four hours is the shortest 
time that it is safe to allow for quinine by the stomach with probability that the 
expected chill will be prevented. The drug acts much more promptly when 
given hypodermically. The hydrobromate is preferred by some to the sulphate 
for subcutaneous use on account of the necessity of using acid to dissolve the 
latter, and the consequent risk of abscess. Such a risk should have no weight if 
the physician has any suspicion that he has to deal with the pernicious form of 
the disease. If the stomach is irritable, the remedy can be given by enema. 

The hypodermic injection of pilocarpine is reported to abort an impending 
chill. 



83 



ACUTE GENERAL INFECTIOUS DISEASES. 



Some prefer divided and smaller to the single and large dose of quinine or one 
of its substitutes, a difference of view which is of minor importance. 

In the remittent forms boldness in the use of quinine is required. Cinchon- 
ism should be induced as promptly as may be, and maintained to a mild degree 
for several days ; the quantity of the drug can then be gradually diminished. 

The treatment of the pernicious forms of periodic fever presents itself under 
three main heads : 

1. The prevention of pernicious paroxysms. 

2. The treatment of the paroxysm when present. 

3. The prevention of a recurrence. 

1. We have seen that very frequently the pernicious character is manifested 
after the occurrence of one or more mild attacks ; consequently, in localities and 
seasons marked by the occurrence of grave cases it is an imperative duty to treat 
every mild case promptly and energetically, a course which unquestionably saves 
many a life. 

2. The management of the paroxysm differs according to the form which it 
assumes ; in other words, is largely symptomatic. Bemiss (Pepper's " System of 
Medicine ") says : " The cure of a congestive chill is one of the most difficult prob- 
lems the physician can possibly encounter." Heat externally, opium and chloro- 
form by the mouth, and morphine and atropine subcutaneously, nutrition by the 
stomach or rectum, according to circumstances, and alcoholics if the action of the 
heart is feeble, are the measures of widest application. 

Whatever the type of the attack, a weak heart calls for alcoholic stimulation. 
Cinchonism is always to be induced as rapidly as possible. 

In the comatose form it is to be remembered that the cerebral and other 
nervous symptoms are not due to congestion, but probably to a combination of the 
malarial and secondary blood-poisons. To quote Bemiss again : " Efforts to nour- 
ish the patient must never be relaxed. One must see many of these cases before 
he can realize how often they recover from conditions apparently hopeless when 
promptly treated and properly nourished." 

The hemorrhagic form, like the others, demands cinchonism and careful 
nutrition, but also haemostatics. Purgative doses of calomel are indicated in 
some cases of each form, but should not be given in a routine manner. 

3. Prompt cinchonism is the chief means of attaining the third aim of treat- 
ment. Removal to a healthy locality should be secured if possible, and the 
general condition of the patient requires careful attention. 

It remains to add that those going to a malarial region can often avoid con- 
tracting the disease by taking advice of a local physician as to hygienic pre- 
cautions, and by moderate divided doses of quinine.] 



CHAPTER XIV. 

TYPHO-MALARIAL FEVER. 

[This is not a distinct disease, but expresses a combination in the same indi- 
vidual at the same time of the effects of the special poison causative of each affec- 
tion. Typhoid being a continued fever, its complication with malaria results in a 
pyrexia of a remittent type. Typho-malarial fever occurs in malarial regions, 
especially in the Southern States, and may be seen in non-malarial regions in the 
persons of those in whom malaria, contracted elsewhere, is in a more or less 
active state. 



DENGUE. 89 

Tlie characteristic symptoms of the two diseases are intermingled, those of 
typhoid, thp graver disease, usually predominating. The history of the case and 
careful observation of the symptoms will generally clear up any doubts felt as to 
the diagnosis in the early stages. It would naturally be supposed that the com- 
bined affections must produce an illness more severe in character and more un- 
favorable as regards prognosis than belongs to simple typhoid. Such does not, 
however, seem to be the case. Woodward's statistics show that the mortality of 
uncomplicated typhoid was far greater among white and colored troops alike 
during our late civil war than was the mortality of typho-malarial fever. 

The treatment as regards the typhoid fever differs in no way from that suit- 
able for cases of the ordinary affection ; the periodic element demands the man- 
agement appropriate to simple intermittent or remittent fever.] 



CHAPTER XV. 
DENGUE. 

[Tms affection has never appeared in Germany, and hence, doubtless, was 
omitted by the author. The name " dengue " is supposed to be a Spanish cor- 
ruption of dandy, the term dandy fever having been applied to the disease by the 
West India negroes on account of the stiff carriage of those affected by it. An- 
other name is "break-bone fever." 

The disease generally appears in epidemics, and is almost exclusively confined 
to tropical and semi-tropical countries. In 1780 an epidemic supposed to be 
dengue prevailed in Philadelphia, and outbreaks have occurred repeatedly in the 
Southern States during this century. In 1880 Charleston, Savannah, New 
Orleans, and other Southern cities were visited by it. 

JEtiology. — As to the causation but little is known. Those who have had 
opportunities of studying the disease consider it both contagious and infectious, 
and the inference that it depends on a specific germ is readily suggested. It 
seems to prefer low lands along the sea-shore, and to be influenced by meteoro- 
logical conditions in that it generally prevails during the summer and disappears 
as cold weather comes on. Neither age, sex, nor condition afford any protection 
from the disease ; it was thought by Dickson that one attack generally confers 
immunity for life. 

Pathology. — The disease is so rarely fatal that few opportunities have been 
afforded for its post-mortem study. So far as is known, it has no peculiar lesions. 
The prominence and the character of the muscle and joint pains have led some 
observers to think the affection related in some way to rheumatism. 

Symptoms and Course. — The onset is usually sudden, but a pronounced chill is 
said never to occur. Prodromata similar to those of other infectious diseases are 
sometimes observed, but the first symptom is very often pain and stiffness in the 
muscles and joints, with frequent swelling of the latter. The large and small 
joints are equally affected, and the pain is increased by motion. With the pain 
there is a rise in temperature and in the frequency of the pulse. The pain is apt 
to increase during the first two or three days and disappear on the fifth, but irregu- 
lar remissions are liable to occur. As the thermometer falls the pain and other 
symptoms diminish, but reappear in full force with any subsequent rise. During 
the later days of the disease a skin eruption appears on the upper part of the body, 
and in severe cases becomes general in about two days. This eruption is very 
variable in character; it may appear simply as an erythema, or simulate the erup- 



90 



ACUTE GENERAL INFECTIOUS DISEASES. 



tions of scarlet fever, rubeola, lichen, or urticaria ; it is apt to be associated with 
well-marked heat and itching of the skin. In mild cases the eruption is evanes- 
cent or absent. Swelling of the lymphatic glands is not uncommon ; in severe 
cases the mucous membrane of the mouth, throat, and nose is reddened, and haem- 
orrhage from the outlets of the body has been observed. Pregnant women are 
apt to miscarry. Delirium is rare in adults, but common in children ; the face is 
generally flushed, and the eyes are injected; the tongue becomes increasingly 
coated as the disease progresses, the appetite is lost, nausea is not uncommon, 
vomiting is rare. The bowels and the kidneys present no constant or distinctive 
symptoms. 

In mild cases recovery is sometimes rapid; sometimes, and especially after 
severe cases, convalescence is very tedious, the muscular and articular pain and 
stiffness passing off gradually, and the glandular swelling lasting for weeks. 
Copious skin eruptions are followed by desquamation. 

Diagnosis and Prognosis. — In the former there can seldom be any difficulty 
during the prevalence of an epidemic. The first cases are the only ones which are 
liable to be mistaken, and even their nature can not remain long in doubt. The 
prognosis is uniformly good. 

Treatment. — We are acquainted with no agent capable of aborting or cutting 
short the disease ; nor is there any known measure of prophylaxis except for an 
individual to keep away from those places in which the affection is known to pre- 
vail. 

The treatment of the attack is simply symptomatic ; notable pain calls for 
opium in some form. Quinine has not seemed to be of service. Debility follow- 
ing the attack demands suitable alimentation and tonics.] 



CHAPTER, XVI. 
YELLOW FEVER. 

[This disease is not a visitant of Germany, but its consideration can not be 
omitted from a text-book on the practice of medicine for use in America. In the 
following description the aim will be to bring out the more important features of 
the disease, while for fuller details the reader is referred to larger works and 
monographs. 

iEtiology. — Yellow fever is an acute infectious disease, confined within certain 
geographical limits, and occurring chiefly in epidemics of greater or less extent. 
In certain localities, notably Havana and New Orleans, a season rarely passes 
without some sporadic cases. The influence of temperature is well established ; the 
disease prevails, namely, during the summer or the warm season, and is abruptly 
arrested by one or two decided frosts ; dampness is favorable to it. That it depends 
ultimately on a special cause and does not originate de novo are undisputed facts ; 
but we still remain in ignorance as to the precise nature of this special cause. 
The poison appears to be more active at night than during the day, prefers low- 
lying districts, and in them hugs the ground to a certain extent. Bad sanitary 
conditions are most important accessory causes of the disease, furnishing the soil 
for the multiplication of the poison. There can be little doubt that, under the 
observance of strict personal and public cleanliness, yellow fever visitations might 
be made simply a matter of history. The transmission of the poison probably 
takes place solely through the atmospheric air, thus finding its way to the blood 
through the lungs ; conclusive evidence is lacking that it gains entrance to the 



YELLOW FEYEE. 



91 



system through the alimentary canal. While the air is the medium of transmis- 
sion, the distance to which the poison can be carried by the air alone is very short ; 
it can, however, be transported to an indefinite distance by fomites, especially if 
inclosed in trunks, packing-cases, letters, and the like. Its vitality may thus be 
maintained for very long periods. It is a remarkable fact that in large cities the 
infection may be of great virulence, but confined to a limited district or districts, 
by carefully shunning which unprotected persons are comparatively safe. An 
infected area is apt to extend itself, but the progress is slow, and is interrupted by 
streams of water, high walls, or simply streets. 

That the disease is not, strictly speaking, contagious is the nearly unanimous 
opinion of those competent to form one. In other words, the poison is not thrown 
off in a matured state from the body of an individual suffering from the disease ; 
but, after being so thrown off, remains in the atmosphere or lodges on solid bodies, 
and then undergoes changes which render it active for evil. One attack of the 
disease renders the system of that person insusceptible for ever after ; the natives 
of a yellow-fever district are far less liable to contract the disease than are those 
who move into the district from elsewhere ; until these have passed through an 
attack they can not consider themselves as acclimated. The negro race is suscepti- 
ble to the disease, though in a less degree than the whites, and in the colored the 
affection is far less fatal. Neither age nor sex has any special bearing on suscepti- 
bility. That fear, anxiety, worry, or anything which tends to depress the nervous 
system increases the individual liability is highly probable. The stage of incuba- 
tion is very variable, ranging from one day to three weeks or even more. 

Pathological Anatomy. — The disease involves no constant and peculiar lesions. 
In rapidly fatal cases, congestion and often haemorrhage are found, especially in 
the nervous system, liver, kidneys, and digestive tract. In fatal cases of longer 
duration more or less parenchymatous degeneration is found. A fatty degenera- 
tion of the liver is quite common, and imparts a yellow coloration to the organ, 
giving rise to the terms cafe an lait, or box-wood liver. Jaundice of the skin and 
tissues generally is also observable after death, and depends upon causes in no way 
connected with mechanical obstruction to the flow of bile into the intestine during 
life. Splenic enlargement is conspicuous by its absence. 

Course and Symptoms. — The onset of the disease is generally sudden, but may 
be preceded for a few days by malaise and other signs of general constitutional 
disturbance; the initial chill is seldom severe, reaction following soon, and the 
thermometer rising to 102°-105° ; hyperpyrexia is rare. The pulse-rate does not 
increase proportionately with the fever. The face becomes flushed and the eyes 
injected and watery; headache and pain in the back are early and usually very 
prominent symptoms. The bowels are confined ; the tongue is apt to be clean if 
it was so before the disease came on ; the stomach is usually somewhat irritable, 
and there may be vomiting ; moderate epigastric tenderness is common ; the mind 
remains clear, as a rule, but. delirium is not very uncommon, and in children a 
convulsion may usher in the attack as in other acute infectious diseases ; the con- 
dition of the urine is at first not remarkable, but albumen may soon appear. This 
hot or febrile stage may last from twelve hours to several days. The pulse gener- 
ally declines in frequency before the fever has reached its maximum. As the 
fever disappears the other symptoms vanish also, and the second, or "stage of 
calm," begins. From this point recovery may be rapid and uninterrupted, the 
whole disease consisting of but a single febrile paroxysm of greater or less intens- 
ity and of short duration. 

In grave cases, and gravity is often foreshadowed in the first stage by marked 
capillary congestion of the surface of the body irrespective of the intensity of the 
other symptoms, and after a stage of calm lasting for some hours, but rarely 



92 



ACUTE GENERAL INFECTIOUS DISEASES. 



exceeding twenty-four, more distinctive symptoms appear. The pulse is very 
compressible, the surface of the body is cool, vomiting occurs or becomes more 
prominent, and haemorrhage is now apt to take place. The escape of blood into 
the stomach, its retention and the changes which it there undergoes, and its 
subsequent expulsion, explain the dreaded and characteristic symptom known as 
"black vomit." Tarry stools sometimes are observed. Haemorrhage elsewhere 
is also common, occurring from the gums, the nose, eyes, uterus, kidneys, into the 
skin, etc. Albuminuria with casts is very common. Jaundice, sometimes of a 
lemon-yellow hue, comes on, and is rarely lacking in severe cases. From this 
symptom the name of the disease is derived. 

In cases marked by more or less complete suppression of urine, coma and con- 
vulsions, probably largely uraemic, come on. Some severe cases are of the " walk- 
ing " type, the patients going about while the malady is far advanced, or even up 
to the time of death. As a rule, however, muscular prostration is marked. 

If the disease does not prove fatal in this third stage, convalescence comes on 
more or less gradually, and is followed by complete recovery ; relapses, however, 
occasionally occur. 

The duration of the affection is variable but, on the whole, short, usually being 
less than a week. 

Diagnosis. — In mild cases the symptoms are not distinctive, and the diagnosis 
at the commencement of an epidemic is not likely to be reached except by an 
experienced observer, and even by him more or less conjecturally. During an 
epidemic the severe lumbar pain, the headache, the suffusion of the eyes, and the 
moderate gastric irritability, are all sufficient for diagnostic purposes. Severer 
cases are also marked by capillary congestion of the surface of the body, and the 
third stage with the black vomit, haemorrhage, jaundice, slow pulse, scanty urine, 
and prostration is characteristic. Of course all the above symptoms are not pres- 
ent in every case. The only disease which can well give rise to confusion is remit- 
tent fever with jaundice. This affection has a different temperature curve, is 
not confined to the yellow-fever zone, is controlled by quinine, and is not accom- 
panied by black vomit. 

Prognosis. — This varies in any given locality with the character of the prevalent 
epidemic. The death-rate is sometimes very high, sometimes moderate ; it is 
greater in hospital than in private practice. 

In the first stage of the disease the chief element in the formation of the prog- 
nosis seems to be the presence of marked and general capillary congestion of the 
skin, a symptom which foretells a severe attack. The absence of this symptom is 
rather less important than its presence. Cases may turn out to be severe in which 
it is lacking. The frequent deceptiveness of the stage of calm is to be remem- 
bered. 

Yellowness, black vomit, and suppression of urine are symptoms denoting the 
greatest gravity, but do not justify the complete abandonment of hope. 

Treatment. — There are no means in our power of aborting the disease. Pre- 
vention is to be attained by cleanliness in its large sense, and by careful quaran- 
tine against things rather than persons. Individuals from infected localities may 
safely be admitted into non-infected localities, provided that they and their cloth- 
ing and effects are thoroughly disinfected. Merchandise, the mails, and the like, 
must be excluded or disinfected. So also vessels and all other means of com- 
munication. 

The earlier proper treatment can be instituted, the better. Absolute rest and 
good ventilation are the first requisites. Emetics and cathartics are not indicated 
by the disease itself ; the condition of the stomach and bowels should be inquired 
into, and indigestible food or an accumulation of faeces should be removed if 



EPIDEMIC CEKEBKO -SPINAL MENINGITIS. 



93 



present. A hot mustard foot-bath early in the attack is useful. For the lumbar 
pains, opium or morphia are indicated. Sinapisms, or other similar external coun- 
ter-irritants, with ice internally, and hydrocyanic acid or chloroform, are service- 
able against gastric irritability. High fever is to be combated by cold spongings, 
the wet pack, and the cold bath. For haemorrhage, styptic remedies may be used, 
though it is doubtful whether, when given internally, they are really of much 
benefit. Of course no medication is to be resorted to which is likely to heighten 
a tendency to emesis. 

Suppression of urine is to be met by dry cups to the loins, diuretic remedies 
internally if the condition of the stomach allows, or the hot-air bath. The results 
of pilocarpine are disappointing according to Bemiss, who states that he has seen 
good effects from large enemata of water, preferably cold, if there be notable fever 
in these cases. Prostration is an indication for the use of alcoholic stimulants, 
among which iced dry champagne ranks high. It will seen that the treatment is 
entirely symptomatic. The disease is self-limited, has a short course, and the 
patient will recover if he can be kept alive until the poison is exhausted. During 
the attack and until convalescence is thoroughly established the management of 
the diet is all-important. Small quantities of the most easily assimilable food 
may be given at short intervals if they are tolerated by the stomach ; if not, ali- 
mentation must be by the rectum, and the lower bowel in this disease is generally 
in a fair condition for this method of nutrition. 

Courage and hopefulness on the part of the physician may do much good, and 
the services of a skillful and experienced nurse are of the utmost importance. I 
am told that in New Orleans, and perhaps elsewhere, it is customary, for those 
who are not protected and can afford this course, to secure in advance a nurse as 
soon as an epidemic breaks out. They then take to their beds at the first sign of 
illness.] 



CHAPTEE XVII. 

EPIDEMIC CEREBRO-SPINAL MENINGITIS. 

{Spotted Fever. Cerebrospinal Fever.) 

iEtiology. — The epidemic form of cerebro-spinal meningitis has been known 
only since the beginning of this century. The first epidemics were observed in 
southern France and in Geneva. Smaller ones occurred in Germany in 1822 and 
1853 ; but it was not till 1863 that the disease became at all frequent among us. 
Since that date there have been more or less extensive epidemics almost every 
year. The southern and central portions of Germany are particularly liable to 
them. Sporadic cases may occur at any time. 

Most of the epidemics appear in the winter and spring. We do not know any 
particular factors which promote the disease. It often seems to be decidedly 
endemic. Barracks, work-houses, and the like have been marked by tolerably 
extensive epidemics. Whether the disease can be carried by patients to places 
previously free from it is still uncertain. It is not directly contagious. Children 
and young adults are the most frequent victims ; but now and then elderly 
persons are attacked. Sex can not be shown to have much influence. 

That the disease is infectious is clearly shown not only by its epidemic and en- 
demic character, but by its whole course. About the infectious agent itself and 
the manner in which infection takes place we have as yet no certain knowledge, 
although micro-organisms have been repeatedly demonstrated in the purulent 



94 



ACUTE GENEEAL INFECTIOUS DISEASES. 



meningeal exudations. They are for the most part diplococci. It is a plausible 
theory, but thus far merely a theory, that the specific poison penetrates through 
the nostrils and the holes in the cribriform plate of the ethmoid bone into the 
cerebral meninges, which are otherwise so perfectly protected. 

[Sanitary conditions seem to play a less important role in this than in many 
other infectious diseases. During the epidemic which visited New England in 
1873 the writer was interne at the Massachusetts General Hospital, and there saw 
a number of cases. The disease was also prevalent among horses at the same 
time, and it is curious to note that a like association of the affection in men and 
animals was observed in Vermont in 1811 and in New York city in 1871. During 
the year 1873, 216 deaths were returned as due to this malady in the city of 
Boston.] 

Pathological Anatomy, — The autopsy discloses an acute purulent cerebro-spinal 
leptomeningitis. It is only in rapidly fatal cases that slight and incipient lesions 
have been met with. As a rule, the extent and intensity of the objective lesions 
correspond to the severity of the symptoms. In the brain the purulent inflamma- 
tion attacks the convexity as well as the base. It is usually most marked along 
the larger blood-vessels and in the fissures of the cortex. Of the spinal cord the 
posterior surface suffers most. Frequently the lumbar portion is more affected than 
the parts above. It is, however, exceptional for the disease to be limited to the 
meninges ; it is prone to extend into the underlying parenchyma. The micro- 
scope reveals clumps of pus-corpuscles about the blood-vessels, where they pene- 
trate into the tissues, and not infrequently there are numerous centers of genuine 
encephalitis. These latter may even be visible to the naked eye. Exceptionally 
there may even be cerebral abscesses of considerable size. The vessels are dis- 
tended with blood, clear into the central ganglia, and ecchymoses are frequent. 
The cerebral ventricles are usually enlarged and filled with a cloudy serum, or even 
with pus. It is plain that these lesions of the cerebro-spinal parenchyma greatly 
modify the clinical picture, and that they must frequently have more to do 
with the severity of the symptoms than has the leptomeningitis itself. 

Clinical History. — Prodromata are relatively rare, and if present they are not 
severe, being confined to general malaise, with slight headache and pain in the 
limbs. Usually the disease begins rather suddenly ; there is intense headache, 
often mainly felt in the back of the head, pain and stiffness in the back of the 
neck, and great general discomfort. It is not rare for vomiting to occur at first. 
Very often there are among the early symptoms such important mental disturb- 
ances as stupor or delirium. There is usually fever from the first. An initial 
rigor may occur, but it is not the rule. 

The intensity of these first symptoms may vary. Subsequently to them 
the course of the disease may vary greatly. First there are very acute, vio- 
lent forms, termed " explosive " (meningitis cerebro-spinalis siderans, meningite 
foudroyante), where the cerebral symptoms are very severe and the patient 
survives only a few days or even hours. Again, there are abortive cases. These 
begin with equally threatening symptoms, but after a few days completely 
recover with remarkable rapidity. The majority of cases last about two to 
four weeks. In severe cases death may come as early as the first week. The 
disease is often protracted to six or eight weeks' duration, or even longer, and 
may end in death after all. Cases that last a good while sometimes exhibit 
a remarkably intermittent character. Finally, the number of mild cases is not 
small in which none of the symptoms are very pronounced, and recovery is 
relatively early. 

The symptoms of the disease may be divided into (1) the severe general symp- 
toms, referable to the brain and spinal cord ; (2) the more localized, nervous symp- 



EPIDEMIC CEREBEO-SPINAL MENINGITIS. 



95 



toms ; and (3) the results of the constitutional infection, including fever and dis- 
eases localized in other parts of the body. 

1. Among the less definite cerebral symptoms neadache is imiDortant. It is 
usually terribly severe. It is chiefly occipital, but sometimes is frontal or tem- 
poral. Like most of the symptoms of meningitis, the headache undergoes very 
frequent changes in intensity during the course of the disease. For a time it may 
remit, only to recur with fresh severity. Marked vertigo and a sense of fullness 
in the head may accompany it. 

The pain in the head is re- enforced by intense pain in the nape of the neck and 
back, due to the spinal meningitis. There is almost always considerable tender- 
ness along the whole spinal column. The erector spinas is contracted, making 
the back straight and rigid, or even producing opisthotonos ; and the head is 
bent backward by the reflex contraction of the muscles in the back of the neck. 

In most of the severe cases intelligence is blunted ; we find all degrees of dis- 
turbance, from slight drowsiness to delirium on the one hand, or deep coma on the 
other. These symptoms likewise may undergo frequent variation in their inten- 
sity. General convulsions occur in very severe cases alone, and are of evil omen. 

The vomiting is also to be regarded as of cerebral origin. It frequently is an 
early symptom, but may be deferred. 

2. Symptoms referable to the individual cerebral nerves are manifold and 
variable. The most frequent disturbances are in the nerves that supply the mo- 
tores oculi. They include strabismus ; nystagmus, or slow movements independ- 
ent of volition ; unilateral or bilateral ptosis ; slow reaction of the pupils, or 
inequality of them, or myosis or mydriasis. In the area of distribution of the 
facial there is often a noticeable contraction of the muscles, giving the face a 
peculiar, painfully distorted look. Trismus, or tetanus of the masseters, is rare and 
usually a bad sign. 

Disturbance of the nerves of special sense is frequent. Deafness may be 
due to the stupor, but is often the result of an extension of the inflammation 
to the acoustic nerve. The purulent inflammation may be propagated as far as 
the labyrinth, or even into the middle ear. Tinnitus aurium is also frequent. 
Disturbances of vision are far less frequently observed, but optic neuritis has 
been repeatedly found by the ophthalmoscope. Severe purulent irido-choroiditis 
has been also observed. It is probably due to extension of the inflammation 
along the sheath of the optic nerve. Conjunctivitis and keratitis sometimes occur ; 
but they are probably caused by external injuries rendered possible by the imper- 
fect closure of the lids, or the diminished sensitiveness of the parts. We have 
several times found the sense of smell diminished. 

Disturbances in the area of distribution of the spinal nerves are, on the whole, 
less frequent. The only one of value in diagnosis is the cutaneous hyperesthesia. 
It is apt to be particularly severe in the extremities, and it may be so extreme that 
the light touch of a finger or a needle causes great pain. Sometimes there is a 
slight twitching in the muscles of the extremities. This has, however, no special 
significance. As might be expected, there is no invariable rule about the reflexes. 
The cutaneous reflexes are usually well marked, and the tendon reflexes may be ; 
but in some cases we have found the tendon reflexes markedly diminished or even 
abolished. Such a condition is probably due to some lesion of the fibers of the 
posterior nerve-roots. 

All of the localized nervous symptoms above enumerated result from one of 
two causes — either the roots of the nerves are affected by the purulent exu- 
dation, or the inflammation extends inward to the central organs themselves. 
This extension is the explanation also of other symptoms sometimes observed — 
viz., hemiplegia, paraplegia, partial convulsions, and aphasia. 



96 



ACUTE GENERAL INFECTIOUS DISEASES. 



3. In addition to all these nervous disturbances, we see also symptoms refera- 
ble to other parts of the body. Of this class there is one cutaneous affection which 
is a very valuable aid to diagnosis. Herpes labialis or herpes facialis is apt to 
appear soon after the beginning of the meningitis. It is seen in more than half 
the cases, and as frequently in severe as in mild attacks. Other eruptions occur 
now and then — e. g., roseola, urticaria, or petechias. Sometimes they are so sym- 
metrically distributed upon the two halves of the body as to suggest the idea of a 
nervous origin. 

The digestive system seldom displays severe symptoms beyond the vomiting 
already mentioned. Anorexia and constipation are, indeed, usually present, as in 
many of the graver diseases. We have seen mild dysentery a few times. Now 
and then a slight jaundice has been observed. The spleen is often somewhat 
swollen, but very rarely attains great size. 

Swelling of the joints has been observed quite often ; it is much more frequent 
in some epidemics than in others. The enlargement may be an early or a later 
symptom. It does not usually prove to be of grave omen. 

The urinary apparatus is seldom affected. The urine may contain some albu- 
men and a few casts. Polyuria is an interesting symptom, probably of nervous 
origin. It is more apt to occur in the latter part of the disease. In a number of 
cases sugar has been found in the urine. Cystitis is a secondary disorder which 
is not very rare, particularly in severe cases where the catheter has been used. 

Pulmonary and bronchial symptoms are likewise secondary. They occur very 
often in bad cases. It is evident how easily the stupor of the patient may lead to 
the inhalation of solid matter, with consequent bronchitis and lobular pneu- 
monia. 

Lesions of the circulatory system are rare. Acute endocarditis has been 
observed only a few times. The pulse is usually somewhat accelerated, seldom 
rendered slower. Very frequently the pulse-rate is remarkably variable, undoubt- 
edly because of variation in the supply of nervous force. Slight irregularities in 
the pulse are also common. 

4. The fever in epidemic meningitis conforms to no single type. It does not 
correspond at all to the severity of the other symptoms ; the worst cases may run 
then course with little or no fever. In most cases the fever has irregular remis- 
sions. It seldom exceeds 104° (40° C). Sometimes the fever exhibits a decidedly 
intermittent character. It is in these cases particularly that we find the variation 
in the intensity of all the symptoms of which mention has been made repeatedly. 
The variations in the temperature do not, however, always run parallel with the 
changes in the other symptoms. In mild cases the fever is usually moderate and 
brief. The abortive attacks may present high temperatures at first, but these 
quickly abate. In case of a fatal issue there is sometimes hyperpyrexia before 
death, reaching 108° to 109° (42°-43° C). In the severer but not fatal cases the 
fever declines slowly but irregularly. The fever may be over, long before the 
other symptoms disappear. 

It is impossible to portray all the forms, symptoms, and courses the disease 
may have. The chief forms have been already mentioned ; but in reality these 
are only types which run into one another without sharply defined border-lines. 
It is in itself a characteristic of epidemic meningitis that most of the more tedious 
cases have a variable, uncertain course. We may even meet with a complete 
intermission of all the symptoms, lasting for quite a while, so that the return of 
the trouble may fairly be called a relapse. 

Sequelae are not rare after severe cases. Persistent deafness is the most fre- 
quent. It results from the complications, already mentioned, which affect 
the labyrinth and the middle ear. Little children may become deaf and dumb. 



EPIDEMIC CEEEBEO-SPINAL MENINGITIS. 



97 



Again, vision may be deranged, because of retinitis, atrophy of tbe optic nerve, or 
corneal opacities, etc. It is not very rare for meningitis to leave grave nervous 
disorders behind it. These are frequently the symptoms of a chronic hydro- 
cephalus. We may observe headache, sudden unconsciousness, or even convul- 
sions, mental impairment, and weakness of the extremities. Or there may be 
localized disturbances due to permanent injury of limited portions of the brain or 
spinal cord, such as hemiplegia, paraplegia, and aphasia. From many of these 
conditions there may be a gradual recovery, but others prove incurable. 

The diagnosis of cerebro-spinal meningitis is not difficult hi a well-developed 
case, particularly if the prevalence of an epidemic puts us in mind of the disease. 
Diagnosis is more difficult in sporadic cases, and most of all when the patient 
does not come under observation till he is very ill and when we can not obtain 
the previous history. Important factors are the abrupt onset, the speedy appear- 
ance of grave cerebral symptoms, the characteristic headache and pain in the 
back, the stiffness of the neck, and the herpes labialis. 

If we find evident symptoms of meningitis, we have still to decide whether the 
case is one of primary epidemic disease, or secondary, perhaps due to extension 
from some other part. Bearing this last possibility in mind, we should examine 
the ears carefully ; for, as is well known, chronic otitis media may set up a puru- 
lent meningitis. Again, it may be very difficult to exclude a tubercular menin- 
gitis. Here we should consider other conditions that might render tuberculosis 
probable, such as the general condition of the patient, heredity, previous pleurisy, 
the results of thoracic examination, or scrofulous disease of the bones or joints. 
The existence of herpes points toward epidemic meningitis, for it is exceptional in 
the other forms of the disease. It is sometimes hard to distinguish between men- 
ingitis and severe cases of other acute infectious diseases — e. g., typhoid fever and 
septic diseases. Here we must weigh all the circumstances carefully. 

This is a good opportunity to mention the secondary meningitis which is said 
to occur with relative frequency just at the time of an epidemic. The combina- 
tion of croupous pneumonia (q. v.) with purulent meningitis has been repeatedly 
observed. Still, it is hard to determine whether the cause of this secondary men- 
ingitis is actually identical with that of the epidemic form. Its diagnosis is 
usually difficult, and not to be made absolutely. In other acute diseases, like 
typhoid and articular rheumatism, when they occur at the time of an epidemic, 
the "tendency to meningitis" is potent enough to make meningeal symptoms 
more frequent than usual. It has not been clearly demonstrated, however, that 
this fact is actually due to the epidemic meningitis. 

The prognosis depends chiefly upon the severity of the cerebral symptoms. Yet 
we should be guarded in our utterances, even when the case seems mild or has 
apparently made the first steps toward convalescence. The disease sometimes 
changes for the worse at a late period. In general the mortality is about thirty 
to forty per cent. Probably this estimate does not take into account many very 
mild cases. 

Treatment is purely symptomatic. There is no specific for meningitis. The 
remedy most employed is cold applications. Ice-bags are placed upon the head 
and, if possible, along the spine. There are long and narrow rubber ones for the 
latter purpose. These applications are borne well by most patients and afford 
decided relief. The local abstraction of blood has also an undeniably beneficial 
influence, however difficult this may be to explain. Leeches are put behind the 
ears, and cupping-glasses on the back of the neck and along the spine. Mercurial 
ointment is often rubbed in, not only locally but also in the same way as in 
treating syphilis. Its use is doubtful. The narcotics are of great value. The 
best is morphine given subcutaneously. It lessens the pain and often affords the 
7 



9S 



ACUTE GENERAL INFECTIOUS DISEASES. 



uneasy and delirious patient rest and sleep. Chloral and bromide of potash may 
also be employed. Iodide of potash is often given internally, to the amount of 
twenty to thirty grains (grm. l - 5-2') in a day. It is said to act as an " absorbent," 
particularly in tedious cases. , 

The fever hardly ever requires special treatment. If the fever intermits, still 
quinine exerts no permanent influence. Bathing involves manipulations which 
most patients find unpleasant and painful, so that baths can seldom be employed, 
at least in the more acute stages of the disease. Later, warm baths are often 
beneficial. Local complications — e. g., affecting the eye or the ear — require special 
treatment. The swelling of the joints which sometimes occurs we have thought 
to be somewhat relieved by salicylic acid. 



CHAPTER XVIII. 

SEPTIC AND PY2EMIC DISEASES. 

(Spontaneous Septicopyemia.) 

The septic and pyagmic processes which follow serious injuries or operations 
belong to surgery ; but analogous diseases occur in persons who are apparently in 
perfect condition. They take the form of an extremely severe acute infectious 
disease, usually fatal. There is often the greatest difficulty in diagnosticating 
these cases during life. Probably the most intelligible way in which to present 
these interesting and clinically important diseases will be to start with their 
pathology, and subsequently to speak of their aetiology and clinical history. 

Pathological Anatomy and iEtiology.— The most striking feature at the autopsy 
of such cases is that there is never a lesion of one organ exclusively. Several, or 
it may be almost all of the organs exhibit numerous limited foci of disease. The 
lesions sometimes consist for the most part of multiple abscesses, sometimes of 
numerous ecchymoses, and sometimes of combinations of the two. The abscesses 
are found chiefly in the lungs, kidneys, liver, spleen, muscles, heart, brain, and 
thyroid gland. Quite extensive purulent inflammation is also found. This attacks 
the joints by preference, but also the pleura and meuinges and the eye, where 
it causes purulent choroiditis, panophthalmitis, and purulent degeneration of the 
vitreous. The ecchymoses are most frequent upon the surface of the body, the 
serous membranes (e. g., the pericardium and the pleura), the retina, and conjunc- 
tiva ; and also in the brain and the pelvis of the kidney. Beside these multiple 
abscesses and ecchymoses, there is frequently another disorder, which seems to be 
the very focus of the disease, viz., acute ulcerative endocarditis (cf. the appro- 
priate chapter). This usually attacks the mitral valve, more rarely the valves 
of the aorta, and quite exceptionally the valves of the right side of the heart. 
Finally come a number of changes common to all severe constitutional infectious 
diseases — acute splenic tumor, " cloudy swelling " of the liver and kidneys, a dry- 
ness and dark-red color of the muscles, etc. 

A glance over this pathological picture makes us feel certain that some per- 
nicious agency pervades the whole system. And this factor we can, in almost all 
cases, demonstrate beyond a doubt to be bacteria. These are found not only in the 
exudations due to the endocarditis, but also in the midst of numerous small foci of 
inflammation situated in the internal organs, where they usually completely fill 
some little blood-vessel with what is called an embolus of micrococci. The large 
foci of inflammation visible to the naked eye are mostly purulent — i. e., are ab- 



SEPTIC AND PYEMIC DISEASES. 



99 



scesses. Most of the internal viscera also contain very minute foci, devoid of nuclei 
and in a state of " coagulation-necrosis." These are visible through the microscope 
alone. They may be combined with ecchymoses, and usually they are when seen 
already surrounded by a zone of secondary inflammation. This necrosis of tissue 
seems to be the first thing which the bacteria accomplish. The cutaneous, retinal, 
and other ecchymoses are frequently attended by the presence of bacteria ; but this 
relation is not always observed. We do not know the reason why the bacteria 
should sometimes cause nothing but necrosis of tissue, sometimes suppuration, and 
sometimes ecchymoses. The prevailing custom is to term the cases of multiple 
abscess pyaemic, and those where there are merely ecchymoses and foci of inflam- 
mation, without actual suppuration, septic in the narrower sense of the term. Bui, 
as the two forms are often combined, we also speak of a " septicopyemia." 

Of course the bacteria, which are the real cause of the disease, must have pene- 
trated into the body from the external world. In fact, careful search will reveal, 
in the great majority of cases, the place of infection. It follows that the idea of 
an actual " spontaneous " pyaemia, arising within the system, must be entirely 
abandoned. 

The factors which most frequently excite septic or pyaamic infection are as fol- 
lows : 1. The condition subsequent to labor or abortion, particularly the latter. 
The raw surface of the uterus furnishes ingress to the septic poison. Nor is it by 
any means the invariable rule that the uterus and its appendages should exhibit any 
considerable pathological change as a result of this absorption. We do find, often 
enough, diphtheritic and gangrenous inflammation at the place where the placenta 
was inserted, or purulent thrombi in the veins of the uterus and of the pelvis ; but 
in other cases the uterus is merely a gate of entrance for the poison, remaining 
itself unharmed. 2. The septic poison may also be absorbed through slight abra- 
sions of the skin, etc. ; and these may be almost completely healed by the time 
the severe symptoms of disease are developed. Bed-sores belong in this category. 
3. Ulcers of the mucous membranes may give rise to infection. This is the expla- 
nation of those cases of sepsis which complicate typhoid fever, dysentery, or diph- 
theria. 4. Lastly, we sometimes find no other source for the pyaemia than a sup- 
purating disease of the bones, joints, or other parts, previously existing. The 
above enumeration by no means exhausts all the possibilities. Still, it will be 
found to explain most cases. The more minutely we search for a possible place 
of entrance for the septic virus, the less often we fail to find one. 

When the poison has once made its way into the system, it can be disseminated 
through various channels. It may be carried by the lymphatics into the general 
circulation. A purulent phlebitis may be excited at the point of infection ; and 
this in turn may excite, chiefly through embolism, secondary abscesses. These 
abscesses occur first in the lungs and then in other organs. It seems to be 
possible for a purulent phlebitis to arise in a vein remote from the place of infec- 
tion. The valves of the heart often greatly promote the dissemination of the 
septic matter. The virus is prone to fasten upon them, probably purely from 
mechanical causes. This results in acute endocarditis. In such a case we must 
regard the endocarditis merely as one of the symptoms of the universal septic 
infection. But the valves are a fertile soil for the propagation of the poison, and 
emboli carry away from them a great deal of infectious matter to the various 
organs ; and so the acute endocarditis becomes in many instances the central factor 
in the whole process. Yet in other cases there is little or no endocarditis. 

Clinical History. — It is our intention to discuss below those cases chiefly which 
are of interest to the physician rather than the surgeon — i. e., where the septico- 
pyaemia is an apparently primary, acute, and grave disease. Many of the essential 
traits of this type of disease are identical with those of the pyaemia which compli- 



100 



ACUTE GENERAL INFECTIOUS DISEASES. 



cates the effects of serious wounds or the inflammation subsequent to childbirth ; 
but it is precisely because no cause at all presents itself that many cases of the 
disease seem so obscure, and are so often Avrongly diagnosticated. Besides, the 
patient is often very ill indeed before the physician sees him ; and this adds greatly 
to the difficulties of a correct diagnosis. 

The beginning of the disease is usually rather abrupt. An apparently 
healthy person is attacked with febrile symptoms, headache, and "rheumatic" 
pains in the muscles, joints, and loins. There may also be gastro-intestinal symp- 
toms of considerable severity, including vomiting and diarrhoea. Usually the 
patient feels ill enough to take speedily to his bed. The symptoms now increase 
rapidly, and develop into a severe illness which may resemble either a bad case of 
typhoid fever or miliary tuberculosis. Or the cerebral symptoms, such as head- 
ache, stupor, and delirium, may become so prominent that the attack seems like 
meningitis. If the trouble in the joints {vide infra) predominates and there are 
signs of endocarditis, the disease may at first be taken for a violent attack of acute 
articular rheumatism. 

Taking up the separate symptoms, we shall first name those which belong to 
every severe acute infectious disease and have nothing characteristic about them. 
In this list belong the general prostration, the anorexia, the mental disturbance, 
the stupor and delirium, the headache, the subjective symptoms of fever, the dry- 
ness of the tongue, and finally the acute splenic tumor which can often be made 
out. There are, however, other and more characteristic symptoms ; and it is chiefly 
upon these that the diagnosis rests, provided we can make one at all. These 
are : 

1. The Course of the Fever. — In many cases it must be confessed that this is not 
at all characteristic. It may even be so like that of typhoid fever as to lead to a 
wrong diagnosis. But in other cases the temperature-curve does aid us greatly, 
viz., when it represents an intermitting fever with marked elevations, reaching 
106° (41° C.) and higher, and often accompanied by a chill and with subsequent 
deep depressions. The curve may thus come to resemble closely that of a quotid- 
ian or even tertian intermittent fever. Sometimes again the course of the fever 
is made up of similar paroxysmal elevations, separated by periods of ordinary re- * 
mitting fever. 

2. Cutaneous Symptoms. — These are very frequent, and a great aid to diag- 
nosis. The hsemorrhages into the skin are of chief importance. They may be 
either punctiform petechiae or more extensive ecchymoses. If petechias, it may 
be very hard to distinguish between sepsis and the purpura of small-pox (q. v.). 
Of other cutaneous appearances, the first in relative frequency is an erythema 
resembling scarlatina. It is not improbable, as we have already said, that many 
cases which have been described as severe scarlet fever occurring during child- 
bed were in reality septic disease. Roseola, wheals, pustulous eruptions, herpes, 
and phlegmonous inflammations have also been observed. 

3. Ocular Disturbances. — The purulent inflammations of the eye, which are 
probably of embolic origin and which may develop into diffuse septic panoph- 
thalmitis, have been known for some time. Lately, Litten and others have called 
attention to more minute changes in the fundus of the eye. These are revealed 
through the ophthalmoscope and have great diagnostic value. Chief among 
them is retinal haemorrhage, which is sometimes accompanied by a white spot in 
the center, corresponding to a necrosis of the retina in that place ; but there may 
be similar white spots without haemorrhage. 

4. Circulatory Disturbances. — An ability to recognize the cardiac lesions 
would be very desirable ; but often this is impossible before death. The pulse is 
indeed frequently much accelerated and irregular ; but such signs alone lead to 



SEPTIO AND PYEMIC DISEASES. 



101 



no definite conclusion. Endocardial murmurs are often wanting, even in cases 
where the autopsy discloses abundant exudation and ulcers upon the valves. 
Still, in some cases of this sort we have found the heart-sounds noticeably deficient 
in clearness. Sometimes we hear blowing sounds, which might, however, quite 
naturally be regarded as functional. There are no noticeable changes in the 
blood. Bacteria have not yet been demonstrated in the blood of the patient during 
life. Sometimes a distinct, though moderate, increase in the number of white 
blood-corpuscles is observed. 

5. The grave cerebral symptoms are for the most part quite analogous to those 
in other severe acute infectious diseases. They may be present, and yet no marked 
objective lesions may be found after death. In other cases they have an anatomi- 
cal basis — in purulent meningitis, haemorrhagic pachymeningitis, cerebral haemor- 
rhage, or abscess. These conditions, just enumerated, may excite localized cerebral 
symptoms, e. g., hemiplegia. 

6. Affections of the joints are comparatively frequent, and of great value in 
diagnosis. We may find purulent inflammation, or even periarticular abscesses. 
If they appear early in the attack, they may, as we have said, lead to an erroneous 
diagnosis of acute articular rheumatism. Abscesses may also occur in the perios- 
teum and marrow ; but it is exceptional for them to cause special symptoms. It 
is, however y possible that many cases of severe purulent "acute osteomyelitis" 
really are constitutional septic disease. Abscesses in the muscles are often found 
at the autopsy, but they again are seldom large enough to enable us to recognize 
them at the bedside. 

7. Renal changes are frequent, but seldom produce striking clinical symptoms, 
or prove of value in diagnosis. The urine often contains a moderate amount of 
blood and albumen ; but yet it may not be essentially altered in cases where the 
autopsy discloses extensive renal abscesses or ecchymoses, or haemorrhages into 
the mucous membrane of the pelvis. In other cases, however, an acute septic 
nephritis is conjoined with the infarctions and abscesses, and then the urine 
exhibits all the characteristics of acute Bright's disease, having a large amount of 
albumen, red and white blood-corpuscles, epithelium, and casts. 

8. The pulmonary symptoms are in part secondary. Bronchitis and lobular 
pneumonia develop as in all other severe constitutional diseases. The pulmonary 
abscesses of themselves give rise usually to no objective symptoms — or, at most, to 
a marked dyspnoea, out of all proportion to the scanty physical signs. Empyema 
is a not infrequent result of infection of the pleura, due to the foci of disease 
which are situated upon the outer surface of the lungs. If the aspirating-needle 
shows the actual existence of empyema, this fact may make the diagnosis of the 
constitutional disease much easier. 

9. Of the abdominal symptoms, we have already mentioned the acute splenic 
tumor. It is almost impossible to diagnosticate infarctions and abscesses in the 
spleen. If the spleen is enlarged and noticeably painful, we may suspect their 
existence. There are sometimes quite severe intestinal symptoms, such as a pro- 
fuse " septic diarrhoea," in cases where the autopsy does not show any particularly 
grave lesions. Still intestinal ecchymoses and intestinal diphtheria have some- 
times been observed. We should mention that often the skin has a faint 
jaundiced hue. This is sometimes the result of duodenal catarrh, but perhaps it is 
at other times haematogenous. 

Course of the Disease and Prognosis.— The entire course of a septic case may 
be comprised within a few days, for a severe attack is always thus quickly termi- 
nated by death. Protracted cases are also seen, where the sufferings last one to 
two weeks, or even longer ; but in these, again, the end is almost invariably 
unfavorable. It is not improbable that there are milder and curable forms. 



102 



ACUTE GENERAL INFECTIOUS DISEASES. 



Our acquaintance with these last is, however, so slight that we can not state any 
particulars about them. 

Diagnosis. — It is self-evident that a disease which combines symptoms so 
manifold and so ambiguous must be very difficult to recognize. We will 
recapitulate the chief diseases to be excluded. A case may greatly resemble 
typhoid fever when there is persistent prostration, diarrhoea, an eruption like 
roseola, and an enlarged spleen. In discriminating we should consider with great 
care the possible aetiology — e. g., external injuries ; and we should look for septic 
retinitis, swelling of the joints, cutaneous ecchymoses, and an intermitting form 
of fever. It is all the more possible for the disease to resemble meningitis, because, 
as we have said, meningeal disturbance may be one of the symptoms of the sepsis 
and color the whole picture. Here the symptoms of septic poisoning already men- 
tioned would be of some value in diagnosis, and the physical signs of endocarditis 
or of a greatly enlarged spleen would be worth still more. There may be equal 
difficulty in the differential diagnosis between acute sepsis and acute miliary tuber- 
culosis. Here we should consider carefully each separate symptom, and, above 
all, the aetiology, searching for something that would explain the occurrence of 
sepsis on the one hand or of acute miliary tuberculosis (q. v.) on the other. 
If we found miliary tubercles in the choroid by means of the ophthalmoscope, all 
doubt would vanish. At the beginning of a septic attack the rigors may arouse 
suspicions of intermittent fever. Usually the early appearance of other symptoms 
corrects this idea ; but, if not, the powerlessness of quinine will. If a severe acute 
nephritis has developed itself in a septic case, all the symptoms may be erroneously 
referred to uraemia. But persistent observation will usually lead us to the right 
conclusion. As to the conditions of great prostration resembling acute sepsis, 
which occur in acute (primary) ulcerative endocarditis and in severe articular 
rheumatism, see the appropriate chapters. 

The treatment can be merely symptomatic. Of course we try again and again 
to cut short the attacks of fever by large doses of quinine, but never with any but 
temporary success. Baths, stimulants, and, if necessary, narcotics are the other 
chief remedies employed. 



CHAPTER XIX. 

HYDROPHOBIA. 

{Rabies canina.) 

iEtiology. Rabies in Dogs. — A peculiar infectious disease sometimes occurs in 
dogs, and more rarely in some other animals — viz., the wolf, fox, cat, cow, and 
horse. Men who are bitten by the animal may catch the disease, and thus become 
the victims of terrible symptoms originating in the central nervous system. 

Two forms of madness are distinguished in dogs — the raving madness and the 
quiet madness. Bollinger describes the raving form as beginning with proclro- 
mata, the melancholy stage, lasting one to three days. The animal is low-spirited, 
timorous, and without appetite. Then comes the stage of irritation or of mania, 
in which the animal is attacked with an impulse to bite. It seems determined to 
run away and rove about, and it utters a peculiar howl. The dog will not touch 
his ordinary food, but often swallows straw, hair, earth, bits of wood, etc. In the 
third or paralytic stage paralysis appears. The dog looks lean and wretched, and 
always dies on the tenth day at the latest. In what is called the quiet madness 



HYDROPHOBIA. 



103 



there is no maniacal stage. The symptoms of paralysis, affecting chiefly the hind 
limbs and the lower jaw, occur earlier and are sooner fatal. Marked pathological 
changes are not found. There are pulmonary and intestinal catarrh and passive 
congestion of the viscera, and the stomach often contains foreign bodies in place 
of the usual partially digested food. 

[On the Western plains hydrophobia is said not infrequently to follow skunk 
bites ; the bite is inflicted during sleep on persons passing the night in the open 
air or in tents to which the animal can gain access.] 

Eabies is transferred to the human being almost invariably by the bite of some 
raving animal ; and this animal is almost always a dog. The poison, which is 
not yet known in its pure form, is evidently contained in the saliva or slaver and 
in the blood of mad animals, and can, by means of these substances, be success- 
fully inoculated upon other animals. Pasteur has discovered another way to pro- 
duce the disease experimentally. He takes minute portions of the brain, medulla 
oblongata, or some other internal viscus of a mad dog, and either injects them 
into the veins of a healthy animal, or trephines, and then inserts them beneath 
the meninges. While this method was being pursued, the remarkable fact came 
to light that the virulence of the poison is greatly aggravated by inoculation 
upon rabbits and guinea-pigs, while by a series of inoculations upon monkeys 
the virulence is diminished. Dogs inoculated with virus thus attenuated remain 
healthy, but acquire through the inoculation an immunity from rabies. They 
may now be inoculated with the strong virus, or be bitten by mad dogs, without 
the slightest harm. If this discovery of Pasteur's be confirmed, we have here a 
fact perfectly analogous to vaccination (cf. the chapter on malignant pustule). 

The liability to rabies does not seem to be universal among human beings. 
About one half of those who are bitten by mad animals exhibit no subsequent 
symptoms. Still this can be only in part due to inherent immunity from the dis- 
ease, and must in part result from imperfect infection. The duration of incu- 
bation till rabies finally breaks out seems to vary greatly. As a rule it is about 
three to six months, but observers have reported instances both of shorter and of 
much longer duration. 

Clinical History. — The disease begins with a general feeling of indisposition, 
anorexia, headache, and uneasiness. This last is partially explained, to be sure, 
by a dread of what is impending. If the bite was in the face, frequent convulsive 
sneezing may occur. Even now, in this prodromal stage, a marked aversion to 
liquids is a usual and early symptom. The attempt to swallow excites slight con- 
vulsive disturbances. Painful sensations may arise once more in the bitten place, 
although this has usually been cicatrized long before, and, according to Penzoldt, 
the neighboring lymph-glands are often found to be swollen. 

Only a day or two later the second hydrophobic stage begins. The especial 
characteristic of this consists in the peculiar attacks of tonic convulsions. The 
pharynx suffers most, but convulsions also seize the muscles of respiration and those 
of the trunk and extremities. A terrible feeling of anxiety and oppression accom- 
panies these attacks, so that one who has once witnessed the sight can never forget 
it. The convulsions always seem to be reflex, and are produced by the slightest 
causes, particularly by any attempt to swallow, or sometimes by the very sight of 
water. They recur at gradually diminishing intervals, and last from a few min- 
utes to half an hour. The excitement of the patient may reach the pitch of delir- 
ium or mania. The pulse is full and rapid. The temperature is usually only 
slightly elevated, but it may be high. There is great thirst, accompanied by burn 
ing pain in the throat. Often there is marked salivation. 

This condition lasts one to three days. Then death occurs, ushered in by vio- 
lent convulsions. Or death may be preceded by a brief third stage of paralysis, 



104 ACUTE GENERAL INFECTIOUS DISEASES. 

during which there are no convulsive attacks. Cases of recovery in man, if they 
ever happen, are extremely rare. 

The result of the autopsy is practically negative. The disease is an infectious 
one, and therefore we should hardly think it a priori certain that such objective 
cerebral lesions would be found as might of themselves account for the grave clini- 
cal symptoms. The microscope has repeatedly detected very minute haemorrhages, 
clusters of lymph-cells around the blood-vessels, etc. The throat may present the 
signs of catarrh. The lungs are congested, and often cedematous. The blood is 
dark, with few clots. The heart, liver, and spleen are apparently normal. 

The diagnosis is usually easy, particularly if we know of the possibility of 
infection. We are guided by the convulsions following attempts to swallow, as 
well as by the whole group of symptoms. Hydrophobia is distinguished from 
traumatic tetanus by the absence of trismus and of the characteristic tension of the 
muscles of the back and abdomen, by the convulsions coming in separate attacks, 
and by the usually greater length of incubation. There is only one form of 
tetanus which bears very great resemblance to rabies, viz., the so-called hydro- 
phobic tetanus {vide infra). It should be mentioned that the mere dread of 
hydrophobia may cause an easily excited person to have the nervous symptoms 
of the disease, but of course without disastrous results. Hysteria, also, may give 
rise to convulsions on swallowing somewhat resembling those of hydrophobia. 

However hopeless treatment seems, we must at least try to mitigate the pa- 
tient's suffering. Narcotics accomplish this best — e. g\, opium or chloral, or, most 
useful of all, the inhalation of chloroform. Curare has been administered repeat- 
edly, and does seem to lessen the violence of the attacks. 

Prophylaxis is extremely important. We can not consider in detail the regu- 
lations which the government should make in order to prevent the spread of the 
disease. As to individual prophylaxis, every suspicious bite should be very thor- 
oughly disinfected, and then cauterized either with nitrate of silver, caustic potash, 
or the red-hot iron. It has also been recommended that the entire wound or scar 
should be excised, along with any swollen lymphatic glands which may be found 
in the neighborhood. Internal remedies to prevent the outbreak of the disease 
are probably quite useless. Cantharides, belladonna, calomel, and arsenic have 
been given for this purpose. The future must determine whether Pasteur's dis- 
covery will afford mankind prophylaxis against hydrophobia. 



CHAPTER XX. 

GLANDERS. 

{Farcy.) 

iEtiology. — Glanders is a disease of the horse and some animals allied to it — 
viz., the ass and mule. It can, however, be transferred to man. It is characterized 
by peculiar new growths, either like nodes ("farcy-buds"), or more rarely diffuse. 
These are very prone to suppurate and break down. Such nodes, and the ulcers 
which they leave behind them, occur most frequently in the mucous membrane 
of the nose. In horses the purulent nasal discharge is one of the earliest and most 
important symptoms of the disease. Similar nodes are found in the larynx, 
lungs, liver, spleen, and kidneys, and often also in the skin. The cutaneous swell- 
ings and deep, crater-like ulcers belong to that form of the disease which is called 
" farcy." The corresponding lymphatic vessels and glands are usually much 



GLANDERS. 



105 



swollen. The animal lias fever, grows weaker and weaker, and almost invariably 
dies at the end of one to three weeks. 

Glanders in man is always referable to infection from a diseased animal, 
although in certain instances it is impossible to demonstrate the source. The 
disease is therefore commonest among persons who have much to do with horses 
— e. g., hostlers, coachmen, farmers, and cavalrymen. The virus is usually con- 
veyed by the pus and nasal secretions of the diseased animals. A little of this 
falls upon some excoriation on the hand or some crack in the skin, and is absorbed. 
Man does not seem very liable to the disease ; it is of rare occurrence. 

Loffler and Schutz have discovered the specific disease-producing agent. These 
investigators were able to demonstrate in all the products of glanders delicate 
bacilli about the size of the bacilli of tuberculosis. These bacilli could be reared 
artificially, and, if inoculated upon horses and other animals, gave rise to a typical 
attack of glanders in every instance. 

Clinical History. — The period of incubation lasts about three to five days, and 
sometimes longer. The first symptoms are local, if the infection has resulted from 
a visible injury. There is considerable swelling and pain in this spot, and usually 
considerable lymphangitis in its neighborhood. In other cases, however, the dis- 
ease begins with indefinite constitutional symptoms, such as fever, headache, and 
pain in the limbs, so that there may be some resemblance to a beginning typhoid 
fever. The local and general disturbances increase, and the disease soon attacks 
other parts of the body. There are usually pustules, or larger abscesses in the 
skin. These burst and discharge offensive pus, leaving behind them irregular, 
deep ulcers. Not infrequently the joints are swollen. The mucous membranes 
are also attacked ; chief among these troubles are ulcers in the nose. The nose 
swells as if with erysipelas, and there is a purulent, foul-smelling discharge. The 
nose rarely escapes. The conjunctivae, throat, mucous membrane of the mouth, 
and the larynx also undergo inflammation and ulceration. A violent, diffuse 
bronchitis develops. Sometimes there is considerable disturbance of the stomach 
and intestine, giving rise to vomiting and diarrhoea. At the same time the con- 
stitutional symptoms become more and more severe. The patient grows stupid or 
delirious. The fever is high. Sometimes it is quite continuous. More rarely 
there are chills and great elevations, as in the fever of pyaemia. The pulse is rapid 
and small. The spleen is seldom much enlarged. The urine may contain a trace 
of albumen. 

In these severe acute cases the termination is almost always fatal. Death 
occurs at the end of about two to four weeks. There are cases with a more chronic 
course, with tedious persistence of the troubles in the skin and mucous membranes, 
and milder febrile and constitutional symptoms. Such attacks appear at first tol- 
erably favorable, but may later assume the acute form, or they may run on for 
months, and at last end in complete recovery. 

The autopsy reveals a condition greatly resembling that in pyaemia. We find 
abscesses in many parts, particularly the muscles and the lungs, and, next in fre- 
quency to them, the spleen, brain, and other viscera. In the mucous membrane of 
the nasal cavities, the pharynx, and the larynx, are found nodes and ulcers, such 
as occur in the horse. As in septicaemia, there are often numerous haemorrhages 
into the serous and mucous membranes. It has already been mentioned that the 
specific bacilli of glanders are present in the abnormal secretions. 

Diagnosis. — "Without the aid of aetiological factors, the diagnosis of glanders 
is often very difficult. Indeed, until recently there have been instances where 
even the autopsy did not suffice to exclude pyaemia. But now that the specific 
bacilli have been discovered, we can clear up all doubts. We can not, however, 
enter into a particular description of the distinguishing characteristics of these 



106 ACUTE GENERAL INFECTIOUS DISEASES. 



bacilli. Their demonstration requires pure cultures. At the bedside also aeti- 
ology is all-important in diagnosis — e. g., exposure to infection or occupation. 
Experience with a limited number of cases renders it probable that in the future 
we shall be able to demonstrate the bacilli, during the life of the patient, in the 
nasal secretions or the contents of the abscesses. The most characteristic symp- 
toms are the nasal and cutaneous. In a case that takes a chronic course there is a 
possibility of mistaking the cutaneous ulcers for syphilitic sores. 

We have already implied that the treatment of acute cases is almost hopeless. 
We must do all we can in the way of cleanliness and disinfection to improve the 
local condition of the skin, the nose, and the throat. Appropriate agents are car- 
bolic and salicylic acids and chlorine-water. Further treatment, by means of 
baths, quinine, and stimulants, should be in accordance with the general rules for 
the care of severe acute infectious diseases. Potassic iodide has been recom- 
mended as an internal remedy. 



CHAPTER XXI. 

MALIGNANT PUSTULE. 

(Anthrax. Charbon. Splenic Fever. Mycosis intestinalis. Carbunculus contagioms.) 

iEtiology. — Malignant pustule is a disease of great interest to general patholo- 
gy, for the poison which produces it is more accurately understood and has been 
more thoroughly studied, from the various points of view of aetiology and mor- 
phology, than the virus of any other infectious disease. Pollender in 1849 was 
the first to discover the poison in question ; and independently of him Brauell, 
some years later, also found it. It is represented by a specific kind of inferior 
organism now universally termed the bacillus of anthrax. These bacilli are very 
minute cylinders, about seven to twelve micromillimetres in diameter. They are 
found in enormous numbers in the blood and organs of animals which die of 
anthrax. Aniline-staining makes them more easily visible. By means of blood 
containing the bacilli, Davaine and others have inoculated many animals with the 
disease, including mice, rats, guinea-pigs, cows, sheep, goats, and birds. The bacilli 
can also be isolated and cultivated, and then produce infection. This is proof 
positive that they are the actual carriers of contagion. The rapid increase of the 
anthrax bacilli in the blood goes on by subdivision. In the artificial cultivations, 
however, the bacilli grow, as Koch has shown, into quite long threads, in which 
shortly appear minute, brilliant egg-shaped bodies (cf. Figs. 10 a and 10 b). The 
threads become disintegrated, setting free the little shining ovoids, the spores of 
anthrax, to grow into bacilli. The bacilli can live only a relatively brief time ; 
but the spores have unusual tenacity of existence. They may remain dried up for 
years and then be brought to further development if placed in favorable condi- 
tions of heat and moisture. If the spores are transferred to animals, they develop 
into bacilli, and there is scarcely room to doubt that men and animals are quite 
as often infected by spores as by full-grown bacilli. There are facts which render 
it not improbable that the anthrax bacilli exist in other places than the bodies of 
men or animals, and may there complete then circle of development. Such places 
are marshes, the banks of streams, and the like. If it is possible for them to be 
carried by high water to the pasture lands, we have an explanation of those 
sudden endemic appearances of anthrax which sometimes occur in places pre- 
viously free from the disease. 

Anthrax in animals is of great practical importance, because its favorite 



MALIGNANT PUSTULE. 



107 



victims are the herbivorous domestic animals — viz., the cow, sheep, and horse. 
'Among these it is terribly destructive. It is remarkable that the carnivora enjoy 
almost complete immunity. The disease usually runs a very acute course in ani- 
mals. Indeed, it often seems like apoplexy ; the apparently healthy animal sud- 
denly falls, suffers for a few minutes from convulsions and dyspnoea, and dies. 
Other cases have a somewhat longer and more intermittent course, but in these 
also recovery is very rare. 

Probably human beings are infected in most cases by direct inoculation. Shep- 
herds, farmers, butchers, and others, who come in contact with animals suffering 

from anthrax, are liable to 
infection through any little 
wound or scratch upon the 
hands. Very often the dis- 
ease is caught from hides, 
han, or other parts of dead 
animals. In workshops and 
factories where wool and 
hides have been used which 
came from diseased ani- 
mals, anthrax has repeat- 
edly occurred. Curriers, 
ropemakers, paper-makers, 
and those who handle horse- 
hair and wool, are all ex- 
posed. Anthrax has also 
earned the name of " rag-pickers' disease." Another way of infection, supposed to 
happen among animals as well as men, is through the sting of insects — e. g., flies 
— bringing the poison from diseased animals. It is not likely that the virus can 




Fig. 10 a.— Anthrax bacilli. (From Koch.) 650 diameters. A From 
the blood of a guinea-pig. B From the spleen of a mouse after 
three hours 1 culture in the aqueous humour. 




05 o 
0 Efc> 



B 




Fig. 10 b.— Anthrax bacilli; spore formation and spore germination. (From Koch.) A From the spleen 
of a mouse after twenty-four hours 1 culture in the aqueous humor, spores arranged like strings of 
beads in the filaments. 650 diameters. B Germination of the spores. 650 diameters. C The same 
with a higher power. 1650 diameters. 

be absorbed through the unbroken skin, or by the lungs. It is certain, however, 
that the intestine may afford ingress to the infectious matter. Koch has proved 
this by putting spores in the food of sheep. Intestinal mycosis in man (vide 
infra) may very possibly be due to a similar mode of infection. Many cases 
of poisoning from eating meat have been referred to the ingestion of the flesh 
of animals who died from anthrax. 



108 



ACUTE GENERAL INFECTIOUS DISEASES. 



Clinical History. — Anthrax in man lias two distinct forms. These may appear 
in combination. The first begins with a local disorder of the skin at the point of 
infection — viz., the malignant pustule, or anthrax carbuncle. The second and 
rarer form presents the symptoms of a severe acute constitutional infection. An 
accompanying cutaneous disorder is sometimes observed. 

1. The malignant pustule usually comes on the hand, the arm, or the throat, 
and appears from three to seven days after infection. A vesicle forms at the 
infected spot, grows rapidly, becomes excoriated, and usually takes on a character- 
istic appearance, being of a dark-bluish or black color. The surrounding parts 
become diffusely swollen and red. Secondary vesicles may surround the original 
one. The swelling becomes more and more extensive. Inflamed lymph- vessels 
or veins radiate in red lines from the pustule, and the neighboring glands are also 
affected. These appearances are accompanied by fever, and more or less prostra- 
tion. In a favorable case the swelling subsides, the scab falls off. and there is at 
last complete recovery. But in other cases the constitutional infection becomes 
more and more prominent, and eclipses the local disorder. The fever and pros- 
tration increase. Severe intestinal symptoms appear, or else stupor, delirium, and 
other nervous disturbances ; and death may ensue after a few days' illness. 

2. Intestinal Mycosis. — A better name would be intestinal anthrax. A quite 
different picture is presented by this second form, which gets its name from the 
marked intestinal lesions. In this the cutaneous disorder, if it exists at all, is 
insignificant, compared with the severe constitutional disturbance. It is only 
within a few years that the labors of Buhl, Waldeyer, E. Wagner, Leube, and 
others have shown that attacks of this land have any connection with anthrax. 
So few cases have thus far been observed that it is impossible at present to give a 
definite and complete description of the disease. 

In cases of this sort the attack is usually rather sudden, beginning with chilli- 
ness, vomiting, headache, and languor. The diagnosis is usually very obscure at 
first, unless the calling of the patient suggests the possibility of anthrax. On care- 
ful examination, we may find some place where the skin is broken, or possibly a 
small characteristic pustule. In a case which came under our own observation a 
pustule had existed on the back of the right hand for some weeks before severe 
symptoms appeared, but had not attracted the attention of the patient at all. In 
this case, therefore, the constitutional infection seems to have come from the local 
disease. But in other cases cutaneous troubles, in the form of small carbuncles, 
may occur secondarily in the course of the disease. Haemorrhages into the skin 
and mucous membranes also occur. 

Of other symptoms, the gastro-intestinal deserve to be mentioned first. Vomit- 
ing occurs frequently, and also a moderate, painless, and sometimes bloody diar- 
rhoea. There is usually severe dyspnoea, and a marked sense of oppression in the 
thorax, but without objective pulmonary signs. Very soon there is collapse ; 
the nose and extremities grow cool ; the pulse is rapid, but small ; and there 
is lividity. In a few instances tetanic or epileptiform convulsions have been 
observed. The temperature is seldom much elevated. It may be subnormal. In 
a few days the prostration becomes complete, and death ensues. 

Mflder forms apparently occur, but here the diagnosis may not be absolutely 
certain. We have seen a few such cases originating in a rope-walk where Russian 
hair was used. The constitutional symptoms were only moderately severe, the 
fever was mild, and recovery occurred after about two or three weeks. , 

Pathology. — In the fatal cases of anthrax the intestinal lesions are the most 
characteristic. Beside the signs of catarrhal inflammation, we find peculiar 
lesions in the mucous membrane of the small intestine, and sometimes in the upper 
portion of the colon. These consist of dark, infiltrated spots, with haemorrhages. 



TRICHINOSIS. 



109 



the spots being somewhat larger than a silver dime. The microscope reveals 
numerous collections of anthrax bacilli, situated chiefly in the lumen of the blood- 
vessels. The spleen is usually only moderately enlarged, but dark and congested. 
There may be ecchymoses in the kidneys, the brain, and the serous membranes. 
Often there is swelling of the lymph-glands. In one case which we saw, with 
slight intestinal lesions, the mesenteric glands were considerably enlarged, and 
the bronchial lymph-glands were perfectly enormous. The bacilli are found in 
all the organs mentioned. 

The diagnosis of a malignant pustule is seldom difficult, particularly if atten- 
tion be directed to the aetiology. All doubt is over if we find the bacilli. The 
cases of intestinal mycosis may be more obscure. Here, too, the demonstration of 
bacilli in the blood is, of course, of the greatest importance, but reports have thus 
far been scanty of endeavors to find them during life in man. 

Treatment. — 1. Prophylactic inoculation. Toussaint and Pasteur were the first 
to show that the virulence of anthrax bacteria can be artificially diminished by 
certain external influences. If the bacilli are kept under cultivation for several 
weeks at an unchanging temperature of 106° to 107'5° (42°-43° C), they pre- 
serve their external appearance completely, as well as their ability to grow, but 
gradually lose their power of infection. Inoculations made with this " vaccine 
virus " produce at most an insignificant disturbance. But what is especially re- 
markable is that the animals thus vaccinated are said to enjoy immunity thereafter 
from infection with actual anthrax. Pasteur was the first to make this assertion ; 
and he proposed that the prophylactic inoculation of sheep and other animals- 
liable to anthrax should be undertaken on a large scale, promising the farmers 
that very great benefit would result. This promise has not yet been completely 
fulfilled, although there can be no doubt that in general Pasteur was correct. Ex- 
periments instituted by Koch and others have shown that, although Pasteur's vac- 
cination protects against the artificial inoculation of anthrax, it does not, at least 
as now performed, afford immunity from the natural anthrax, which usually 
results from infection within the intestine. Still this is a field where further dis- 
coveries can be confidently expected. 

2. The treatment of malignant pustule is purely surgical. Cauterization with 
caustic potash, nitric acid, carbolic acid, etc., must be tried at the commencement 
of the disease. Later, the main thing is to combat the inflammation by ice, rest, 
and elevation of the part. Incisions may be indicated. The treatment of intes- 
tinal mycosis must be purely symptomatic. We may try the effect of calomel, 
salicylic acid, and vigorous stimulants. 



CHAPTER XXII. 

TRICHINOSIS. 

(Trichinatous disease.) 

The Natural History of Trichinae.— The trichina spiralis, one of the class of 
round worms or nematoda, has long been known to occur occasionally in the mus- 
cles of men and certain animals ; but it was not until 1860 that Zenker showed 
that trichinae are capable of exciting in man a dangerous and sometimes fatal dis- 
ease. Since then numerous individual cases and quite extensive epidemics have 
been reported ; and the labors of Virchow, Leuckart, and others have taught us 
the anatomy and mode of development of this peculiar parasite. 



110 



ACUTE GENERAL INFECTIOUS DISEASES. 



The trichina appears in two shapes — as intestinal trichina and as muscular tri- 
china. The intestinal form is a small white worm, visible to the naked eye. The 
female is 3-4 mm. long, the male only 1-1 '5 mm. They have well-developed 
digestive and sexual organs. The male is distinguished by two little processes at 
the tail. The muscular trichina (vide Fig. 11) is a small worm 07-1 mm. long. 

It is found coiled up among the muscular fibers, inside 
a connective-tissue capsule, which is often calcified. 

The events in the life of the trichina are remarkable. 
If living muscular trichinae reach the human stomach, 
viz., through the eating of trichinatous pork, the capsules 
are dissolved, and the trichinae, thus set free, grow in 
two or three days into sexually perfect intestinal trichinae. 
In the uterus of the impregnated female the eggs develop 
into embryos, which are born already hatched. The 
birth of embryos begins seven days after the ingestion of 
the muscular trichinae, and seems to continue for some 
time. A single female is said to produce more than one 
thousand embryos. These latter begin their travels soon 
after birth, and reach the voluntary muscles. As to the 
routes they choose, we are still somewhat in doubt. Some 
authorities state that the trichinae penetrate through the 
walls of the intestine and the abdominal cavity into the 
connective tissue. Others affirm that they enter the lym- 
phatic vessels, or exceptionally the blood-vessels. They 
penetrate into the primitive fibers of the muscles, and 
cause them to disintegrate. Finally, they coil themselves 
up, attain the size of muscular trichinae in about four- 
teen days, and become encapsulated. Each capsule usu- 
ally contains but one, although it may inclose as many 
as four. The capsule is formed partly by an excretion 
from the trichina, and partly from the reflex hyperplasia 
of the surrounding connective tissue. The process of 
development is now complete. The muscular trichinae 
seem, unlike the intestinal form, to have a very long 
lease of life, and usually endure till the death of their 
host. They are often found accidentally at autopsies. 
They are most abundant in the diaphragm, the intercos- 
tal muscles, the muscles of the larynx and throat, and in 
the biceps. 

iEtiology of Trichinosis— The only cause yet known 
for trichinatous disease in man is the ingestion of trichin- 
atous raw or underdone pork— e. g., smoked ham. Swine are pre-eminently sub- 
ject to trichinae. They probably become infected in various ways, e. g., from the 
faeces of human beings and swine suffering from trichinosis, or through the inges- 
tion of the trichinatous flesh of other swine. The waste of slaughter houses is 
often fed out to swine, and the disease thus disseminated. Many affirm that 
swine are also infected by eating rats infested with trichinae. 

Clinical History. — The symptoms in man correspond in general to the devel- 
opmental and vital processes of the trichinae, as above depicted. In individual 
cases, however, the separate stages are quite often obscured, probably because all 
the parasites do not develop simultaneously, or because there are relapses. The 
first symptoms are gastro-intestinal. At the commencement there is a feeling of 
pressure in the epigastrium, with nausea and vomiting. Later, diarrhoea is promi- 



Fig. 11.— (From Heller.) An 
isolated primitive bundle 
with two free trichinae in 
the sheath of the sarco- 
lemma. Much enlarged. 



TEICHINOSIS. 



Ill 



nent, becoming* in some cases so violent as to remind one of cholera. It is not 
impossible, although rare, to find intestinal trichinae in the stools. Sometimes 
there is constipation instead of diarrhoea. In some cases the initial gastrointes- 
tinal symptoms are but slight. Frequently, even in the beginning of the disease, 
there is complaint of pain and stiffness in the muscles, too early for it to be due 
to the migrations of the trichinae. 

The genuine severe muscular symptoms, due to the myositis produced by the 
trichinae in the muscles, do not begin till the second week, or even later. In 
many cases, where the invading parasites seem to be relatively few in number, the 
muscular symptoms are slight or wholly absent. In the more severe cases, how- 
ever, they may be extremely violent and distressing*. The muscles become swol- 
len, firm and hard, very tender on pressure, and very painful. The patient avoids 
all movement and contraction of the muscles as much as possible, lying, with 
flexed arms and legs either extended or likewise flexed, motionless in bed. The 
masseters and the pharyngeal and laryngeal muscles are attacked, so that there 
is difficulty in mastication and deglutition, and hoarseness. The participation 
of the motores oculi causes pain in the eyes. The condition of the diaphragm, 
intercostals, and abdominal muscles causes serious difficulty in respiration. There 
is distressing dyspnoea, and expectoration is so hampered that secretions accumu- 
late in the air-passages. Some of the fatal cases of trichinosis are principally due 
to this impairment of respiration. The condition may be aggravated by diffuse 
bronchitis or lobular pneumonia. 

Third in the list of important symptoms comes oedema. It appears, toward the 
end of the first week, in the eyelids. Somewhat later it involves the upper and 
lower extremities. What produces it is not quite clear. It has been regarded as 
in part inflammatory and in part the result of occlusion and thrombosis of the 
smaller lymphatics. Cutaneous eruptions also develop — e. g., vesicles, wheals, 
petechiae, and pustules. Frequently there is profuse i3erspiration, consequent 
upon which abundant crops of miliaria or sudamina may appear. 

In well-marked cases there may be quite high fever and other severe constitu- 
tional symptoms in addition to the local disturbances already discussed. The 
temperature may for a time reach 104° to 106° (40°-41° C.) ; but the fever is 
seldom continuous for any length of time, being usually interrupted by fre- 
quent and considerable intermissions. There are also a rapid pulse, headache, 
stupor, and other symptoms suggesting typhus or typhoid fever. In fact, the first 
case in which trichinosis was recognized at the autopsy (by Zenker of Dresden) 
had been regarded before death as typhoid. 

Pathology. — The autopsy reveals little that is characteristic excepting the 
changes in the muscles. There are sometimes the signs of haemorrhagic catarrhal 
inflammation of the small intestine. The spleen is not enlarged. Very often 
the liver is decidedly fatty. What should cause this in trichinosis has not yet 
been determined. The lungs often present islets of lobular pneumonia, or even 
sometimes of gangrene. The trichinae are found in the muscles, beginning with 
the fifth week. They can be recognized by the naked eye as little whitish lines. 
We have already named the muscles chiefly infested. Under the microscope 
we see the fibers in which the trichinae lie transformed into a fine granular 
mass. The nuclei of the muscular fibrillae are greatly increased in number in the 
neighborhood of the coiled-up parasite. Finally, the sarcolemma collapses, and 
becomes greatly thickened upon its external surface by a hyperplasia of connect- 
ive tissue. 

Treatment. — The trichinae may still be alive in pork that has been smoked or 
salted or half -cooked — e. g., many sausages are unsafe. The only possible but 
perfectly reliable prophylaxis, as far as the individual is concerned, is therefore to 



112 ACUTE GENERAL INFECTIOUS DISEASES. 



avoid all such food. A real protection for the public against the disease is also 
afforded by governmental microscopic inspection of meat, as already established 
in many places. 

The treatment of trichinosis, when already existing, should have for its first 
aim to destroy the trichinae before they leave the intestinal canal. Unfortunately, 
we are not yet acquainted with a thoroughly reliable means for this end. The 
following have been recommended for trial : benzine, 3 j to i j (grm. 4-8) pro die, 
in gelatine capsules ; glycerine, of which large doses can be taken with impunity, 
e. g., a tablespoonful every one or two hours ; and picric acid, gr. ^-j (grm. 0*03- 
9*05) pro die, in pills. If we make the diagnosis at the beginning of the disease, 
it is both rational and advantageous to give purgatives — e. g., senna, castor-oil, 
and, best of all, calomel, in repeated half -grain (grm. 0'03) doses. Later on, when 
the invasion of the muscles has already begun, we are unfortunately almost with- 
out resource. The muscular pains can be alleviated by narcotics, poultices, and 
chloroform-oil as an embrocation.* Protracted warm baths are excellent. Sali- 
cylic acid is also said to do good in many cases. 

* Generally one part of chloroform to ten of olive-oil. It is not officinal in Germany, but is weaker 
than the linimentum chloroformi (U. S. P.). — Tuans. 



DISEASES OF THE RESPIRATORY ORGANS. 



SECTION I. 
Diseases of the Nose* 

CHAPTER I. 

CORYZA. 

(Snuffles. Rhinitis.) 

JEtiology. — The well-known symptoms of coryza depend upon a catarrhal 
inflammation of the nasal mucous membrane. Although this catarrh may often 
be due to infectious influences, still we can not deny that it is one of those dis- 
eases which may be caused by taking cold. Daily experience teaches us how often 
coryza follows an evident exposure to cold, like wetting the feet. We may men- 
tion its contagiousness as an argument in favor of its infectious character, and 
this may be illustrated by the fact that it may be conveyed by handkerchiefs, 
kissing, etc., but an experimental transmission of common coryza has not yet been 
successful. 

Coryza may also arise from the action of chemical irritants or mechanical irri- 
tants, like dust, on the nasal mucous membrane. The iodine coryza, which occurs 
from the internal use of iodine, is especially noteworthy. In this form iodine 
can easily be detected in the nasal secretion. The idiosyncrasy of many people to 
ipecacuanha is also well known, the very smell of it setting up a coryza. A 
severe coryza is the chief symptom, too, in hay fever, which is probably due to 
the action of the pollen of certain grasses on the respiratory mucous membrane. 
Finally, we must bear in mind that coryza may often be only a symptom of 
another disease like measles, syphilis, or glanders, and that severe purulent 
inflammation of the nasal mucous membrane may be excited by the presence of 
the secretion from a gonorrhceal or blennorrhoeal conjunctivitis. 

The symptoms of coryza are in most of the milder cases of a local nature only. 
The secretion is troublesome ; at first it is scanty and mucous, but later it becomes 
more abundant, more watery, and sometimes purulent. The nasal passages are 
not infrequently closed from the swelling of the mucous membrane. The patient 
necessarily has to breathe through the mouth, which gives rise to the well-known 
nasal speech. This closure of the nares may give rise to dangerous attacks of 
dyspnoea in children, especially in infants, who have to breathe through the nose 

* Special treatises on the pathology and therapeutics of nasal diseases are to be found in the follow- 
ing works : Michel, " Krankheiten der Nasenhohle." Fraenkel, " Diseases of the Nose," in " Ziems- 
sen's Cyclopaedia." Stork, "Klinik der Krankheiten des Kehlkopfes, der Nase, und des Kachens," 
etc., etc. 

8 



1U 



DISEASES OF THE RESPIRATORY ORGANS. 



when sucking" at the breast. The sense of smell is always diminished. The local 
sensations of pain and burning are due chiefly to a mild inflammation of the skin 
of the nostrils and upper lip set up by the irritation of the secretion. The symp- 
toms are more severe if the cavities adjacent to the nose are attacked by catarrh, 
and if in them accumulations of secretion occur. Marked pain in the forehead 
occurs in catarrh of the frontal sinuses. The sinuses of the ethmoid and sphenoid 
bones, and the antrum of Highmore, may also be implicated. Much more fre- 
quently a severe coryza sets up an inflammation in adjacent mucous membranes. 
Thus we find following a coryza a conjunctivitis, an affection of the ear, a sore 
throat, or a laryngitis. In persistent coryza an eczema is not infrequently ex- 
cited on the skin of the upper lip, and mention has already been made of the fact 
that coryza may sometimes act as the exciting cause of an erysipelas. 

In severe coryza we may sometimes have quite a marked general disturbance, 
and often slight elevations of temperature. The " coryza fever " in children, for 
instance, is well known. 

Treatment. — Special treatment is usually unnecessary, for most cases recover 
of themselves in a few days. With abundant secretion, especially in fresh cases, 
Hager's " coryza remedy " [as an inhalation] is worthy of trial ; this consists of 
ten parts each of alcohol and carbolic acid, and five parts of ammonia- water. A 
snuff of calomel is also greatly praised. When the secretion forms abundant dry 
scabs an attempt should be made to wash them out by injections of warm fluids 
like warm milk. The upper lip and the nostrils should be smeared with vaseline 
or simple ointment to protect the skin from the action of the secretion. Only in 
the rare cases of a severe purulent catarrh can an energetic local treatment of the 
nasal mucous membrane be necessary. Here we may use douches, sprays, or 
inhalations of astringents like tannin or alum, or we may apply caustics like 
nitrate of silver. 



CHAPTER H. 

CHRONIC NASAL CATARRH. 

(Ozcena. Chronic Rhinitis. Stinknase.) 

iEtiology. — While acute nasal catarrh only rarely runs into a chronic con- 
dition, chronic diseases of the nose are quite frequent, and they develop very 
gradually and usually last for years. Since most of these diseases, from the 
decomposition of the secretion which accompanies them, are attended by an 
extremely offensive odor from the nose, they are usually given in practice the 
general name of "ozsena." We must not forget, however, that under this term 
are brought together morbid conditions which anatomically and even setiologi- 
cally are very different from one another. In some cases no cause at all can be 
found. These we call " simple ozsena," or " rhinitis chronica atrophicans,' 1 ' 1 from 
the most common anatomical lesion. In other cases, however, the ozsena is noth- 
ing but a local syphilitic or tubercular disease of the nasal mucous membrane and 
the deeper parts (vide infra). Demme has been able to demonstrate with cer- 
tainty the tubercular nature of the long-known "scrofulous ozaena," which 
frequently occurs in children, by the discovery of tubercle bacilli in the nasal 
secretion. 

Pathological Anatomy. — We distinguish two forms of simple chronic catarrh 
of the nasal mucous membrane, the hypertrophic and the atrophic. In the 
former the membrane is thickened, red, and swollen. In the atrophic form, 



CHEONIC NASAL CATARRH. 



115 



which is commoner, and which, is almost always found in true ozaena, the mem- 
brane is very much thinned. Not only the connective tissue itself with the 
vessels and glands, but the structure of the turbinated bones, is involved in the 
atrophy in the more marked cases, so that we see a considerable dilatation of the 
nasal passages. In many cases of old ozaena we find deeper-seated anatomical 
changes, numerous ulcerations, and often circumscribed necrosis of the nasal 
bones. In almost all such cases, however, it is extremely probable that we have 
to do with specific processes, syphilis, or still more frequently tuberculosis. 

Symptomatology. — The leading symptom in most chronic nasal affections is 
the extremely repulsive odor from the nose, which has given the disease its name 
(o£>ti», to stink). The patient's friends are annoyed by this stench, while he him- 
self often does not notice it at all. The odor arises from the nasal secretion, 
which decomposes under the influence of the bacteria of putrefaction. This 
secretion is usually not abundant in ozsena, but it has a tendency to dry in dis- 
colored crusts. On the posterior wall of the pharynx we often see the dried scabs 
of the secretion from the nose, and a dry chronic catarrh of the naso-pharynx is 
often associated with a chronic rhinitis. The local symptoms of ozsena are 
usually only moderate. If there is a marked thickening of the mucous mem- 
brane, or if the secretion stops the nasal passages, respiration through the nose is 
impeded, and the patient has to breathe with his mouth open. When the frontal 
or sphenoidal sinuses are involved, the patient often complains of headache, dizzi- 
ness, fullness in the head, etc. If pieces of the bony structure of the nose become 
necrotic, and are discharged, the nose sinks in, and we have the well-known 
characteristic "saddle-nose." 

The diagnosis of ozsena can easily be made by the smell and by finding the 
scabs of secretion sticking to the posterior wall of the pharynx ; but a more inti- 
mate acquaintance with the finer changes can be obtained only by rhinoscopy. 
In most cases of ozaena this shows the atrophy of the turbinated bones, and also 
permits us to recognize the presence of ulcerations, etc. In the rare cases of 
hypertrophic rhinitis we see marked swelling and enlargement of the mucous 
membrane, by which the nasal passages may be almost entirely closed. We may 
refer to the special works on rhinoscopy and nasal diseases for a fuller account of 
these changes. 

Treatment. — The treatment of ozaena can be made effective only by the aid of 
local applications as prescribed by specialists. Even then the treatment is a 
prolonged one and demands much patience on the part of both patient and physi- 
cian. Beside local applications we must also bear in mind the necessity of consti- 
tutional treatment, especially in syphilis and tuberculosis. 

The object of local treatment is to remove the secretion in order to get rid of 
the bad odor. Nasal douches, with disinfectant solutions like permanganate of 
potassium, are here most useful. The solution is carefully injected into the nose, 
or the fluid is allowed to run gently into one nostril from an irrigator while the 
patient keeps his head bent forward ; it then runs through the naso-pharynx and 
out through the other nostril. The patient soon learns to retain the fluid in the 
pharynx and eject it from the mouth. All nasal douches must at first be used 
with care and under the eye of the physician. The fluid should be injected at the 
lowest pressure possible, so that none of it may enter the adjacent cavities or the 
Eustachian tube. Furthermore, all solutions used as a douche must be lukewarm 
— 90° to 95° (25°-28° E.). Beside the regular use of douches, painting and the 
insufflation of powders, like boracic acid, etc., are sometimes employed. The 
insertion of tampons of dry absorbent cotton is to be recommended ; under their 
use the secretion dries less easily and the odor is diminished. These tampons 
should be changed daily. In hypertrophic rhinitis, painting with nitrate of silver 



116 



DISEASES OF THE EESPIEATOEY OEGANS. 



or tincture of iodine is recommended. Of late many attempts have been made 
to treat chronic nasal catarrh by the galvano-cautery. With regard to the details 
of this as well as of other methods, we must refer to special treatises on the 
subject. 

CHAPTEE III. 

NOSE-BLEED. 

(Epistaxis.) 

Although in many cases nose-bleed is only a symptom of some other disease, 
still we are justified in a short description of it, partly because frequently repeated 
nose-bleeds often first call our attention to some other existing disease, and partly 
because the treatment is of practical importance. 

Many people are subject to habitual nose-bleed, which comes on either from 
slight causes, from violently blowing the nose, from physical exertion, from over- 
heating, or even without any special cause. This habitual nose-bleed is sometimes, 
but by no means always, the sign of a general haemorrhagic diathesis, which is 
hereditary in many families. (See the chapter on Haemophilia.) In other cases 
the nose-bleed is the result of some chronic disease. It occurs especially in leu- 
kaemia, in disease of the heart, in contracted kidney, and as a symptom of the so- 
called haemorrhagic diseases, like scurvy, purpura haemorrhagica, etc. It is 
also not uncommon in acute febrile diseases, like typhoid and scarlet fever. 
Finally, diseases of the nose itself may give rise to haemorrhage. The occurrence 
of nose-bleed as a form of so-called " vicarious menstruation " has often been 
described, but we must always be very guarded in admitting it as a fact. 

In many cases nose-bleed is a very transitory symptom, wholly without danger, 
and in one sense it may even be advantageous. When there is headache or a 
feeling of fullness in the head, it is often actually better after an epistaxis. Nose- 
bleed is dangerous, however, when it takes place in people who are already weak 
and anaemic, or when it is so persistent and abundant as to cause a marked general 
anaemia. The latter is recognized by the pallor of the face, by the appearance of 
general weakness, by vertigo, tinnitus, and a weakened pulse. In such cases the 
physician's interference is always necessary. In every case of nose-bleed it is 
important to examine the posterior wall of the pharynx in order to see whether 
the blood is not flowing backward from the posterior nares. The haemorrhage is 
often thought to stop when no more blood comes from the nostrils, and yet the 
blood keeps flowing posteriorly. 

In every severe nose-bleed rest is the chief thing to be enjoined, and the patient 
must be told to avoid unnecessarily blowing, wiping, or drying the nose. By 
quietly and persistently closing the nostrils with a handkerchief a thrombus is 
often formed without any further medication, and the bleeding stops. The appli- 
cation of cold water (iced water), in which a little vinegar may be put, is a good 
thing. If the bleeding does not stop, we may next try a tampon of common 
absorbent cotton or styptic cotton in the nostril from which the blood comes. If 
this does not succeed, the posterior nares must be plugged by means of a " Bel- 
locq's canula." In case of emergency we may use an elastic catheter which is 
passed through the inferior meatus into the pharynx and out by the mouth. The 
tampon is fastened to the catheter and brought up into the posterior nares by 
drawing the catheter back through the nose. Internal remedies to check the 
blood are very uncertain in their action. Ergotine, in one-grain pills (grm. 0*05), 
every three or four hours, is the first one to employ, if we wish to try to check the 
bleeding by this means. 



ACUTE LARYNGEAL CATARRH. 



117 



SECTION II. 
Diseases of the Larynx. 
CHAPTER I. 

ACUTE LARYNGEAL CATARRH. 

{A cute Laryngitis.) 

JEtiology. — Taking cold plays a prominent part in the aetiology of acute laryn- 
geal catarrh, as every one knows. Its influence can not properly he wholly 
denied, since the more intimate relation between taking cold and the origin of 
a catarrh is still unknown. The disposition to laryngitis differs very much in 
different people, so that some take a catarrh much more easily and more fre- 
quently than others. Beside cold, direct irritants which attack the laryngeal 
mucous membrane often set up a laryngitis ; among these are in particular the 
inhalation of smoke and of injurious gases and vapors. Many laryngeal catarrhs, 
too, arise from excessive speaking, shouting, or singing, particularly if other 
injurious influences act on the larynx at the same time. Finally, laryngitis may 
appear as a complication or as a secondary affection in other diseases, especially in 
measles, less frequently in typhoid, scarlet fever, and erysipelas. Catarrh of the 
larynx is very often combined with catarrh of the nose, the pharynx, and the 
larger bronchi. 

Symptomatology. — Although the symptoms of laryngitis usually make the 
diagnosis easy and certain, yet an accurate understanding of the extent and 
intensity of the catarrh can be obtained only by a laryngoscopic examination,* 
which therefore should be employed in every severe case. The laryngeal mirror 
shows a decided reddening and swelling of the mucous membrane, varying with 
the intensity of the catarrh, and most marked on the true and false vocal cords 
and between the arytenoid cartilages. We often see small collections of mucus 
here and there on the membrane. In individual cases different parts of the 
larynx are especially affected. In intense inflammations superficial erosions are 
often met with, especially on the vocal cords. In other cases the mucous mem- 
brane shows a grayish-white coloring in some places, due to a thickening of the 
epithelium. Small haemorrhages in the mucous membrane are also occasionally 
seen. Very often we see on phonation an incomplete closure of the glottis, so that 
a little oval space is left between the vocal cords. This slight " catarrhal paresis 
of the vocal cords " is probably of muscular origin, and depends chiefly upon an 
affection of the thyro-arytaenoid muscles. 

Of the other symptoms of laryngeal catarrh, hoarseness is particularly to be 
mentioned, for in many cases the diagnosis of laryngitis can be made from this 
alone. It is either due directly to the anatomical changes of the cords, or to the 
paresis just mentioned. The degree of hoarseness is of course very different in 
different cases, and varies from a simple " roughening " or " deadening " of the 
voice to a complete loss of voice (aphonia). 

* More extensive observations on laryngoscopy and on many details of the pathology of laryngeal 
diseases, which have been carefully investigated by specialists and which can not be mentioned here, 
are to be found in the following works: Tiirck, "Klinik der Krankheiten des Kehlkopfes," 1866. 
Semeleder, " Laryngoskopie," 1863. Tobold, " Laryngoskopie," 1874. Stork, " Klinik der Krank- 
heiten des Kehlkopfes, der Nase, u. des Eachens," 1880. Mackenzie, " Diseases of the Throat and 
Nose," 1880. B. Fraenkeland v. Ziemssen, " Diseases of the Larynx," in Ziemssen's " Cyclopaadia." 



118 



DISEASES OF THE EESPIEATOEY ORGANS. 



The cough, in laryngitis may be very severe, and is often recognizable by its 
harsh, hoarse ring as a " laryngeal cough." It is at first usually dry, and later on 
it is associated with a scanty nmco-purulent expectoration, which is sometimes 
tinged with blood. 

Pain in the larynx is usually only moderate. The subjective symptoms consist 
chiefly of a disagreeable feeling of itching, burning, and dryness in the throat. 
After prolonged speaking, however, the pain in the larynx may sometimes be quite 
severe. External pressure on the larynx is often somewhat painful. Difficulty 
in swallowing, when it occurs, is usually due to an accompanying pharyngitis, 
but it may also be dependent upon an affection of the epiglottis and the arytaenoid 
cartilages. 

The general health is affected in very different degrees. Many patients feel 
quite well except for the hoarseness, while others are affected with considerable 
debility, mild headache, and even at times slight febrile disturbances. 

Dyspnoea is not present in the common laryngitis of adults, even if there is 
decided swelling of the false vocal cords or of the ary-epiglottic folds. There is, 
however, a severe form of acute laryngitis, the so-called laryngitis hypoglottica 
acuta gravis (chorditis vocalis inferior), affecting not only children, but adults, 
in which well-marked symptoms of suffocation may be present. In this form 
there is an acute, very well marked swelling of the mucous membrane in the in- 
ferior, " sub-chordal," laryngeal space, which leads to a stenosis. 

In children, however, on account of the greater narrowness of the child's 
larynx, symptoms of stenosis are not rare, even in the milder forms of laryngitis, 
and therefore they have led to the establishment of a special disease, the so-called 
false croup. 

The false croup of children usually follows a slight coryza. A harsh, hollow, 
ringing cough comes on, almost always suddenly and usually at night, by which the 
child is awakened out of sleep. The paroxysms of coughing are broken by long- 
drawn, noisy inspirations. The child is anxious and restless, the respiration is 
labored, the pulse is rapid. Such attacks recur several times during the night. 
The next day the child is quite lively, plays about, and has at most a slight cough. 
The next night, rarely sooner, the same severe attacks are repeated. After that 
there remains, as a rule, nothing but a slight catarrh, which completely disap- 
pears in a week or two. These sudden attacks have their origin partly in 
a marked swelling of the mucous membrane, occurring during sleep, partly 
in a neglected accumulation of secretion, and probably often also in a reflex 
spasm of the glottis. No other anatomical cause than a simple catarrh of the 
larynx is apparent, and on examining the pharynx, and, if possible, the larynx, 
also, we find no trace of that diphtheritic process which is always present in pure 
laryngeal croup. It is remarkable that many children, and sometimes several 
children of the same family, have a specially marked predisposition to false 
croup. The statement, therefore, that a child has had the croup several times 
almost always means that it has had this form of false croup just described. 

Acute laryngitis lasts only a few days in mild cases, and a week or more in 
severe cases. With improper care and unreasonable conduct on the x^atient's part 
an acute catarrh may run into the chronic form. We hardly ever see a fatal 
result in adults, even in the severe form, or in the false croup in children. 

The treatment of acute laryngitis requires that especial attention be paid to the 
removal of all injurious influences. In every severe laryngitis the patient should 
stay in his room, and children are better off in bed. The patient should talk as 
little as possible. In all severe cases smoking, too, is to be forbidden. It is a good 
plan to furnish plenty of warm drink. Hot milk, mixed with Seltzer or Ems 
water, is readily taken by most patients. If there is an inhaler at our disposal, we 



CHEONIC LARYNGITIS. 



119 



may let the patient inhale simple steam or a one- or two-per-cent. solution of 
common salt. Inhalations of astringents are usually unnecessary. The patient 
may also breathe simple steam without any special apparatus. When there is 
marked irritation from coughing we may give a little morphine. With more marked 
local symptoms, especially if there is much pain on swallowing from swelling of 
the epiglottis and the mucous membrane over the arytsenoid cartilages, the patient 
may suck pieces of ice slowly. In severe cases of acute laryngitis, with evident 
symptoms of stenosis, ice must be energetically used as an internal and an external 
application. Sometimes, too, a few leeches applied in the region of the larynx 
afford distinct relief. Among external applications a mustard plaster over the 
front of the neck is to be recommended when there are marked local symptoms. 
Cold, wet compresses about the neck are also of advantage in all cases. 

In the false croup of children we should use, as a rule, the same treatment as 
has just been described. The child should take warm drink, and a mustard paste 
or hot poultices should be applied to the neck. , We should be rather cautious with 
regard to the favorite treatment with emetics, although it can not be denied that 
they sometimes work very well. 

These means are entirely sufficient for the treatment of acute laryngitis. Cer- 
tainly it is only exceptionally that we fiud ourselves led to employ in acute laryn- 
geal catarrh an energetic local treatment of the laryngeal mucous membrane, like 
painting with a 1-15 solution of nitrate of silver. 

We must bear in mind that a rational hardening process is of distinct prophy- 
lactic value in persons, especially in children, with a recognized tendency to 
laryngitis, sore throat, etc. The best method is to bathe the neck and chest with 
cold water regularly morning and night. 

[A mild emetic can do no possible harm in false croup, and very often cuts the 
attack short. The application of a sponge, moistened with water as hot as the 
child will bear, to the region of the larynx deserves mention.] 



CHAPTER II. 

CHRONIC LARYNGITIS. 

( Chronic Laryngeal Catarrh.) 

./Etiology. — Chronic laryngitis develops from an acute catarrh, or comes on 
gradually from the action of injurious influences on the larynx (see the preceding 
chapter). Chronic laryngitis, therefore, is in many cases a disease arising from 
the occupation, and is seen especially in singers, public speakers, criers, inn-keep- 
ers, etc. It is very frequent in drunkards, and in such cases it is almost always 
associated with a chronic pharyngitis. It is frequently stated that too long a 
uvula sets up a chronic laryngitis by constant irritation of the entrance to the 
larynx, and that if the uvula is amputated the disease is cured. 

Symptomatology.— A laryngoscopy examination is very desirable in acute laryn- 
geal catarrh, but it is the physician's absolute duty to make one in every chronic 
laryngitis, for only too frequently a persistent hoarseness is referred simply to 
catarrh when the laryngoscope gives quite another cause for it, such as paralysis 
of the vocal cords or new growths. Furthermore, we must always remember that 
a chronic laryngitis may be a complication of tuberculosis or syphilis. On the 
other hand, those physicians who make a specialty of laryngology often neglect 
a careful and satisfactory examination of the rest of the body when there are 
laryngeal troubles. 



120 



DISEASES OF THE RESPIRATORY ORGANS. 



The laryngoscopic appearance in chronic catarrh, may be so like that in an acute 
catarrh that we can not distinguish between them without the history obtained 
from the patient. The redness of the mucous membrane, however, is usually less 
intense, and the vocal cords have more of a dirty grayish-red appearance. Quite 
frequently in persistent catarrhs a thickening of particular parts of the mucous 
membrane is developed, especially of the folds between the arytaenoid cartilages. 
This swelling is of practical importance, because it furnishes a mechanical hin- 
drance to the closure of the arytaenoid cartilages, and in that way contributes to 
the development of the hoarseness. We also find limited and marked thickening 
of the epiglottis, the false vocal cords (especially in public speakers and preachers), 
and the true vocal cords. Tiirck has described a peculiar form of chronic laryn- 
gitis, in which rough prominences are formed in the middle of the true vocal 
cords, under the name of chorditis tuberosa. We not infrequently find in 
chronic catarrh superficial erosions, especially on the true vocal cords. We also 
very often see a disturbance of motion of one or both vocal cords, due to muscular 
paresis, which is sometimes real and sometimes due to mechanical conditions. 

The other symptoms of chronic laryngitis are hoarseness, cough, and abnormal 
sensations in the larynx. The hoarseness is of every degree, from mere rough- 
ness, frequent " cracking " of the voice, to almost complete aphonia. The cough 
is ringing, hoarse, deep, and rough. The expectoration is scanty, usually simply 
mucous, but sometimes a little bloody. The subjective sensations in the larynx 
are a feeling of burning and itching, and of dryness and tickling. They usually 
increase after any protracted use of the voice. 

We must also mention as a very rare but practically important and peculiar 
form of chronic laryngitis the chorditis vocalis inferior hypertrophica (Gerhardt), 
or laryngitis hypoglottica chronica hypertrophica (Ziemssen). In this form there 
is a very gradual hypertrophy, and finally a contraction of the mucous and espe- 
cially the submucous connective tissue in the inferior laryngeal space. More 
rarely the same changes are seen in the upper part of the larynx. The special 
symptom of the disease, beside a chronic hoarseness, is the appearance of a gradu- 
ally increasing stenosis of the larynx. The respiration is always labored, the 
inspiration noisy and protracted. In many cases there are at times such attacks of 
suffocation that life can be prolonged only by tracheotomy. The diagnosis can 
be made only by the aid of the laryngoscope. We see beneath the glottis a little 
fissure between the thick and swollen mucous membrane of the laryngeal walls. 

The precise aetiology of this disease is as yet unknown. It aj)pears to have 
nothing to do with syphilis, contrary to the former belief. 

The treatment of chronic laryngeal catarrh is always a tedious and laborious 
task, the success of which depends in great measure upon the good will and 
energy of the patient. In the first place, then, we should endeavor to remove as 
far as possible those injurious influences which have excited and kept up the 
catarrh. It is often easier to give good advice here than to follow it. Neverthe- 
less, it is the task of the physician to impress upon the patient the urgent neces- 
sity of taking care of the larynx, and to forbid as far as possible all protracted 
speaking, singing, staying in smoke or dust, smoking, and drinking alcoholic 
liquors. 

Local treatment takes the second place. Among the most useful means to 
employ are inhalations of astringent solutions, like a one-per-cent. tannin solution 
or a two-per-cent. alum solution. When there is great sensitiveness of the larynx, 
the patient may also inhale narcotics, a mixture of fifty parts of cherry-laurel water 
with a thousand parts of water, or a f our-per-cent. solution of bromide of potas- 
sium. The inhalations should be used two or three times a day, and last about five 
minutes each time. Direct applications to the larynx are much more effective 



LAKYNGEAL PERICHONDRITIS. 



121 



than inhalations, but these can be employed only by the aid of a laryngeal mirror. 
Of these we use, first of all, nitrate of silver, at first in a weak solution (one to 
thirty) ; later in a more concentrated form (one to ten or even one to five). These 
applications are made every two or three days. Beside nitrate of silver, the larynx 
may also be painted with pure tincture of iodine, or with iodine and glycerine, or 
with concentrated solutions of alum or tannin. 

Water-cures are also often prescribed in chronic catarrh of the larynx. These 
are so far of advantage that, from the greater care which the patient takes, and 
from the good air, the catarrh improves. Empirically, we prescribe, especially for 
" full-blooded " patients, the cold sulphur springs, like Nenndorf, Eilsen, or Weil- 
bach, or the sulphate of sodium waters, like Carlsbad and Marienbad, while we 
send those of delicate constitutions to Ems, Salzbrunn, Salzungen, Eeichenhall, or 
Ischl. 

The treatment of laryngitis hypertrophica, when it leads to stenosis, must be 
mechanical. Schrotter, in particular, has devised several methods in order to 
dilate the stenosis gradually by the introduction of bougies and harder dilators. 
The details of this treatment are to be found in the later special works referred to 
above. 



CHAPTER III. 
LARYNGEAL PERICHONDRITIS. 

iEtiology and Pathological Anatomy.— The inflammation of the perichon- 
drium of the laryngeal cartilages is in very rare cases apparently a primary 
disease. It is much more frequently secondary to other laryngeal affections, 
especially tuberculosis and syphilis of the larynx. Furthermore, it develops 
secondarily in severe acute diseases, most frequently in typhoid fever, more 
rarely in small-pox, diphtheria, etc. Superficial ulcerative processes in the mu- 
cous membrane often precede the perichondritis in these cases, and the participa- 
tion of the perichondrium in the inflammation arises from their gradual deep- 
ening. Anatomically, we have to do as a rule with a purulent inflammation, 
which usually leads to the formation of circumscribed abscesses. Most laryn- 
geal abscesses have their origin in the perichondrium.* The perichondrium is 
in part destroyed by the abscess and in part elevated from the cartilage. The 
cartilage then becomes necrotic, breaks in pieces, and is expelled in small particles 
or in masses. 

Perichondritis occurs most frequently in the cricoid and arytenoid cartilages, 
much more rarely on the internal or external surface of the thyroid cartilage. 
Hence we distinguish an internal and an external perichondritis. A perichon- 
dritis of the epiglottis has also been repeatedly observed. 

Symptomatology. — In the rare cases of primary perichondritis marked laryn- 
geal symptoms are speedily developed in a person previously healthy. These 
symptoms are pain and tenderness on pressure over the larynx, hoarseness, and 
cough ; and to them are usually soon added the signs of a dangerous stenosis of 
the larynx. In secondary cases, which occur almost always in patients who are 
already seriously ill, the symptoms of stenosis are often the first to point to a severe 
disease of the larynx. On laryngoscopic examination, beside the general redness 
and swelling in particular places, we can sometimes recognize a circumscribed 
protrusion of the mucous membrane caused by the abscess. We often find, 
besides, a considerable collateral oedema of the surrounding mucous membrane, 



* Pure submucous abscesses, the so-called phlegmonous laryngitis, occur only in very rare cases. 



122 



DISEASES OF THE EESPIEATOEY ORGANS. 



winch frequently has a greater share in the production of stenosis than has 
the primary affection itself. The dreaded oedema of the glottis (oedema of the 
ary-epiglottic ligament) in typhoid, tuberculosis of the larynx, etc. , is usually due 
to perichondritis of the cricoid or arytenoid cartilages. Finally, we can see 
with the laryngoscope, especially in perichondritis arytaenoidea, a considerable 
disturbance of motion of the affected arytenoid cartilage, and also of the vocal 
cords. In the later stages, if the abscess has been opened, or if it breaks of its own 
accord, and the whole cartilage or a part of it is expelled, we can make out the 
extent of the destruction that results more accurately by the laryngoscope. 

Laryngeal perichondritis terminates fatally in a great number of cases from 
the appearance of stenosis. In other cases the most threatening symptoms may be 
averted for a time, but the primary disease, such as tuberculosis, finally comes to 
an unfavorable termination. In the rare cases in which recovery occurs after 
primary perichondritis or after the termination of the primary disease, such as 
typhoid, this recovery is often incomplete, since a chronic stenosis of the larynx 
remains from the ensuing cicatricial contractions. 

The diagnosis is usually difficult during the first period of severe symptoms of 
stenosis, since it is difficult to make a laryngoscopic examination, and it is also 
not always easy to determine the condition. We are usually justified, however, 
in making the diagnosis if, in those diseases which we have mentioned, in which 
we know by experience that a perichondritis quite frequently occurs, the danger 
of suffocation arises in addition to the other laryngeal symptoms. It is of prac- 
tical importance to recognize stenosis of the larynx with certainty, for it demands 
a speedy therapeutic interference. 

Treatment. — In the beginning of the affection we may try to reduce the inflam- 
mation by the internal and external application of ice or by leeches ; but if ste- 
nosis of the larynx occurs, surgical interference is usually necessary, for only in 
very rare cases do we see the abscess open of itself and a subsidence of the 
dangerous symptoms follow. In the majority of cases the patient can be saved 
from suffocation only by the timely performance of tracheotomy. The laryngeal 
abscess has been repeatedly opened internally by laryngologists with favorable 
results. If a chronic stenosis of the larynx remains after a favorable termina- 
tion of the disease, either the patient must wear a tracheal canula all his life, or 
the attempt may be made to dilate the stenosis gradually by the methods referred 
to in the preceding chapter. 



CHAPTER IV. 

CEDEMA OF THE GLOTTIS. 

The practical importance of the subject demands a brief special description of 
oedema of the glottis, by which name we mean oedema of the entrance of the lar- 
ynx, especially of the ary-epiglottic ligaments. We have already learned to 
recognize laryngeal perichondritis as one of its most frequent causes. In less 
deeply seated inflammations in the larynx and its neighborhood, however, oedema 
of the glottis may sometimes occur as a dangerous complication, especially in 
cases of laryngitis occurring in the course of severe acute diseases, like typhoid, 
small-pox, or erysipelas, or in inflammations of the larynx arising from severe 
mechanical or chemical irritation, like hot steam or corrosive substances, or from 
wounds of the larynx, or, finally, from foreign bodies in the larynx. The col- 
lateral oedema in angina Ludovici, in intense inflammations of the parotid gland, 



TUBEKCULOSIS OF THE LARYNX, 



123 



or the tonsils, etc., may in rare cases extend to the ary-epiglottic ligaments. Fi- 
nally, oedema of the glottis occurs in rare cases as a complication of general oedema 
of the body, as a result of Bright's disease, disease of the heart, emphysema of the 
lungs, etc. CEdema of the glottis has been repeatedly observed to come on quite 
suddenly, especially in Bright's disease. 

The chief symptom of oedema of the glottis is dyspnoea, which comes on as 
a result of the stenosis of the entrance of the larynx, and is sometimes most 
extreme. At first this is chiefly on inspiration, but it soon comes on with 
expiration also. Respiration, especially inspiration, is accompanied by a loud 
laryngeal stridor. As a result of the incomplete entrance of the air, the efforts 
at inspiration involve the neck, the epigastrium, and the sides of the thorax. 
We see with the laryngoscope, if the examination be successful, an ©edematous 
swelling of the ary-epiglottic ligaments, and often a swelling of the epiglottis and 
the false vocal cords. Sometimes we succeed in feeling the swollen parts with 
the finger. 

If the dyspnoea reaches a degree which threatens life, an operation is the only 
thing which can afford relief. Laryngologists attempt to reduce the swelling 
by long incisions in the oedematous parts. If this does not succeed, tracheotomy 
must be performed. If the immediate danger to life is thus averted, further 
treatment should be directed to the disease which has given rise to the oedema. 



CHAPTER V. 

TUBERCULOSIS OF THE LARYNX. 

{Laryngeal Phthisis. Consumption of the Larynx.) 

JEtiology. — Since tuberculosis of the larynx is in most cases combined with 
tuberculosis of other organs, especially of the lungs, we must refer to the descrip- 
tion of tuberculosis of the lungs for the general aetiology and pathology of the 
disease. A particular description of the special appearances in laryngeal tuber- 
culosis is, however, justifiable, because tuberculosis may at times begin in the larynx 
and may remain isolated there, at least for a time; and, furthermore, in many 
cases of laryngeal tuberculosis, which are evidently combined with pulmonary 
tuberculosis, the laryngeal symptoms are predominant in the clinical picture of 
the disease. Many physicians have, wrongly as we think, disputed the fact that 
tuberculosis can begin in the larynx. Clinical experience not infrequently teaches 
us that men, who up to that time were apparently in good health, are attacked 
with hoarseness, the disease being at first thought to be a common laryngitis, 
but at last, by its later course, proving to be a tuberculosis. In spite of the most 
careful examination, there are not to be found at first the slightest physical 
signs of disease in the lungs, and not till later do the manifest signs of a pul- 
monary tuberculosis succeed the symptoms of a laryngeal affection. In such cases 
it seems to us an affectation to claim that there is a primary pulmonary tubercu- 
losis which could not be made out at first. Everything is much more in favor of 
the opinion that the tubercular poison, the tubercle bacilli, may sometimes first 
fix upon the larynx, excite the first symptoms of tuberculosis there, and only later 
attack the lungs. 

In the majority of cases of laryngeal tuberculosis the symptoms are developed, 
of course, secondarily in the course of chronic pulmonary phthisis. We shall 
see that in these cases the disease of the larynx is to be considered as the result of 



DISEASES OF THE RESPIRATORY ORGANS. 



an infection of the mucous membrane of the larynx by the tuberculous sputum 
which passes over it. In about one fourth of all cases of pulmonary tuberculosis 
this complication occurs, if we include all the mild diseases of the larynx. 
Marked and extensive tuberculosis of the larynx is much rarer, however. 

Pathological Anatomy. — In its anatomical appearances the laryngeal affection 
which complicates pulmonary phthisis or occurs primarily is at first usually a 
simple catarrh of the mucous membrane, which does not differ in any remarkable 
way from any other laryngeal catarrh. Shallow erosions, too, on the vocal 
cords or between the arytaenoid cartilages have nothing characteristic in them- 
selves. In fact, it is even hard to decide whether the simple laryngeal catarrh and 
superficial ulcere in the larynx, which often occur in phthisical patients, are really 
in every case specific tubercular affections. Perhaps they are often only the result 
of the mechanical irritation from the frequent cough or of the chemical irritation 
from the sputum. This question is to be decided finally only by the discovery of 
the special tubercle bacilli in the laryngeal affections of phthisical patients. 

The more marked changes in the larynx in phthisical patients, however, are 
without doubt always of tubercular origin. In these we find a characteristic 
tubercular infiltration, with the formation of miliary tubercles in the mucous and 
submucous tissues. When the infiltrated parts break down, extensive ulcers are 
formed which always extend farther, and whose favorite seat is on the arytaenoid 
cartilages, the vocal cords, and the epiglottis. From the latter the ulcers not infre- 
quently extend to the back of the tongue. In severe cases we often find a marked 
collateral oedema in the neighboring parts from the inflammation, and sometimes 
the tubercular perichondritis which has already been described. 

Clinical Symptoms. — In the beginning of tuberculosis of the larynx the laryn- 
goscope usually shows nothing but the appearances of a simple catarrh. In the 
later stages, however, most of the special signs of the destructive tubercular pro- 
cess, like ulcers, infiltration, etc., can be very satisfactorily made out. In fact, 
we often get in this way a better picture of the disease than we do at the autopsy, 
for the hyperemia and swelling of the parts are much diminished in the cadaver. 

The other clinical symptoms of tuberculosis of the larynx vary very much with 
the extent and intensity of the process. Sometimes they consist merely in mod- 
erate roughness and hoarseness of the voice, but in other cases they increase to a 
most painful condition, which generally comes on in tuberculosis. This is especi- 
ally the case if the ulceration involves the epiglottis and the arytaenoid cartilages. 
Swallowing is then extremely painful, so that the nutrition is very often impaired, 
and painful attacks of coughing frequently occur. If severe ulcerations attack 
the vocal cords, and their free mobility is imxDaired to a marked degree, the hoarse- 
ness increases, and finally reaches a complete aphonia. Death finally occurs from 
the increase of the general inanition, or rarely from oedema of the glottis. 

The diagnosis of tnberculosis of the larynx is not difficult if pulmonary 
phthisis is already known to be present. When attention has been called to it 
from the onset of hoarseness or from some disturbance in swallowing, we recognize 
the character and seat of the changes by the aid of the laryngoscope. The diag- 
nosis, however, may present much difficulty in cases where we are not sure that 
an affection of the lungs co-exists. As has been said, the symptoms at first are not 
unlike those of a simple catarrh, and the suspicion of the existence of tuberculosis 
is first aroused from the stubbornness of the disease, the condition of the patient, 
some inherited taint, the onset of fever, and the remarkable emaciation. With 
the changes in the larynx which have been described the distinction between 
tuberculosis and syphilis may be very' difficult. In syphilis of the larynx, how- 
ever, we find that co-existing changes in the pharynx are much commoner 
than in tuberculosis, and the cicatricial formation which is visible in many 



PARALYSES OF THE LARYNGEAL MUSCLES. 125 



places furnishes, besides, a very characteristic evidence of syphilis. The diagnosis 
of tuberculosis of the larynx, however, is made perfectly certain in all doubtful 
cases by the presence of tubercle bacilli in the patient's expectoration or in the 
secretion from the ulcer, which often can be easily obtained by the aid of a fine 
laryngeal brush. In regard to the laryngoscopic appearances, we may also say 
that a thick infiltration of the epiglottis with a partial ulceration of the same is 
an appearance which is almost exclusively confined to tuberculosis. 

The treatment is in the milder cases the same as in catarrh of the larynx, and 
then it is sometimes of decided benefit. When ulcers make their aj)pearance we 
may try to obtain improvement by cauterization with nitrate of silver, or by 
using inhalations of astringents or iodoform (see the chapter on pulmonary tuber- 
culosis). In the cases just described we are very soon reduced to a purely pallia- 
tive treatment. The constant use of cracked ice, and especially a lavish employ- 
ment of narcotics, form the best means of lessening the pain and the difficulty in 
swallowing. Subcutaneous injections of morphine a quarter of an hour before 
each meal often afford great relief. Beside this, we can paint the larynx with 
strong solutions of morphine, blow in powdered morphine, or let the patient 
inhale solutions of morphine or bromide of potassium. Cocaine, which is an 
excellent local anaesthetic, excels all these, however, in potency (von Anrep). If 
we paint the ulcerated mucous membrane at the entrance of the larynx with a ten- 
or twenty-per-cent. solution of cocaine, in a few minutes such an anaesthesia of the 
affected parts ensues that swallowing may take place without any pain. The fol- 
lowing formula may be used : 

Cocaini muriatis l'0-2'0 ; 

Alcohol 2'0 ; 

Aquae destillatae 8*0. M. 

Unfortunately, the action of cocaine is extremely transitory, so that the paint- 
ing must always be repeated anew. 



CHAPTER VI. 
PARALYSES OF THE LARYNGEAL MUSCLES. 

1. Paralyses in the Distribution of the Superior Laryngeal Nerve.— The supe- 
rior laryngeal nerve, arising from the vagus, is the sensory nerve for the mucous 
membrane of the upper portion of the larynx down to the glottis, and also for 
the mucous membrane of the epiglottis and its neighborhood. Beside this, it also 
supplies motor fibers to the crico-thyroid muscle. Clinical experience renders it 
probable that the superior laryngeal nerve also supplies the depressors of the 
epiglottis, the thyro-epiglottideus, and the arytaeno-epiglottidei muscles, and per- 
haps also the arytaenoideus muscle. The last three muscles mentioned, however, 
perhaps derive some motor fibers from the recurrent nerve also (the inferior 
laryngeal nerve). 

Paralysis of the crico-thyroid muscles and of the depressors of the epiglottis 
is seen most frequently after recovery from diphtheria. It is usually a part of a 
more extensive paralysis, and, in addition, is frequently associated with anaesthe- 
sia of those parts of the mucous membrane which, as we have seen, derive their 
sensory fibers from the superior laryngeal nerve (von Ziemssen). 

Paralysis of the thyro-epiglottideus and the arytaeno-epiglottidei muscles is 



126 



DISEASES OF THE RESPIRATORY ORGANS. 



recognized by the immobility and the erect position of the epiglottis, which is 
directed toward the back of the tongue. 

Paralysis of the crico-thyroid muscles makes the voice rough, and especially 
renders the production of high tones impossible, since for this purpose we need 
the action of this muscle as a tensor of the vocal cords. The detection of this 
paralysis by the laryngoscope is extremely difficult. Its chief signs are a con- 
cavity of the edges of the vocal cords, a lack of visible vibration in them, and 
perhaps, in unilateral paralysis, a higher position of the vocal cord on the sound 
side. 

For paralysis of the arytsenoideus muscle, vide infra. 

2. Paralyses in the Distribution of the Inferior Laryngeal or Recurrent Nerve. 

— The recurrent nerve supplies with sensory fibers the mucous membrane of the 
inferior cavity of the larynx below the glottis, and it is the motor nerve for all the 
laryngeal muscles except the crico-thyroid, and except possibly the depressors of 
the epiglottis (vide supra). The muscles innervated by it are arranged according 
to their function in the three following groups : 

a. The openers of the glottis — the posterior crico-arytsenoid muscles alone. 

b. The closers of the glottis — the lateral crico-arytaenoids and the arytsenoideus 
(transverse and oblique). 

c. The tensors of the vocal cords — the thyro-arytaenoids, which act usually 
as closers of the glottis, but which very often produce the fine differences in 
tension in the vocal cords which are necessary in singing and in modulations of 
speech. They accordingly have the same task as the coarser-working crico- 
thyroid muscles, which are innervated by the superior laryngeal nerve. 

The motor fibers for all these muscles have their special origin in the accessory 
nerve, from which they pass into the trunk of the vagus, and from this into the 
laryngeal nerves. 

Most of the paralyses of the recurrent nerve are of peripheral origin. Except 
in the pure muscular pareses {vide supra), which arise not infrequently in the 
course of other laryngeal affections, peripheral paralyses of the vocal cords occur 
with the greatest relative frequency from an abnormal pressure on the trunk of 
the recurrent nerve, especially in aneurism of the arch of the aorta, which may 
cause a left-sided paralysis. Tumors of the bronchial glands, cancer of the 
oesophagus, thyroid or mediastinal tumors, and, in rare cases, even large pericar- 
dial effusions, may also cause a paralysis of the recurrent on one side. Paralyses 
on the right side are seen quite frequently in contractions at the apex of the right 
lung and in the rare cases of aneurism of the subclavian artery. The paralyses of 
the laryngeal muscles, which are sometimes met with after recovery from diph- 
theria (q. v.), also belong to the peripheral paralyses of the recurrent nerve, 
and their cause is to be found in a degeneration of the branches of the affected 
nerves. In other cases the paralysis of the recurrent nerve is due to an affection 
of its fibers in the vagus or even in the accessorius. Excluding certain injuries from 
operations, these affections are usually due to new growths which cause a paraly- 
sis of conduction. Paralyses of the recurrent nerve also arise from affections of 
the nucleus of the accessory nerve in diseases of the medulla, in the different 
forms of acute bulbar paralysis, in chronic bulbar paralysis, in multiple sclerosis, 
etc. The frequent hysterical paralyses in the distribution of the recurrent nerve 
are to be regarded as cerebral paralyses. Finally, paralyses of the laryngeal mus- 
cles are sometimes observed for which we are not in a position to find any cause. 

1. Complete Paralysis of the Recurrent Nerve.— Paralysis of all the laryngeal 
muscles supplied by the recurrent nerve occurs quite frequently in the pressure 
paralysis of the trunk of the recurrent, or of its fibers in the vagus. With the 
laryngoscope (see Fig. 12) we find the vocal cord on the paralyzed side in a middle 



PARALYSES OF THE LARYNGEAL MUSCLES. 



127 




Fig. 12. — (From Ziemssen.) Position 
on inspiration in paralysis of the left 
vocal cord, or paralysis of conduc- 
tion in the recurrent nerve. 



position, often falsely called a " cadaveric position," and completely motionless on 
respiration, and also on phonation. On phonating as strongly as possible, the 
vocal cord on the sound side passes beyond the 
median line, the arytenoid cartilage also crosses 
the line, and consequently the glottis is put in an 
oblique position. The other symptoms are some- 
times so slight that without a laryngoscopic ex- 
amination we do not even think of a paralysis. 
The speech, however, is usually not as pure ; it 
often breaks into a falsetto, and the patient is 
easily tired by speaking. With bilateral paralysis 
of the recurrent nerve, which is very rare, we find 
both vocal cords motionless in a middle position. 
Complete aphonia exists, and it is impossible to 

cough, since in coughing we have to make at first a complete closure of the 
glottis. There is no dyspnoea, however, if the patient keeps quiet. 

2. Paralysis of the Dilators of the Glottis, the Posterior Crico-arytsenoid 
Muscles. — Bilateral paralysis of these muscles is a very rare phenomenon, but clin- 
ically it is of the utmost importance, since it results in a condition of most marked 
inspiratory dyspnoea. This condition develops gradually, and usually without 

any cause that has been satisfactorily determined. 
There is probably some affection of the nerves 
themselves which finally leads to the paralysis.* 
In most cases the disease lasts for years. The 
dyspnoea increases, especially from external causes, 
to severe attacks of suffocation, and tracheotomy 
is frequently necessary. In paralysis of the dila- 
tors of the glottis the respiration is so changed that 
inspiration only is difficult, protracted, and noisy, 
while expiration is free and unhindered. This 
depends on a valve-like action of the vocal cords. 
They are drawn together by the dilatation of the 
thorax on inspiration, while the current of air in expiration easily pushes them 
aside. Phonation is usually entirely undisturbed. With the laryngoscope (see 
Fig. 13) we find the glottis changed to a small slit, which grows narrower instead 
of wider on inspiration. 

The prognosis is usually unfavorable. Only in the hysterical can these 
apparently severe conditions appear and disappear again in a short time. 

3. Paralysis of the Thyro-arytaenoid Muscles.— The paralysis or paresis of 
these muscles, which run into the vocal cords, and which are their chief tensors, 
is one of the most frequent of the paralyses of the laryngeal muscles. It 
occurs especially in acute and chronic catarrh of the laryngeal mucous mem- 
brane, and is often the chief cause of the accompanying hoarseness. It also 
frequently develops in the course of an habitual over-exertion of the voice in 
singers and public speakers, and it is one of the commonest causes of hysterical 
aphonia. 

Paralysis of the thyro-arytaenoid muscles may be bilateral or unilateral. It 
is frequently associated with a paresis of the other closers of the glottis, the arytse- 
noidei and the crico-thyroid muscles. With the laryngoscope (see Fig. 14), in 
the ordinary bilateral paresis of the thyro-arytaenoid muscles we see that on pho- 




Fig. 13.— (From Ziemssen.) Complete 
bilateral paralysis of the posticus 
at the moment of inspiration. 



* It is remarkable, however, that a purely mechanical hindrance to the dilatation of the glottis may 
occur from the formation of anchylosis in the crico-arytsenoid articulation. 



128 



DISEASES OF THE RESPIRATORY ORGANS. 



nation the glottis does not close completely, but that an oval space is left between 
the vocal cords. 

In unilateral paralysis the affected cord shows a concavity of its edge. The 
voice is always more or less hoarse and low, and the speech is strained. 

In many cases, after a cure of the original catarrh, a complete recovery from 
the paralysis may follow by taking good care of the voice. Hysterical paralyses 
are diagnosticated by their sudden disappearance and reappearance, usually after 
some psychical disturbance. They are quite common in children of the age of ten 
to fourteen years, especially in girls. (See the chapter on hysteria.) 

4. Paralysis of the arytsenoideus muscle is rarely an isolated phenomenon. It 

is sometimes seen in laryngeal catarrh or in hysteric- 
al aphonia. The voice is quite hoarse, and with the 
laryngoscope (see Fig. 15) we find on phonation that 
the whole anterior part of the vocal cords closes well, 
but that the cartilaginous glottis remains open as a 
triangular gap on account of the imperfect motion of 
the arytenoid cartilages toward each other. "When 
the thyro-arytsenoids are paralyzed with the arytse- 
noideus, the glottis shows on phonation a narrow 
hour-glass opening (see Fig. 16). Both the anterior 
and the posterior portions of the glottis fail to close, 
while the vocal processes take their usual median position on phonation from the 
normal turning of the arytaenoid cartilages inward by the action of the lateral 
crico-arytaenoid muscles. 

5. Paralysis of the lateral crico-arytsenoid muscles, as an uncomplicated con- 
dition, has never been observed with certainty. Some cases of a complete and 
simultaneous paralysis of all the closers of the glottis have been described, how- 




Fig. 14.— (From Ziemssen.) Pa- 
ralysis of both internal thyro- 
arytenoid muscles in the 
course of an acute laryngitis. 




Fig. 15.— (From Ziemssex.) Paraly- Fig. 16.— (From Ziemssex.) Bilateral 

sis of the arytsenoideus in acute paralysis of the thyro-aryteenoids 

laryngitis. ' combined with paresis of the ary- 

tsenoideus. 

ever, in which the vocal cords are immovable laterally and the glottis remains 
abnormally wide open. 

We may expect success from the treatment of paralysis of the vocal cords only 
when the primary disease is capable of cure. If catarrhal or other diseases of the 
larynx co-exist, we must first treat these by the methods already mentioned. 
Paralysis from the compression of tumors, etc. , may be relieved in rare cases by 
extirpation or by partial resolution of the tumors when of strumous origin. In 
catarrhal, diphtheritic, and the so-called " rheumatic " pareses — that is, those 
which occur without any assignable cause — and also in all hysterical aphonias, 
electricity often works very well. A very rapid recovery sometimes occurs in 
hysterical paralyses, but it is not always permanent. We usually use external 
faradization of the neck or galvanization through the larynx, combined with fre- 
quent changes of the current. Ziemssen has made electrodes for the endo- 
laryngeal irritation of single muscles. Internally we may prescribe preparations 



SPASM OF THE GLOTTIS. 



129 



of iron and small doses of quinine, especially in anaemic patients. Subcutaneous 
injections of strychnine are also of advantage, in doses of gr. ^ to gr. £ daily (grm. 
0*003 to 0-01). Methodical efforts at speaking and breathing are of great service in 
hysterical aphonia. 



CHAPTER VII. 

SPASM OF THE GLOTTIS. 

(Millar's Asthma. Thymic Asthma.) 

JEtiology. — Spasm of the glottis is a disease which occurs almost exclusively in 
children under three years of age, and which consists of attacks of spasmodic 
closure of the glottis, and consequently of most severe dyspnoea. Boys are more 
frequently attacked by this disease than girls, but the cause of this is wholly 
unknown. The old name of thymic asthma arose from the old idea that the 
attacks were due to an increase in the size of the thymus gland, but this opinion 
is wholly unfounded. The relation between spasm of the glottis and rachitis is 
remarkable, but it is unexplained. Nearly two thirds of all the children who 
suffer from spasm of the glottis are rachitic, but the opinion which was once held 
that spasm of the glottis has a special relation to the rachitic craniotabes is not 
clearly proven. The fact that it is often combined with eclampsia, in that the 
attacks of spasm of the glottis are aggravated by eclamptic attacks, and that the 
two alternate with each other, is an argument in favor of a central origin for 
the disease. In the cases which come on, as they often do, at the time of denti- 
tion, we think it possible to assume a reflex origin for the spasm, just as we may 
in those cases which seem to follow a laryngitis due to taking cold. 

Symptomatology. — The single attacks usually come on suddenly by day or by 
night, either without any cause or from some external influence, like crying, 
swallowing fluid, or some psychical disturbance. They usually begin with a deep 
inspiration, followed by complete cessation of respiration. The child becomes 
pale, cyanotic, looks anxiously about, rolls his eyes, and makes strained and 
labored efforts at respiration. In severe cases there is a temporary loss of con- 
sciousness, and tonic and clonic spasms in the muscles of the extremities and 
the trunk, as has been mentioned. The attack lasts from some seconds up to two 
minutes. In very severe cases the attack may be immediately fatal. As a rule, 
however, the spasm passes off, deep, noisy inspirations follow, and in a short time 
the child is completely well. The severity of the attacks varies, moreover, in 
different cases, and it varies very markedly, too, in the same child. Sometimes 
we have only one attack or a small number of them, while in other cases they 
may come on ten or twenty times a day, and even oftener, and may last with 
yarying intensity for months. If the child reaches his third year the disease 
almost always disappears, but quite a large number of the children who suffer 
from spasm of the glottis die before that age, either in the attack itself or from 
other affections. 

Pure spasm of the glottis hardly ever occurs in adults, but similar attacks are 
sometimes observed in hysteria. 

The treatment must be especially directed to the child's general condition. 
The child is usually pale and emaciated, and if we succeed in improving its nutri- 
tion with iron and cod-liver oil, the attacks become less frequent, milder, and 
finally may wholly disappear. The child should also be kept in moderately warm 
air and guarded from any exposure to cold. Internal remedies to prevent the 
9 



130 



DISEASES OF THE RESPIRATORY ORGANS. 



recurrence of the attacks are very uncertain in their action. We may employ 
bromide of potassium, ten to thirty grains daily (grm. 0* 5-2*0) ; musk, ten drops of 
the tincture every hour or two ; oxide of zinc, etc. 

In the attack itself the child must be raised up. The face should be sprinkled 
with water, or, if the attack be of long duration, a cool shower-bath should be 
given. Friction should be applied to the skin, aided by mustard, or a mustard 
plaster to the chest and calves. If the attacks are very frequent and intense, 
we must use narcotics, either inhalations of chloroform or subcutaneous injec- 
tions of morphine, with care, in doses for a child of ¥ V to X V of a grain (grm. 0*001 
to 0*005). 



CHAPTER VIII. 
DISTURBANCES OF SENSIBILITY IN THE LARYNX. 

Disturbances of sensibility in the laryngeal mucous membrane have been 
observed especially in the distribution of the superior laryngeal nerve, in the epi- 
glottis, and in the superior cavity of the larynx above the glottis ; but in rare cases 
they are also observed in the lower portion of the larynx, which is supplied with 
sensory fibers by the recurrent nerve. They are most frequently associated with 
motor disturbances, particularly with hysterical paralyses, but they are also quite 
often found in paralyses of diphtheritic origin. Anaesthesia of the larynx is rec- 
ognized by the lack of sensation which the patient shows when we touch special 
parts of the larynx with the point of a sound. The choking and coughing reflexes 
are almost always absent, so that we can touch the whole entrance of the larynx 
with the finger without causing discomfort. 

The absence of the reflexes may sometimes be dangerous, especially in severe 
diphtheritic and bulbar paralyses, for, as a result of it, small portions of saliva may 
reach the larynx in swallowing, and fail to be coughed up, but may be drawn 
down into the lungs, where they set up a bronchitis and a lobular pneumonia. 
This danger is especially great if, at the same time, the patient can not cough 
forcibly, as is frequently the case in imperfect closure of the glottis. Hysterical 
anaesthesia is the only form where there is no fear of the development of inhala- 
tion diseases in the lungs. 

An effective prophylaxis against the dangerous condition just described is 
possible only by feeding patients, who have much weakness in swallowing and 
coughing, by means of the oesophageal tube. 



CHAPTER IX. 
NEW GROWTHS IN THE LARYNX. 

Since new growths in the larynx are of interest rather to specialists and sur- 
geons, we will here only glance briefly at them. We must remember especially, 
however, that they can be recognized only by the aid of the laryngoscope. It 
unfortunately often happens that a patient is treated for a long time without 
success for a " chronic laryngeal catarrh," until the laryngoscope finally shows 
that a new growth is the cause of the hoarseness. It is of especial importance, 
however, to make a diagnosis as early as possible, particularly in carcinoma, 



NEW GKOWTHS IN THE LARYNX. 



131 



since the earlier the operation is done the better is the chance for success {vide 
infra). 

A. Benignant New Growths in the Larynx. 

1. Papilloma is one of the commonest new growths in the larynx. It forms 
glandular, cauliflower-like excrescences, which are usually situated on the ante- 
rior part of the vocal cords, rarely on the false cords. The base of the swelling is 
broad or pediculated. We do not know the special cause of their origin. They 
sometimes develop upon an existing chronic catarrh. 

2. Fibroma in the larynx is comparatively common. The tumors known as 
" laryngeal polypi " are usually fibromata. They are generally situated on the 




Figs. 17 and 18.— (From Ziemssen.) Pediculated fibromata. 



vocal cords and form whitish or reddish-brown swellings, from the size of a pea to 
that of a cherry, and are usually pediculated (see Figs. 17 and 18). People who 
use their voices very much are especially liable to the formation of fibromata. 

3. Cysts and " mucous polypi " rarely occur. They are probably due to the 
retention of the secretion in a mucous gland from the stoppage of its orifice. 
We find them in the ventricles of Morgagni, on the epiglottis, etc. 

The symptoms which are excited by benignant tumors in the larynx depend 
partly upon the situation and partly upon the size of the new growth. Small 
polypi may go on wholly without symptoms, and are found only by chance on 
laryngoscopic investigation. Usually, however, the presence of hoarseness, press- 
ure, and itching in the larynx, or respiratory disturbances, when the tumor is a 
large one, are the symptoms which give occasion for an examination. 

B. Malignant New Growths. Carcinoma of the Larynx. 

Carcinomata develop usually in old people, either primarily in the larynx or 
secondarily from affection of the neighboring organs. In the first case the vocal 
cords or the ventricles of Morgagni are the points most frequently attacked. An 
extension of the disease to the larynx is seen especially in cancer of the tongue or 
pharynx, rarely in cancer of the oesophagus. 

The symptoms of cancer of the larynx develop slowly. Hoarseness, disturb- 
ance in swallowing, pains in the larynx often shooting up into one ear, the 
appearance of respiratory symptoms, and finally the signs of general weakness 
and emaciation which are seen in almost all forms of carcinoma, form the picture 
of the disease. The diagnosis is possible only by the aid of the laryngoscope. 
Beside this, a digital examination may at times be of diagnostic value by the detec- 
tion of the characteristic hardness about the entrance or in the neighborhood of the 
larynx. A general description of the laryngoscopic appearances can not be given 
on account of the diverse character of the cases. We see the uneven, injected 
new growth, covered with mucus and often ulcerated, and beside this at times 
the secondary appearances of catarrh, a developing perichondritis, etc. With a 
little care the diagnosis is usually tolerably easy. It may be hard, however, at 



132 



DISEASES OF THE RESPIRATORY ORGANS. 



times, to distinguish it from tuberculosis or from syphilis. We may be aided in 
such cases by the discovery of the tubercle bacilli (!) or by the results of anti- 
syphilitic treatment ( ! ). All the other organs of the patient therefore must always 
be carefully examined. 

Surgical treatment is the only one for all laryngeal new growths. We must 
refer to the special works for all the details. Laryngologists have devised numer- 
ous instruments for the removal of benignant polypi by which, under the guid- 
ance of the laryngoscope, the new growth is cut, snared, squeezed, or torn off. 
The performance of the operation is made much easier by the advantage of the 
local ansesthesia of the laryngeal mucous membrane due to painting with cocaine 
(see p. 125) . In carcinoma of the larynx a total extirpation of the larynx, with 
the insertion of an artificial larynx later on, is the only thing which can give a 
lasting result. This operation was first successfully performed by Billroth, and 
later by other surgeons. If an operation is impracticable, the only aim of treat- 
ment is to alleviate the patient's symptoms by narcotics, morphine, cocaine, etc. 



CHAPTER X. 
SYPHILIS OF THE LARYNX. 

Pathological Anatomy. — Syphilis of the larynx shows itself at times merely as 
a catarrhal inflammation of the mucous membrane, syphilitic catarrh of the 
larynx, which presents no peculiarities anatomically, and the special significance 
of which can be made out only by the co-existence of other symptoms of syphilis. 
In other cases, however, we meet with coarser anatomical lesions, syphilitic infil- 
tration of the mucous membrane, either in the form of mucous patches {plaques 
muqueuses) or in the form of denser nodular masses which have a great tendency 
to break down and form ulcers. The patches, which are quite analogous to the 
broad condylomata of the external skin, form soft whitish elevations of the 
mucous membrane, which consist of a granulation tissue rich in cells. They 
are situated chiefly in the upper part of the larynx, on the epiglottis, the ary- 
epiglottic ligaments, and the posterior wall of the larynx. They are only rarely 
seen on the vocal cords or lower down. The denser infiltrations, "gummous 
nodules," are situated on the epiglottis, on the anterior surface of the posterior 
wall of the larynx, and on the true and false vocal cords, and they show a 
marked tendency to ulceration, as has already been said, so that syphilitic ulcers 
are an almost constant lesion in severe laryngeal syphilis. They are situated on 
the above-named spots, and are especially frequent on the epiglottis, which may be 
almost completely destroyed. As general diagnostic signs of syphilitic ulcers, we 
may mention their reddened, dense, often sinuous edges, and also their tendency to 
extend deeply on one side while on the other they begin to cicatrize. As a result 
of then deep excavation, we sometimes have a secondary perichondritis with a 
loss of cartilage. The cicatrization is important in a diagnostic point of view, for 
it hardly ever is seen in tubercular or carcinomatous ulcers. It is also of great 
significance in the further course of the disease, since by the formation of cicatri- 
cial bands and deformities we may have marked permanent disturbances of 
speech, swallowing, and especially of respiration from stenosis of the larynx. 

The symptoms which are due to syphilis of the larynx vary, of course, with 
the seat and extent of the affection. If the vocal cords are attacked by catarrh or 
ulceration, hoarseness arises ; but in affections of the epiglottis, the arytenoid car- 
tilages, and the parts adjacent, the complaint is merely of disturbance in swallow- 



ACUTE CATARRH OF THE TRACHEA AND THE BRONCHI. 133 



ing. In many cases subjective symptoms are entirely absent, and a laryngoscopic 
examination alone discloses the condition of the larynx. 

The larynx is only rarely the sole seat of syphilitic disease. We usually find 
analogous changes at the same time in the pharynx, the naso-pharynx, the nose, 
etc. Co-existing disease of these organs is of great diagnostic importance. 
Syphilis of the skin, of course, often occurs at the same time. 

As regards the time of its appearance, we usually reckon syphilis of the larynx 
among the " secondary symptoms," which first appear in the second or third 
month after the primary infection. The first symptoms of the disease, however, 
may come on much later, and we also meet with relapses and second attacks of 
syphilis in the larynx. 

The treatment consists chiefly in the general treatment of syphilis. As soon 
as the larynx is attacked we should try to cure the affection as rapidly as pos- 
sible in order to prevent the deeper-seated disturbances and the more extensive 
cicatricial formations. We may best accomplish this by energetic inunction, by 
rubbing mercurial ointment, forty to eighty grains (grm. 3-5), into the skin daily. 
This is aided further by the exhibition of iodide of potassium internally, fifteen to 
forty-five grains (grm. 1-3) a day. By this general treatment syphilis of the 
larynx is often completely cured without any local treatment. It is of advan- 
tage, however, especially with severe syphilitic ulcers, to cauterize them a few 
times with strong solutions of nitrate of silver. It is also of advantage to paint 
the ulcerations with iodine and glycerine (iodine, 0*2 ; potassii iodidi, 2 ; glycerine, 
10), or with a solution of corrosive sublimate (hydrargyri bichloridi, 0*5 ; setheris 
sulphurici, 20). 

The treatment of the subsequent cicatricial stenosis, which gives rise to respira- 
tory symptoms, consists of the mechanical methods of dilatation which have been 
already mentioned. 



SECTION III. 
Diseases of the Trachea and the Bronchi. 
CHAPTER I. 

ACUTE CATARRH OF THE TRACHEA AND THE BRONCHI. 

{Tracheitis and Acute Catarrhal Bronchitis^) 

iEtiology. — Acute catarrh of the larger air-passages, of the trachea, and larger 
bronchi, is a frequent disease, and it may often arise from taking cold. It is con- 
ceivable that the inhalation of cold, damp air sometimes directly affects the mucous 
membrane of the upper air-passages. Bronchial catarrh is very often associated 
with a coincident catarrh of the larynx, and more rarely of the pharynx. In the 
ordinary mild forms the catarrh is usually confined to the trachea and the first 
large branches of the bronchi, while the finer bronchi remain healthy. 

More intense inflammation of the bronchial mucous membrane is the result 
of active mechanical or chemical irritation. A severe bronchitis develops after 
the inhalation of noxious gases, nitrous and sulphurous oxides, chlorine, bromine, 
etc., as is often observed in operatives. The inhalation of smoke and dust, 
especially vegetable dust, works in the same injurious fashion, and the followers 



134 



DISEASES OF THE EESPIEATOKY OEGANS. 



of many trades and employments, like millers, colliers, etc., are especially subject 
to disease from this cause. In this form of bronchitis the catarrh often extends to 
the finer bronchi. 

The bronchitis which develops in the course of other acute and chronic diseases 
is still commoner than the primary forms already mentioned. It is often due to 
infectious causes, like certain infectious diseases, especially measles and whooping- 
cough. In these diseases bronchitis is one of the most constant local affections, 
and is probably immediately dependent upon the primary infection. Bronchitis, 
however, develops secondarily in most of the other acute infectious diseases, and 
is largely due to the inhalation of noxious substances from the upper part of the 
air-passages. This is the explanation of the bronchitis in diphtheritic processes in 
the pharynx and larynx, in so far as it does not depend upon a direct extension 
of the disease, and also of the bronchitis in small-pox, etc. Bronchitis may also 
be met with ir. all other forms of severe disease, because retentions of secretion, 
inflammations, formations of thrush, etc., arise in the cavity of the mouth and 
pharynx, and from them chemical or organic irritants may easily be inhaled into 
the bronchi. The imperfect expectoration in all severe diseases is a still more 
harmful factor than this inhalation. The secretion remains in the bronchi, pro- 
cesses of decomposition arise in the stagnating mucus, bacteria collect and lead to 
a bronchitis, and finally to a lobular pneumonia which is so often found (vide 
infra). The swallowing and inhalation of portions of saliva, which easily decom- 
pose, is also a frequent cause of secondary bronchitis. 

We do not know how far we may claim that infectious agents act as a cause 
of primary bronchitis, yet it is not improbable that many cases have such an 
aetiology. It can certainly be asserted that such is the case in whooping-cough, 
which will be described in a special chapter. Febrile bronchial catarrh some- 
times appears as an epidemic outbreak, usually associated with catarrh of the 
other respiratory mucous membranes. It has been called influenza {grippe), and 
is of an infectious character. 

Finally, we must mention that an acute bronchitis is sometimes merely an 
exacerbation of a previous chronic bronchitis. 

The predisposition to acute bronchitis varies in different people. We do not 
know definitely on what ground such an increased predisposition to bronchial dis- 
ease rests, nor why we meet with it sometimes in weak and anaemic people 
and at other times in the so-called " full-blooded " persons. Bronchitis is more 
frequent in children and old people than in those in middle life. Most of the 
cases occur in the spring and autumn. 

Symptoms. — Pain in the chest may be present in some cases of simple catarrhal 
bronchitis, but usually only in a moderate degree. In severe tracheitis patients 
often have a painful feeling of soreness in the neck and behind the upper part of 
the sternum, and this is increased on coughing. The mucous membrane of the 
bronchi, apparently, has no nerve-fibers which are sensitive to pain, and the pains 
in the chest which are often present in bronchitis are, as a rule, muscular pains 
in the intercostal muscles, due to the severe paroxysms of coughing. 

Cough is one of the most constant symptoms of bronchitis, and by it usually 
the attention of the patient or of the physician is first called to the existing 
thoracic affection. The cough may of course be due to a laryngitis, if that is also 
present. There is no doubt, however, but that a cough may be excited in a reflex 
manner from the mucous membrane of the trachea and of the larger as well as of 
the finer bronchi. Experiments have shown that the point of bifurcation of the 
trachea is especially irritable, and many severe paroxysms of coughing maybe due 
to an irritation of this very spot from the accumulation of secretion. The 
intensity of the cough, moreover, is very different in individual cases, which is 



ACUTE CATAEKH OF THE TEACHEA AND THE BEONCHI. 135 



due in part to the degree and extent of the bronchitis and in part to the reflex irri- 
tability of the person affected. 

The expectoration consists of the secretion from the inflamed mucous mem- 
brane. Its abundance and consistency vary very much in the different cases. 
We distinguish a catarrh with an abundant secretion, and the so-called "dry 
catarrh." In the latter only a little viscid sputum is expectorated, but in the 
former the expectoration is more abundant and muco-purulent. Very often in 
the beginning of the disease the expectoration is scanty and viscid — the sputum 
crudum of the old physicians ; and later it becomes more abundant, more fluid, and 
more purulent — the sputum coctum. In catarrh of the finer bronchi the expecto- 
ration may contain little mucous or muco-purulent casts of the bronchi. A simple 
catarrhal expectoration shows nothing peculiar under the microscope. The pus- 
corpuscles are often swollen and show more or less marked fatty degeneration. A 
slight admixture of blood may occasionally be present in severe bronchitis, but it 
usually has no special significance, being at times merely the result of severe 
fits of coughing. A more marked and persistent admixture of blood is seen in 
the catarrhal sputum in some cases of intense bronchitis in drunkards, so that we 
may even speak of a " hemorrhagic bronchitis. " 

Dyspnoea is usually entirely absent in simple bronchitis, but marked shortness 
of breath may be noticed in extensive catarrh of the finer bronchi. 

Physical Examination. — We may obtain direct evidence of the condition of 
the tracheal mucous membrane, with due practice, by the laryngoscope. We 
see a reddening of the tracheal mucous membrane, and sometimes an abnormal 
abundance of secretion on it, if there is a tracheitis. Other methods of physica] 
examination are at our service for judging of the changes in the bronchi. 

Inspection of the thorax shows nothing abnormal in the milder forms of bron- 
chitis. The respiration is somewhat accelerated and the expiration prolonged in 
severe bronchitis, especially if the finer bronchi are affected. Percussion in 
uncomplicated bronchitis shows nothing abnormal in the pulmonary resonance. 
Auscultation, too, shows nothing unusual in many cases of mild catarrh limited 
to the trachea and large bronchi, but in the cases where the smaller bronchi are 
the seat of the catarrh and there is a marked accumulation of secretion in them ? 
we hear, beside the vesicular respiration, the so-called rhonchi which almost 
wholly hide it. In dry bronchitis we speak of humming or buzzing sounds, 
sonorous rhonchi, or shrill, whistling sounds, sibilant rhonchi, according to their 
pitch. These sounds are probably due to stenosis, and are caused by the passage 
of the air through narrow portions of the bronchi. The narrowing occurs in part 
from the swelling of the mucous membrane, in part from the accumulation of 
secretion. The masses of secretion themselves, if they are set in vibration at the 
same time, may possibly take part in the production of the humming noises. If 
the amount of secretion collected in the bronchi is more abundant and of a more 
fluid consistency, it gives rise to "moist rales" on the passage of the air. These 
are distinguished as " medium " or " small moist rales," according as they occur in 
the larger or smaller bronchi. 

Other symptoms of disease are often present beside those already mentioned 
as being directly due to the bronchitis. The general health is usually disturbed 
in a severe bronchial catarrh. The patient does not feel well and has less appe- 
tite than usual. A moderate amount of fever is often present, especially toward 
evening. An increase of temperature above. 102° or 103° (39° C.) is rarely seen 
except in children. The patient sometimes complains of headache, which is 
increased by severe coughing. 

The separate forms of bronchitis are distinguished chiefly by the degree of 
extension of the catarrh. 



136 DISEASES OF THE RESPIRATORY ORGANS. 



1. Catarrh of the Larger Bronchi.— This is the common form of simple bron- 
chitis after taking cold, after irritation on the bronchial mucous membrane, etc. 
Many cases of secondary bronchitis also remain confined to the larger bronchi. 
The symptoms are moderate, although the irritation from coughing may some- 
times be quite severe. Auscultation gives the coarser humming sounds [rhon- 
chi], or, as has been said, in many cases nothing at all abnormal, so that we can 
recognize the disease only from the subjective thoracic symptoms, the cough, and 
the expectoration. With good care uncomplicated bronchitis runs its course in 
a few days, or at most in a few weeks, and goes on to complete recovery ; but 
with a lack of care on the patient's part, or where the irritation has been severe, 
the disease may of course continue for a long time, and finally run into a chronic 
bronchitis. 

2. Catarrh of the Finer Bronchi— Capillary Bronchitis— A simple primary 
bronchial catarrh rarely extends to the finer bronchi in adults. The secondary 
bronchitis, however, which develops in other severe diseases (vide supra), often 
extends into the ultimate divisions of the bronchi, and finally leads to the forma- 
tion of nodules of lobular pneumonia — " catarrhal pneumonia " (vide infra). We 
recognize the implication of the finer bronchi by hearing the high, shrill, whist- 
ling rhonchi [sibilant rhonchi], or the abundant small, moist rales. Respiratory 
symptoms may be quite marked in extensive catarrh of the finer bronchi. Res- 
spiration is evidently accelerated and expiration is usually prolonged. There is 
often quite a severe cough. The expectoration is muco-purulent and usually not 
very abundant. 

Capillary bronchitis in children is of great practical importance. Every bron- 
chitis in young children has, as experience tells us, a tendency to attack the 
smaller bronchi. Extensive bronchitis is seen especially in weak children who 
are rachitic or predisposed to tuberculosis. Children have an especial predisposi- 
tion to be attacked with bronchitis at the time of the first dentition, but it is also 
seen at an even earlier age. 

The parents' attention is usually called to the disease by the appearance of a 
cough, which is excited especially by the child's crying. Small children never 
expectorate, for they swallow the secretion which is coughed up into the pharynx. 
The rapidity of respiration is very striking, it being increased to sixty or eighty, 
or even more, in a minute. The respiration is also labored, but it is usually super- 
ficial, and in severe cases interrupted. We often see a retraction of the lower lat- 
eral portions of the thorax on inspiration as a result of the imperfect entrance of 
air into the smaller bronchi. The expiration is often noisy and groaning in chil- 
dren. We hear extensive small, moist rales over the lungs. In severe cases the 
child becomes restless, anxious, often markedly cyanotic, and finally apathetic 
and stupid. In such cases, however, we have no longer to deal with simple 
bronchitis, but catarrhal pneumonia has already developed. The disease almost 
always runs its course with fever, the temperature rising to 104° (40° C.) and 
over. The pulse is increased to 120 or 140 or more per minute. The duration of 
the disease is seldom less than two or three weeks, and it often lasts much longer. 
Death may ensue, especially in ill-nourished children, partly as a result of general 
weakness, and also directly from the imperfect respiration. In such cases we find 
at the autopsy not only diffuse bronchitis, but also almost always lobular 
pneumonia. In many cases a gradual recovery finally takes place in spite of the 
most severe symptoms. 

The secondary bronchitis in children in measles, whooping-cough, diphtheria, 
etc., has the same tendency to involve the finer bronchi and to lead to lobular 
pneumonia. 

In conclusion, we must mention that acute bronchitis in old people also readily 



ACUTE CATARRH OF THE TRACHEA AND THE BRONCHI. 137 



attacks the finer bronchi, and may be dangerous partly from the general exhaus- 
tion, partly from the occurrence of respiratory symptoms, as in lobular pneumonia. 

Diagnosis. — The diagnosis of bronchitis presents no special difficulty. It is 
obtained directly by the discovery of the rhonchi on auscultation. If these fail, we 
conclude that there is a mild catarrh of the larger bronchi from the presence of 
cough and expectoration, if no cause for the cough is to be found in an affection of 
the larynx. The question is more difficult, but it must always be considered, 
whether a given bronchitis is a common primary catarrh or secondary to some 
other affection. This question naturally can be decided only by a very careful 
examination of the body. "We must always remember, furthermore, that severe 
pulmonary affections may be at first quite latent, and show objectively merely the 
signs of simple bronchitis, while later pneumonia, a tubercular affection, or 
something similar, develops. A bronchitis which is unilateral, or in which the 
signs are to be found in circumscribed localities, must therefore be regarded as sus- 
picious. It has long been known that bronchitis in the apices of the lungs, the 
* apex-catarrh," is often the first objective change to be met with in pulmonary 
phthisis. We can only conjecture, and not pronounce with certainty on objective 
evidence, whether nodules of lobular pneumonia are present or not in diffuse 
bronchitis affecting the finer bronchi. 

From what has been said, it is clear that we should be guarded in our prognosis 
in judging of every severe bronchitis, especially in children and old people. The 
prognosis in the milder forms of bronchitis is of course always very favorable. 

Treatment. — The prophylaxis of primary bronchial catarrh consists in the 
removal of all the injurious influences mentioned which, as experience shows, may 
give rise to a bronchitis. A careful hardening of the skin to the effects of a change 
in temperature is of service in persons, particularly children, who have a special 
tendency to bronchitis, as we have already said in regard to the prophylaxis of 
laryngitis. It is very important to remember, in this connection, that we can also 
be successful in our prophylactic measures against secondary bronchitis. Keep- 
ing the mouth and pharynx clean, urging deep inspirations, and aiding expec- 
toration by the timely use of tepid baths and shower-baths, may often check a 
bronchitis or keep it within bounds, while it inevitably arises if the patient be 
neglected. 

Simple hygienic measures suffice in the treatment of mild cases of acute bron- 
chitis. The patient should be kept warm, should remain in his room, or, if there 
be any fever, in bed. Diaphoretic remedies have long been praised as especially 
potent in the treatment of acute bronchial catarrh. The patient, therefore, should 
drink hot tea, pectoral tea* (Brustthee), or elder tea, etc., or hot milk mixed with 
Seltzer, a remedy whose efficacy is frequently praised by the patient. Local 
treatment of the mucous membrane by inhalations is usually illusory, for only 
the smallest part of the inhaled fluid reaches the bronchi. We may, however, 
always prescribe inhalations of warm steam, or a one- or two-per-cent. solution of 
common salt, especially with a dry cough and a secretion which is hard to loosen. 

Otherwise we must employ symptomatic treatment. A mustard plaster or a 
cold, wet compress about the chest does good service with severe subjective thoracic 
symptoms. In severe cases a few dry cups may be very useful in adults, but local 
abstractions of blood are never necessary in simple bronchitis. If there is trouble- 
some irritation on coughing, so as* to disturb the rest, we may prescribe small 
doses of morphine, five to ten grains of Dover's powder (grm. 0*3-0 '5), fifteen to 

* A favorite German household remedy, consisting of an infusion of eight parts of althsea, three 
parts of licorice, one part of orris-root, four parts of colt's-foot, and two parts each of mullein and anise- 
seed. — Tkans. 



138 



DISEASES OF THE RESPIRATORY ORGANS. 



twenty drops of cherry-laurel water, etc. When expectoration is difficult, we may 
use the so-called expectorants — ipecac, chloride of ammonium, apomorphine, etc. 

We have already repeatedly mentioned the use of tepid baths and shower-baths, 
indicated in severe diffuse bronchitis developing secondarily in the course of other 
acute diseases. 

Tepid baths with shower-baths, two or three times a day, are also to be used as 
a most powerful remedy in severe cases of capillary bronchitis in children. The 
baths assist expectoration and guard against the possibility of the development of 
lobular pneumonia. Wet packs applied to the thorax or over the whole body are 
serviceable in milder cases. As to other remedies, we use the same as in adults. 
With weak children our care must be to keep up the strength by furnishing the 
most nourishing food possible and giving small amounts of wine. An emetic 
is sometimes indicated in cases with an abundant accumulation of mucus in the 
bronchi, and is of good service. As experience has shown, we should use opiates 
with small children only with the greatest care. 

In the bronchitis of old people our chief aim should be to keep up and improve 
the patient's strength. We prescribe liquor ammonii anisatus, infusion of senega, 
etc., to aid expectoration, which is usually difficult, since the cough is feeble. 
Tepid baths may be of advantage, but they must be used with care. 



CHAPTER n. 

CHRONIC BRONCHITIS. 

(Chronic Bronchial Catarrh.) 

iEtiology. — Chronic bronchial catarrh may develop gradually from external 
causes, or, in rare cases, it may follow an acute bronchitis. The same noxious 
influences which excite an acute bronchitis may, by the frequent repetition of 
their action, result in a chronic bronchitis. 

In a large number of cases severe chronic bronchial catarrh is not an independ- 
ent disease, but occurs as a complication or a result of other diseased conditions. 
The combination of chronic bronchitis with emphysema of the lungs {vide infra) 
is the most common. A large number of cases also are the result of some form 
of heart disease, like valvular disease or myocarditis, or of disease of the vessels, 
leading to stasis in the pulmonary circulation, and finally to a chronic catarrh of 
the bronchi. Chronic bronchial catarrh in renal diseases also depends, in part 
at least, upon circulatory disturbances. Finally, we find a more or less extensive 
chronic catarrh of the bronchi in other chronic affections of the lungs and pleura, 
as in tuberculosis or pleurisy. 

Chronic bronchitis is seen especially in adults and old people, and more fre- 
quently in men than in women. 

Pathological Anatomy. — Chronic bronchitis is characterized anatomically by a 
marked venous hypersemia of the bronchial mucous membrane. The whole tissue 
itself is often thickened, and the surface of the membrane is swollen. In old cases, 
however, we finally meet with an atrophy of all the layers of the mucous mem- 
brane. One of the most frequent results of a chronic bronchitis is a cylindrical 
dilatation of the middle and lesser bronchi — bronchiectasis. This arises gradually 
from the loss of elasticity of the diseased bronchial walls, increasing their ten- 
dency to give way, as well as from the pressure of the stagnating secretions. 

Symptoms and Course of the Disease. — The symptoms which are due to chronic 



CHRONIC BRONCHITIS. 



139 



bronchitis are disturbances of respiration, cough, and expectoration. To these 
should be added the results of a physical examination. 

The cough is of very different severity in different cases. Usually it is worse 
early in the morning, in the evening, and at night, than in the daytime. The 
amount of expectoration is also subject to great variations. In many cases there 
is a dry cough (catarrhe sec, vide infra), in which only small amounts of tough, 
viscid sputum are expectorated. In other cases the expectoration is more abund- 
ant and muco-purulent, and sometimes very abundant and quite thin. Microscop- 
ically, it has no special characteristic appearances, but it contains only the usual 
elements of sputum — pus-corpuscles mixed with pavement epithelium, often many 
bacteria, sometimes needles of fat acids, and rarely a few pointed octahedral crys- 
tals, the so-called asthma crystals (vide infra). Small amounts of blood may be 
seen in severe chronic bronchitis, but they do not have any bad significance. 

Dyspnoea of moderate degree may also be present in uncomplicated and exten- 
sive bronchitis. In the cases in which it is severe, however, it is usually due to 
other conditions affecting the heart or lungs. 

Physical Examination. — The percussion in bronchitis shows no special change 
in itself. At most the resonance may be somewhat tympanitic from the relaxa- 
tion of the lung-tissue, especially in the lower and posterior portions of the lungs, 
or, with an abundant retention of secretion in the bronchi, it may be a little 
diminished. Auscultation may give either rhonchi, whistling, hissing, humming, 
etc., or moist rales, according to the extent of the catarrh and the amount and 
consistency of the secretion. The sounds are usually to be heard over the whole 
lung, or especially over the whole of the lower lobes, because here the catarrh is 
usually most marked, and retention of secretion is most apt to occur. The respi- 
ratory murmur in some places may be quite obscured by the rales. Otherwise it 
is vesicular, sometimes exaggerated, sometimes rough and indefinite. Expiration 
is usually prolonged. The respiratory murmur may be much diminished, or 
even entirely suppressed in places where the bronchi are stopped by secretion, 
which happens most frequently in the lower lobes. 

Except in mild cases, we usually distinguish several different forms of chronic 
bronchial catarrh, which may run into one another. 

1. The dry chronic catarrh (catarrhe sec of Laennec) is the form in which the 
mucous membrane has only a very slight secretion. The cough is usually very 
troublesome and labored, but the patient raises only a little tough sputum, or 
none at all. On auscultation we hear sibilant rhonchi, but no moist rales. This 
form of catarrh is usually associated with pulmonary emphysema, and asthmatic 
attacks are also frequent. The disease is stubborn and usually lasts for years. 

2. The so-called bronchial blennorrhoea is that form of chronic bronchitis in 
which we find a very copious secretion from the mucous membrane. The cough 
is therefore associated with a very abundant and quite thin expectoration, the 
amount of which in the twenty-four hours may exceed a pint (half a litre). The 
expectoration runs together in the sputa-cup and usually separates on standing, the 
more purulent portion sinking to the bottom, and the sero-mucous portion, which 
is usually frothy on the surface, remaining at the top. Numerous moist rales are 
heard in the lungs, especially in the lower portions. These diminish if large 
amounts of sputum are coughed up. Anatomically, the bronchi are almost always 
found dilated in this form of chronic bronchitis. 

3. The so-called serous bronchorrhoea (" catarrhe pituiteux v of Laennec) is 
quite rare but very interesting. It is characterized by the expectoration of a very 
large amount of frothy, purely serous, thin sputum. The cough usually comes on 
in very violent paroxysms which last from half an hour to an hour or more. 
The respiratory symptoms are quite severe, especially during these attacks, and 



140 



DISEASES OF THE RESPIRATORY ORGANS. 



have given rise to the old and useful term "asthma humidum" The expec- 
toration collected in twenty-four hours may amount to one or two quarts (litres). 
Examination of the lungs usually gives very abundant and extensive moist rales. 
The resonance on percussion is normal or a little diminished, from the accumula- 
tion of secretion. 

The special cause of this peculiar disease is quite obscure. It is either an 
independent, very chronic trouble, which may last for years with a varying course, 
or it may occur secondarily in other affections, especially in chronic contraction of 
the kidney. Wo once saw a very severe case of the independent and apparently 
quite uncomplicated form in a young woman who had high fever at various 
times, and who was much broken down physically. 

Course of the Disease. — The course of most chronic bronchial catarrhs is very 
protracted. The disease usually has frequent remissions and fresh exacerbations. 
The patient is tolerably well in the pleasanter time of the year if he takes good 
care of himself, but in autumn and winter, or after exposure to various noxious 
influences, the catarrh grows worse and the patient's symptoms increase. If the 
disease has lasted for years, we usually find symptoms in the lungs, like emphy- 
sema or chronic tuberculosis, or in the heart, like secondary dilatation and hyper- 
trophy of the right ventricle, which symptoms gradually become more severe. 
The details of these conditions are to be found in the appropriate sections. 

Diagnosis. — The diagnosis of chronic bronchitis is not difficult in itself, and 
may easily be made by considering the patient's symptoms and by judging of the 
result of the physical examination. We must always consider, however, whether 
bronchitis is not a result or a complication of some other chronic disease. There- 
fore in every case of chronic bronchitis the heart and the urine must be carefully 
examined, as well as the lungs. 

Prognosis. — Chronic bronchitis is in most cases a very stubborn affection which 
frequently shows improvement, but from which complete recovery is rare. The 
prognosis also depends greatly upon the patient's circumstances and upon the 
possibility of his taking care of himself and avoiding all harmful exposure. In 
secondary bronchitis the question whether the bronchitis is capable of material 
improvement or not of course depends mainly upon the prognosis of the primary 
disease. 

The danger in primary chronic bronchitis comes from the final development 
of its sequelae, especially from the gradual appearance of pulmonary emphysema, 
dilatation of the heart, etc. 

Treatment. — The only hope of success in severe cases in any method of treat- 
ing chronic bronchitis is in removing the patient completely, at least for a time, 
from the action of injurious influences. The favorable action of the baths and 
health resorts that are employed depends largely upon this, that patients enjoy in 
them complete bodily rest and are far better protected from dust and the changes 
in the weather than at home. We must make the patient comprehend the neces- 
sity of this condition as the basis of any other treatment. If he can not go to a 
suitable climate during the cold season, he must keep his room in all unpleasant 
weather, but at other times he may be permitted to stay in the open air. Further- 
more, the patient must be warned to avoid as completely as possible those harm- 
ful influences which his calling and manner of life entail, and among which 
especially is the bad air in our inns and restaurants. Food should be easily 
digestible and, in people inclined to corpulence, sparingly taken. Alcohol is to 
be permitted only in a moderate degree. We combat the tendency to constipa- 
tion, which is often present, by dietetic remedies, by taking fruit, especially grapes, 
prunes, etc., honey, Graham bread, or by mild laxatives, like the bitter waters, 
Friedrichshall, Ofner, etc. 



CHEONIC BEONCHITIS. 



141 



If the circumstances of the patient permit and his condition requires it, we 
should send him south in the autumn in order to avoid the evils of a northern 
winter. The rule is to send patients with a bronchial catarrh when there is much 
secretion to health-resorts with a dry climate — for example, to the western Eiviera, 
San Eemo, Bordighera, Mentone, Cannes, etc. The somewhat dry yet cooler 
climate of Meran, Gries, or Arco is suitable for patients with a stronger constitu- 
tion. Patients with dry bronchitis usually find themselves at their best in a 
warm but not too dry climate. If we wish to be sure of avoiding the winters 
cold, we must choose Sicily, Egypt, or Madeira for a residence. Of the more 
northern winter resorts we may mention here places on the eastern Eiviera, 
Nervii, Spezzia, etc., except Venice, Pisa, or Eome. 

We must recommend especially, in bronchitis, a suitable summer residence 
outside of large and dusty cities. Any private country residence in a well-wooded 
and protected place is of advantage. If we wish to send patients to a bath, 
Marienbad, Kissingen, or Homburg are proper places for corpulent people who 
also suffer from digestive disturbances, while we may send weaker patients to 
Ems, Soden, Badenweiler, Ischl, or Eeichenhall. Milk cures, whey cures, and 
grape cures are also prescribed in many cases of chronic bronchitis, the milk cure 
in particular for weak and anaemic individuals. A summer residence on the sea, 
best on the Baltic, is very serviceable for many patients with bronchitis. 

The inhalation treatment is much employed in chronic bronchitis, but we 
should not cherish too high hopes from its use. The best inhalations in dry 
catarrhs are simple steam, a two-per-cent. solution of common salt or bicarbonate 
of sodium, Ems water, etc. In cases with marked secretion, inhalations of oil of 
turpentine are most to be praised. The simplest way is to pour a teaspoonf ul of 
oil of turpentine into hot water and inhale the vapor as it arises. The so-called 
turpentine-pipe, however, is more convenient and more efficacious. This consists 
of a flask, which is filled to the height of several inches with water and then with 
a layer of oil of turpentine some two centimetres thick. Two glass tubes, open at 
both ends, are passed through the cork. One straight tube extends down into the 
layer of water ; the lower end of the other is free in the upper part of the flask. 
The outer portion of this last tube is long enough to be bent at an angle and forms 
the mouth-piece of the pipe which the patient sucks. He thus breathes the air 
which is filled with turpentine vapor. We have treated many patients in this 
way, who, for a number of hours a day, " smoked " their turpentine-pipes. 

In the treatment of chronic bronchitis much use is made of the "pneumatic 
treatment," * that is, the inhalation of artificially compressed air, or the expiration 
into rarefied air by the aid of the transportable pneumatic apparatus (Walden- 
burg, etc.). In many cases the results are not unfavorable, but they should not 
be overestimated. Special pneumatic cabinets have also been constructed in 
many places, such as Ems and Eeichenhall. 

The different alkaline mineral waters — Seltzer, Ems, Victoria, etc. — are next to 
be mentioned among internal remedies, which may also be used efficaciously at 
home. The numerous expectorants, like ipecac and apomorphine, are especially 
valuable in dry bronchitis. In bronchial blennorrhcea we know empirically 
that the internal use of balsams causes a distinct diminution of the secretion. 



* Details of the pneumatic treatment may be found in the following works: E. v. Vivenot, Jr., 
" Zur Kenntniss der physiologischen Wirkungen und der therapeutischen Anwendung der ver- 
dichteten Luft," Erlangen, 1868. "Waldenburg, "Die pneumatische Behandlung der Bespirations- und 
Cireulationskrankheiten," Berlin, 1880. Knauthe, " Handbuch der pneumatischen Therapie," Leip- 
zig, Wigand, 1876. Schnitzler, " Die pneumatische Behandlung d. Lungen- u. Herzkrankheiten," 
Wien, 1877 (40 Seiten). Oertel, " Handbuch d. respiratorischen Therapie " (v. Ziemssen's " Allg. 
Therapie," ii, 4), Leipzig, Vogel, 1881. 



142 DISEASES OF THE RESPIRATORY ORGANS. 



Oil of turpentine is the most active, and may be given internally in gelatine cap- 
sules, two or three capsules a day, or mixed with milk, in doses of ten or fifteen 
drops two or three times a day. Balsam of copaiba and balsam of Peru are also 
used internally. We should be very sparing of narcotics at first, but in severe 
cases we can not wholly dispense with them. 

[The iodide of potassium in doses of five to ten grains thrice daily is sometimes 
distinctly curative. An out-door life, free diet, moderate alcoholic stimulus, 
tonics, and woolen clothing do much to promote recovery.] 

Local applications to the chest in the form of embrocations, mustard plasters, 
dry cups, or cold, wet compresses are to be used, especially with severe dyspnoea, 
or with pain and a feeling of oppression in the chest. Regular cold sponging of 
the chest serves to harden and strengthen the patient. 

Warm baths are very well borne by many patients with chronic bronchitis. 
Sometimes, too, vapor baths, if taken with caution, may be of service, especially in 
strong and corpulent patients. 

In all secondaiy chronic catarrhs our chief attention, beyond the symptomatic 
treatment of the bronchitis, must be directed to the treatment of the underlying 
disease. If we succeed in once more regulating the heart's action where there is 
uncompensated heart disease, or in establishing diuresis where there is renal dis- 
ease, we may also in that way cause improvement in the existing bronchial 
catarrh. 



CHAPTER III. 

FCETTD BRONCHITIS. 

{Putrid Bronchitis.) 

iEtiology. — By putrid or foetid bronchitis we mean that form of bronchitis in 
which the secretion of the mucous membrane undergoes a putrid decomposition, 
and in which, consequently, the expectoration takes on a peculiar and extremely 
foul odor. The cause of foetid bronchitis is usually the entrance of the bacteria 
of putrefaction into the bronchi by means of the inspired air. Only in rare cases 
does it arise from a pulmonary gangrene of embolic origin {vide infra). 

The opportunity for the agents of putrefaction to enter the bronchi with the 
inspired air is of course often given, but a foetid bronchitis naturally is excited 
only when they can remain there and increase. Their retention and their further 
development is chiefly favored, as we know, by diseased conditions which already 
exist in the bronchi. A great number of cases of foetid bronchial catarrh there- 
fore develop secondarily upon other pulmonary affections of longer standing. 
Thus the expectoration may quite suddenly change and take on a foetid character 
in the course of a chronic or rarely of an acute bronchitis or of phthisis. Bron- 
chiectasis {vide infra) greatly favors the development of this putrid change, for 
in it the retention and stagnation of large amounts of secretion furnish the aid 
and occasion for it. If a putrid decomposition of the secretion begins in one part 
of the bronchial system, the further extension of the process follows from direct 
infection. 

In rare cases putrid bronchitis also develops in lungs which were apparently 
previously sound — primary foetid bronchitis. 

Symptoms and Course ; Anatomical Changes.— If a foetid bronchitis arises in 
the course of some other chronic pulmonary disease, its appearance may be marked 
by a sudden impairment of the general condition, by high fever, often associated 



FCETID BEONCHITIS. 



143 



with numerous chills, and by an increase of the thoracic symptoms, like pain and 
cough. The change in the expectoration, the peculiarity of which was first 
accurately described by Traube, is most characteristic. There is a most repulsive, 
sweetish, putrid smell. The expectoration is usually quite abundant ; the con- 
sistency is rather thin. On standing, the sputum shows a very marked division 
into three layers. The upper layer consists of a very frothy, muco-purulent 
stratum, consisting in part of individual masses, from which a number of coarser 
or finer fibers float down into the middle layer. This middle layer consists of a 
dirty-green muco-serous fluid. At the bottom of the vessel is found the third 
layer, which is often the thickest, and is composed entirely of pus. It consists of 
pus-corpuscles which have sunk to the bottom, and is of rather a thin, greasy con- 
sistency. With the naked eye we generally recognize a number of little whitish- 
gray plugs and particles in it. These so-called " Dittrich's plugs," which are easily 
crushed under a cover-glass, are quite characteristic. Microscopically, they con- 
sist of decomposed pus-corpuscles, detritus, and bacteria, and usually contain 
very many needles of fat acids arranged in bundles (see Fig. 19). 

We often find also in the sputum large masses of fungi, especially great 
bunches of twisted leptothrix fibers, which, by an unpracticed eye, may readily be 
mistaken for elastic fibers. The latter are, of 
course, never found in the expectoration of a 
simple foetid bronchitis, but only in the deep- 
seated, destructive processes in the lung, like 
gangrene. On chemical examination of the 
sputum, the ordinary products of putrefaction 
may be found, volatile fat acids, especially 
butyric and valerianic acids, also sulphuretted 
hydrogen, leucine, tyrosine, etc. 

The breath of the patient, as well as the 
sputum, is very often foul-smelling, and so 
offensive that he becomes a burden to his asso- 
ciates. Fig. 19.— Crystals of fat acids. 

The signs which foetid bronchitis gives on 
physical examination are those of an ordinary bronchitis. In a great number of 
cases we also find signs of consolidation and contraction of the lung, of pleurisy, 
etc., which do not belong to foetid bronchitis as such, but are due to complications 
or sequelae. 

The most frequent of these sequelae is the development of a " reactive " lobular 
inflammation, a pure pneumonia, which follows a catarrh which has attacked the 
finer bronchi. These pneumonias frequently run into gangrene, so that we very 
often find a number of larger or smaller nodules of pure gangrene beside the ex- 
tensive foetid bronchitis in the lungs. In many of these cases the foetid bronchitis 
is certainly the primary process, and the development of the nodules of gangrene 
is secondary ; yet we shall see later that the reverse may also be true. Foetid bron- 
chitis and gangrene of the lungs run into each other so often, both clinically and 
anatomically, that there is no sharp line to be drawn between them. If the 
nodules are superficial, and reach the pleura, the infection attacks this, and we 
have a purulent, or even an ichorous pleurisy. 

The smaller and medium-sized bronchi are almost always found in a condition 
of cylindrical dilatation in old foetid bronchitis. Their mucous membrane is in- 
tensely inflamed, and often ulcerated superficially. On its surface we see in the 
cadaver the greasy purulent masses and the plugs which we find in the expectora- 
tion during life. 

Whatever may be the case with the general course of foetid bronchitis, its 




144 



DISEASES OF THE EESPIEATOEY OEGANS. 



beginning is often quite sudden and acute, both, in the primary and in the second- 
ary cases, as we have said. The patient is attacked with fever, which may often 
be quite high, and with a stitch in the side, and cough, and expectoration. Later, 
the characteristic peculiarities described above appear. The further course of the 
disease is almost always very chronic, lasting for years, but subject to many 
variations. Very often manifest improvement, and even apparent recovery, takes 
place, until suddenly there is a new attack of fever and thoracic symptoms. The 
general condition and nourishment of the patient may be quite good for a long 
time, except during the periods of marked exacerbation of the disease. Patients 
with chronic foetid bronchitis often appear somewhat bloated, but also pale and 
slightly cyanotic. Peculiar clubbed thickenings of the terminal phalanges of the 
fingers gradually develop, as in many cases of bronchiectasis. Slight oedema 
of the lower extremities is also sometimes present. 

Symptoms referable to other organs may be wholly absent. We see most 
frequently disturbances of the stomach, loss of appetite, and nausea, which proba- 
bly comes from swallowing the foetid sputum. Patients also complain of occa- 
sional rheumatic pains in the muscles and joints, which may perhaps be due to an 
absorption of septic matter. 

The danger of the disease lies in the possible extension of the process to 
the lungs in the development of pulmonary gangrene and its sequelae. We 
hardly ever find a simple foetid bronchitis in the cadaver, but we almost 
always see other processes besides, which have been mentioned above — reactive 
pneumonia, pulmonary gangrene, etc. These processes develop very readily, 
and make very rapid progress in old, decrepit people, who live under bad 
external conditions, and in whom putrid processes in the lungs are very often 
present. 

The diagnosis of foetid bronchitis is not difficult in itself, for the diagnosis of a 
putrid process in the lung may be made from the stinking sputum alone. It is 
often a hard question to decide whether we have to do merely with a foetid bron- 
chitis, or with a pulmonary gangrene also, and we often can not answer this 
question with certainty. Decisive indications of gangrene are derived from 
physical examination, dullness, bronchial respiration, and large, moist rales, 
and also the discovery of elastic fibers and fragments of parenchyma in the 
expectoration. 

The prognosis must be made with care in every case of foetid bronchitis. If 
the external circumstances of the patient are favorable, he may remain in toler- 
able health for years. We must always be prepared for the appearance of new 
exacerbations of the disease and of affections of the lung itself. 

Treatment. — The chief aim of treatment must be to bring the putrid processes 
in the bronchi to a stand-still by the death of the agents of putrefaction. The 
difficulty of fulfilling this task lies in the impossibility of getting the disinfecting 
material to act on the bronchial mucous membrane in the necessary amount and 
concentration. Nevertheless, we can, without doubt, at least relieve a foetid bron- 
chitis and keep it in check by the judicious use of inhalations. Inhalations of a 
two-per-cent. solution of carbolic acid are most useful, given for five or ten min- 
utes several times a day. These, however, are sometimes not well borne if long 
continued, and they may excite mild symptoms of carbolic poisoning — like head- 
ache, malaise, and dark carbolic urine. We have often used with good results 
the " carbolic mask " recommended by Curschmann, a kind of respirator fastened 
in front of the nose and mouth, containing cotton in a special receptacle impreg- 
nated with carbolic acid, equal parts of carbolic acid and alcohol, or other remedies 
like turpentine or creasote. Many patients can wear these masks, with occasional 
interruptions, for many hours a day. Turpentine is most used next to carbolic 



CROUPOUS BRONCHITIS. 



145 



acid. Both inhalations and the internal exhibition * of turpentine are of distinct 
value. We may also try acetate of lead internally, one or two grains (grm. 
0*05-0 "10) in powder every two hours. 

In other respects all the general hygienic and symptomatic methods of treat- 
ment recommended for common chronic bronchitis are also useful in foetid bron- 
chitis. The sputum should be disinfected by putting strong carbolic acid, chloride 
of lime, etc., into the sputa-cup to lessen the bad odor for the attendants. It is a 
very good plan to keep the carbolic spray at work in the patient's room as often 
and as long as possible. 



CHAPTER IV. 

CROUPOUS BRONCHITIS. 

(Fibrinous or Pseudo-membranous Bronchitis.) 

CROUPOUS bronchitis is a peculiar form of disease of the bronchial mucous 
membrane, of very rare occurrence, in which there is a formation of extensive 
fibrinous patches in the bronchi. Only that form of croupous bronchitis which 
occurs primarily in the bronchi is to be considered here, and not the secondary 
form, which on the one side is associated with diphtheria in the pharynx and 
larynx, and on the other with croupous pneumonia. 

The aetiology of the disease is as yet wholly unknown. From analogy with 
other well-known croupous inflammations of mucous membranes, we must look 
here for some noxious influence which destroys the epithelium, but up to this time 
we are entirely ignorant of its character. Individuals in youth and middle age, 
somewhere between ten and thirty years of age, are the chief victims. Men are 
attacked somewhat more frequently than women. The disease comes on either 
in people who were previously healthy — the essential croupous bronchitis ; or in 
people who have already suffered from some other disease, especially some chronic 
pulmonary affection — the symptomatic, secondary croupous bronchitis. It is not 
certain whether the last-named cases can have the same serological relation as 
the cases of pure primary fibrinous bronchitis. Fibrinous bronchitis has been 
observed in the course of typhoid fever. 

Symptoms and Course. — Primary fibrinous bronchitis occurs in two forms, 
acute and chronic. The acute form begins quite suddenly with fever, cough, pain 
in the chest, and severe dyspnoea which speedily develops. The fibrinous coagula, 
which alone render the diagnosis possible, appear in the expectoration either at 
once or after the existence for some days of what is apparently simple catarrhal 
bronchitis. 

These coagula form complete casts of the bronchi, and are more or less branch- 
ing. They are of a whitish color and of quite a dense, elastic consistency. The 
main stem may be a centimetre thick, and from it the further ramifications 
branch, dividing dichotomously. The largest casts are ten or fifteen centimetres 
long. On section, we usually find a free lumen within, and generally recognize a 
definite laminated structure in the membrane. In many places they are enlarged 
and swollen. Microscopically, we find white blood-corpuscles in and near the 
hyaline substance, and also red blood-corpuscles, sometimes epithelial cells, and 
quite often the peculiar pointed octahedral crystals which are also found in the 
expectoration in bronchial asthma {vide infra). The so-called "spirals" (vide 



* From a communication of Lepine, turpin, a hydrate of turpentine, seems to be more eifective than 
turpentine, in doses often to twenty-five grains (grm. 0-5-1-5) a day. 

10 



146 



DISEASES OF THE RESPIRATORY ORGANS. 



infra) have also been found in the expectoration of fibrinous bronchitis. Chem- 
ically the casts consist of coagulated albumen. Their solubility in alkalies, espe- 
cially in lime-water, is of therapeutic importance. 

On coughing, the patient usually raises a simple mucous or muco-purulent 
expectoration beside the casts, and in this sputum the casts are imbedded. They 
are often first discovered by pouring the whole amount of "sputum into water, 
when they unfold and spread out. The expectoration also contains not infre- 
quently a slight admixture of blood. 

The subjective symptoms of the patient may be very violent. The dyspnoea 
sometimes attains a high and alarming degree. It ceases when a large cast is 
expectorated after a severe paroxysm of coughing. Such attacks may recur every 
day or two. In other cases, however, the subjective symptoms are comparatively 
slight. 

Physical examination of the lungs gives little that is characteristic. In uncom- 
plicated cases percussion gives nothing abnormal, or at most the signs of an 
acute emphysema. Auscultation gives the ordinary signs of bronchitis, not char- 
acteristic in themselves, such as rhonchi, or moist rales. If a large bronchus 
is plugged, the respiratory excursions and the respiratory murmur are almost 
entirely absent in the corresponding portion of the lung, but after the expectora- 
tion of a cast the murmur once more becomes audible. 

The duration of acute cases is sometimes only a few days, at most a few weeks. 
In favorable cases the fever, which at times is quite high, soon disappears, the 
respiratory symptoms grow milder, the expectoration of the casts ceases, and there 
is a complete and permanent recovery. In severe cases, however, death often 
ensues with all the symptoms of suffocation. The acute form sometimes becomes 
chronic, but this is rare. 

The chronic form of fibrinous bronchitis may last for years. Usually the con- 
dition grows worse periodically, at varying intervals of time, and at each exacer- 
bation casts are expectorated, while in the interval there is apparently merely a 
simple bronchial catarrh. Some observations are also recorded in medical litera- 
ture of people who have expectorated these casts at intervals for years without any 
special disturbance of their health or then nutrition. In some cases other chronic 
pulmonary affections, like tuberculosis, finally develop. 

The pathological anatomy of fibrinous bronchitis is not yet satisfactorily 
known on account of the rarity of the affection. The changes in the lungs found 
at the autopsy of fatal cases have usually been complications, like pneumonia, 
pleurisy, or tuberculosis, which stood in no direct relation to the fibrinous bron- 
chitis. A loss of epithelium has been discovered in some cases in the parts of the 
bronchial mucous membrane that were attacked. 

Prognosis. — In all acute cases the prognosis should be guarded, for we know 
that about one fourth of the cases terminate fatally. The chronic cases, as has 
been said, are usually very protracted and are subject to frequent recurrences, 
but they differ from the acute cases in being much less dangerous. 

Treatment. — We make special use for inhalations of those remedies which, as 
we have said, are able to dissolve the casts. We usually employ a two-to-five-per- 
cent, solution of carbonate and bicarbonate of sodium, and above all lime-water, 
either alone or diluted with an equal volume of water. The internal administra- 
tion of iodide of potassium, in doses of twenty to forty-five grains (grm. l'S-S'O) a 
day, proves of advantage in many cases. Energetic inunction with mercurial 
ointment is sometimes of service. Expectoration of the casts may be aided in many 
cases by the timely use of emetics. We do not know any remedies which are 
able to prevent a return of the attacks in the chronic form. The treatment, except 
at the time of the attacks, is the same as in ordinary chronic bronchial catarrh. 



WHOOPING-COUGH. 



147 



CHAPTER V. 

WHOOPING-COUGH. 

(Pertussis. Tussis convulsiva.) 

JEtiology. — By the name " whooping-cough " we mean a specific disease of the 
mucous membrane of the air-passages which is chiefly seen in children and is 
characterized by a peculiar violent and paroxysmal cough. Sporadic cases are of 
almost constant occurrence in large cities, but the disease often appears in epi- 
demic outbreaks. Epidemics of whooping-cough follow epidemics of measles with 
remarkable frequency. 

Whooping-cough is without doubt contagious, and therefore often attacks one 
child after another in the same family. Kindergartens, orphan-asylums, and nur- 
series aid very much in extending the disease. The contagious element seems to 
be connected with the air expired by the patient, particularly with the secretion 
from the mucous membrane expectorated after coughing. Children are most 
subject to an attack up to the age of six years ; from that age the disposition to 
the disease decreases rapidly with increasing years. Whooping-cough is seen, 
indeed, in adults, but it is quite rare, and almost always comparatively mild and 
rudimentary. 

The epidemic onset, the contagiousness, and the whole course of the disease 
favor the theory of its infectious nature. The presence of the organisms, which 
are supposed to be the poison of the disease, has not yet been certainly demon- 
strated, although many have claimed to discover characteristic organisms in the 
sputa of patients. These statements, however, all conflict, and lack well-attested 
and methodical proof. If a patient has once had the disease, he is almost inva- 
riably secure against a new attack. 

Symptoms and Course of the Disease. — Whooping-cough begins with the symp- 
toms of a catarrh of the trachea and bronchi, which develops more or less rapidly 
and which at first often shows nothing characteristic. We can at this period 
make a tolerably probable diagnosis only at a time when an epidemic is prevailing, 
or in case the child's associates have already been attacked with the disease. The 
cough is often quite severe at the beginning, but it does not yet come on in dis- 
tinct paroxysms. Examination of the chest shows nothing peculiar except a few 
rhonchi. There is often a coryza, with frequent sneezing, and there is sometimes 
a mild conjunctivitis. The child is restless and feverish, especially toward night. 
The temperature may repeatedly reach 103° or 104° (39°-40° C.) in this initial 
fever. The duration of this first so-called catarrhal stage varies, but it usually 
lasts a week or ten days. 

The catarrhal stage gradually passes into the second, convulsive stage, without 
any sharp boundary. The cough becomes more violent and comes on in the 
separate paroxysms of whooping-cough which are characteristic of the disease. 
We do not know the particular reason why the cough has this paroxysmal char- 
acter, but a nervous factor probably plays the chief part in it. 

The peculiarity of the attack consists in the violent, paroxysmal fits of cough- 
ing, which are from time to time interrupted by deep, long-drawn, loud, and 
shrill inspirations, due to the occurrence of a spasmodic contraction of the glottis. 
The child becomes markedly cyanotic during the attack, the veins in the neck 
swell, and tears come into the eyes. Haemorrhage into the conjunctiva, nose- 
bleed, and in some cases haemorrhages into other organs, like the ear, the skin, 



148 



DISEASES OF THE EESPIEATOEY OKGANS. 



and the brain,* often come on as a result of this stasis. Vomiting very often 
occurs either during a paroxysm or at its close. Involuntary evacuations of urine 
and fasces may also follow from the violent contraction of the abdominal muscles. 
Exceptionally we observe still more severe symptoms with a paroxysm ; a com- 
plete spasmodic cessation of respiration with imminent danger of suffocation, or 
sometimes general convulsions. 

The paroxysms vary with the severity of the disease, frequently appearing 
ten or fifteen times in twenty-four hours ; sometimes with greater frequency — 
fifty times or more. They also occur at night as often or even oftener than in 
the daytime. They come on either spontaneously or from some special predis- 
posing cause. We may, for example, excite a paroxysm artificially by pressing 
on the larynx or by making the child cry. If there are several children with 
whooping-cough in the same room and a paroxysm attacks one of them, the 
others, as a rule, soon begin to cough too. Some prodromal symptoms often pre- 
cede the peculiar paroxysm, such as general uneasiness, rapid respiration, or 
vomiting. At the end of a paroxysm many children remain very feeble and 
exhausted, but others recover very rapidly and are playing again quite briskly a 
few minutes after. 

In general the child feels quite well in the interval between the paroxysms, 
but the effects of the violent attacks of coughing may of course often be seen. 
Beside the occasional haemorrhages into the conjunctiva, we find the eyelids 
somewhat swollen, their veins dilated and blue, and showing through the skin. 
A small ulcer is quite frequently formed on the frasnum of the tongue, the 
origin of which is to be referred to mechanical causes. The tongue is violently 
protruded in the severe paroxysms of coughing, and the frasnum is thus pulled or 
torn, or injured by the sharp lower incisors. 

Physical examination of the lungs shows nothing abnormal in uncomplicated 
cases except a few moist rales or rhonchi. Sometimes the rhonchi are wanting or 
are present in small numbers only a short time before a paroxysm, but in other 
cases an intense diffuse bronchitis is developed, which often leads to the develop- 
ment of a lobular pneumonia (vide infra). 

The fever, which is usually present in the first or catarrhal stage, is absent in 
the convulsive stage. The child is free from fever for the most part. We often 
find a slight rise of temperature up to 100° or 101° (38°-38'5° C), but only toward 
night. Higher and more persistent fever points to the development of complica- 
tions, especially on the part of the lungs. 

The convulsive stage seldom lasts less than three or four weeks, and often 
much longer, up to three or four months. The paroxysms gradually become less 
frequent and less violent (stadium decrementi), until they finally disappear 
entirely ; but relapses and fresh exacerbations also occur in this stage. Finally, 
however, the disease, in uncomplicated cases, goes on to a permanent and com- 
plete recovery. 

Complications and Sequelae. — The severe results which sometimes follow whoop- 
ing-cough are probably only partly due to the direct action of the specific causes of 
the disease, and partly also to complications of a secondary nature whose origin is 
merely favored by the whooping-cough. The most important are complications 
in the lungs. A lobular, catarrhal pneumonia often develops after a severe 
bronchitis which involves the finer bronchi. In such cases the respiration becomes 
hurried and superficial, the fever higher, and the general condition worse even 
in the times between the paroxysms. On examination of the lungs, we hear 



* Not long ago we observed the very rare occurrence of a hemiplegia during a paroxysm of whoop- 
ing-cough. 



WHOOPING-COUGH. 



149 



numerous moist rales, especially over the lower lobes, and we can sometimes make 
out dullness on one or both sides if there is extensive pneumonic infiltration. 
Such cases are always very protracted, and many children succumb, partly from 
the disturbance of respiration and partly from general weakness and inanition. 

Complications in other organs are much rarer. Among the most frequent are 
attacks of diarrhoea which exhaust the child's nutrition. Many observers have 
also mentioned the quite frequent occurrence of a croupous or diphtheritic 
inflammation in the pharynx and larynx in the course of whooping-cough. 
Finally, a case under our own observation may here be mentioned, in which 
death occurred with severe nervous symptoms, convulsions, and coma. At the 
autopsy very numerous capillary haemorrhages were found in the brain. 

Pulmonary emphysema is the first thing to be mentioned among the sequelae 
of whooping-cough. Prom the marked pressure which the severe and frequent 
outbursts of coughing exert from within upon the alveoli of the lungs, they gradu- 
ally become dilated. An acute lobular emphysema ("acute pulmonary infla- 
tion ") is set up which sometimes passes into a typical chronic pulmonary emphy- 
sema {vide infra). Chronic bronchial catarrh may also remain for a long time 
after an attack of whooping-cough. 

A third important sequel of whooping-cough is pulmonary tuberculosis. The 
bronchitis and lobular pneumonia which occur during a whooping-cough some- 
times do not improve, especially in weak children with a tubercular tendency. 
The fever continues high, the child grows thin, and constantly becomes more and 
more miserable. At the autopsy we find cheesy nodules in the lungs, cheesy bron- 
chial glands, and at times tuberculosis of other organs. These cases signify that 
when a tubercular infection is present, but is still latent, the whooping-cough acts 
as an exciting cause for the outbreak of the disease, or that a greater receptivity 
to infection with tubercular poison is created by the whooping-cough. 

The diagnosis of whooping-cough can not be made with certainty, as we have 
said, until the second or convulsive stage. It is easy then, however, since the 
characteristic attacks occur in no other affection of the lungs in like manner 
and with like frequency and duration. If we have no opportunity to observe the 
attack itself, and have to depend upon the description of the friends, the diagnosis 
is sometimes more uncertain. In such cases, however, certain signs are often 
present : the child has a bloated aspect, or we may find slight haemorrhages into 
the conjunctiva, or ulcers on the fr3enum of the tongue, which make the diag- 
nosis highly probable. Under some circumstances we may also make the attempt 
to bring on the paroxysm artificially {vide supra). 

The prognosis is favorable with the majority of children if they are previously 
strong and healthy. Very young children are in more danger than older ones. 
There is danger if secondary pneumonia develops and if the general nutrition and 
strength of the child suffer. As soon as the diagnosis is certain we must call the 
attention of the parents to the probable long duration of the disease. Attention 
must also be paid to the possibility of the development of sequelae, especially in 
weak children suspected of tuberculosis. 

Treatment. — Since the disease is protracted and is not devoid of danger, it is our 
duty, when an epidemic of whooping-cough prevails, to guard children from it as 
far as possible. If one child in a family is taken ill, the other children must be 
rigorously kept away from him. If circumstances permit, we should prefer to 
send them away to another place free from whooping-cough. 

The treatment of the disease itself has unfortunately produced no very favora- 
ble results up to the present time. The number of " specifics " employed is very 
great, but none of them have proved their specific quality by shortening the dura- 
tion of the disease. Of late we have tried chiefly inhalations, especially inhala- 



150 



DISEASES OF THE RESPIRATORY ORGANS. 



tions of a one- or two-per-cent. solution of carbolic acid, for the purpose of com- 
bating the infectious nature of the disease. Sometimes, indeed, this seems , to be 
of some service. We may also try turpentine, benzine, twenty or thirty drops on 
a sponge wet with hot water, and similar remedies. Of internal remedies, qui- 
nine and belladonna or atropine have won the most repute. Quinine is to be 
tried in five- or ten-grain powders (grm. 0'3-0"5) twice a day in older children. 
It should be used, if possible, at the beginning of the disease. We give belladonna 
in powders, extractum belladonnas, gr. T ^ to % (grm. 0 '005 -0*01) at a dose, three to 
five times a day. We may at the highest reach one sixtieth of a grain (grm. 
0 *001) of sulphate of atropine a day with children, although care and attention 
are needful to avoid the appearance of symptoms of poisoning, dilated pupils and 
dry mouth. We can not do without narcotics in severe and frequent attacks. 
Small doses of morphine or chloral may be used with care. Inhalations of chlo- 
roform and ether have also been used after this formula : 

^ Chloroformi 30; 

^Etheris sulph 60; 

01. terebinth, rect 10. 

M. One to two teaspoonfuls inhaled from a towel. 

The internal use of bromide of potassium may sometimes mitigate the paroxysms, 
in doses of fifteen to forty-five grains (grm. l'0-3*0) a day. 

Beside employing the remedies mentioned, certain hygienic directions must 
be given to the parents. The child must be kept in the best and purest air pos- 
sible. In summer it should be taken out of doors a great deal if there is no 
fever. City children should be sent to the country in summer if possible. Beside 
that, we should take care that the child has good strengthening food. Frequent 
warm or tepid baths are highly to be recommended, especially when there is a 
severe bronchitis, in order to avoid as far as possible the danger of the develop- 
ment of lobular pneumonia. 

The complications and sequelae are to be treated according to the usual rules. 



CHAPTER VI. 

BRONCHIECTASIS. 

(Bronchial Dilatation.) 

Dilatation of the bronchi is not a separate disease, but it is a result of various 
affections of the lungs and bronchi. Nevertheless, we will speak of it briefly in 
this connection since many cases of bronchiectasis present the appearance of quite 
a characteristic disease. 

We distinguish anatomically the cylindrical and saccular bronchiectases. 

Cylindrical bronchiectasis consists of a uniform dilatation of a bronchial tube, 
and occurs most frequently in the medium-sized, or rarely in the finer bronchi of 
one or more lobes of the lung. It is usually due to a long-continued bronchitis, 
and develops most frequently in cases of emphysema, and also in, whooping- 
cough, measles, and sometimes in phthisis, etc. The primary process is probably 
always the atrophy which follows the catarrh, and the diminished resistance of 
the bronchial walls thus occasioned. The dilatation of the lumen of the bronchus 
is produced gradually, partly by the traction of the thorax during inspiration, 



BRONCHIECTASIS. 



151 



and still more by the increased pressure in the bronchi due to the frequent and 
violent fits of coughing, and finally, perhaps, by the constant pressure of the 
stagnating secretion. 

The diagnosis of cylindrical dilatation of the bronchi is only a probable one. 
We suspect that a bronchiectasis has formed if the conditions are fulfilled 
which we know lead to it. In the chronic bronchial catarrh of emphysema we 
judge that there is cylindrical dilatation of the bronchi if the secretion is very 
abundant and comparatively thin, and separates on standing in a sputa-cup. The 
dilatation is usually emptied by a severe paroxysm of coughing, such as is apt to 
occur in the morning if the secretion collects in great quantity during the night. 
Physical examination usually gives numerous small and medium moist rales, 
especially in the lower lobes. The respiratory murmur sometimes loses its vesicu- 
lar character in marked cylindrical bronchiectasis, and has a more indefinite and 
tubular quality. 

Saccular bronchiectases are spherical or oval dilatations which are confined to 
a definite portion of the bronchial tube. They may attain a diameter of several 
centimetres. The bronchus passes suddenly or gradually into the dilatation, and 
it is often obliterated so that the bronchiectasis forms a completely closed cavity. 
The wall of a saccular bronchiectasis loses in great measure the character of a 
normal bronchial wall. As a rule it is atrophied to a high degree, the atrophy 
involving not only the mucous glands, but also the muscular fibers, the elastic 
elements, and even the cartilages, so that the bronchiectasic cavities seem lined 
with nothing but a thin membrane. In other cases, however, we find hyper- 
trophic processes, which involve the connective tissue of the mucous membrane, 
and lead to band-like projections and swellings. Finally, ulcerative processes 
may develop on the inner surface of a bronchiectasis and attack the surrounding 
lung-tissue and change the bronchiectasis to a typical ulcerating cavity. 

Only rarely, for example in emphysema, do we find a single saccular bron- 
chiectasis surrounded by tolerably normal lung-tissue. Its origin, then, is to be 
referred to causes like those which have been given above for the much com- 
moner cylindrical bronchiectases. In the great majority of cases we find saccular 
bronchiectases, singly or in large numbers, surrounded by indurated and con- 
tracted lung-tissue. They form one of the complications of "pulmonary con- 
traction " [fibroid phthisis], which is almost always associated with contraction of 
the pleura. Since Corrigan's day we have with good reason looked upon this con- 
traction as the chief cause for their origin. By the gradual shrinking and retrac- 
tion of the lung, which as a rule has become adherent to the costal pleura, a trac- 
tion is exerted upon the bronchial walls from without to which they gradually 
yield. Thus arises the frequent combination of pulmonary contraction with the 
formation of bronchiectases. This combination is usually unilateral, and involves 
the whole lung or only one of the upper or lower lobes. This form has been 
described from a histological stand-point as a chronic interstitial pneumonia, 
and it has been believed possible to make a sharp distinction between it and the 
chronic tubercular processes in the lung. 

We often see the form of pulmonary contraction in question developing as a 
result of pleurisy. Laennec first advanced the opinion that in such cases the 
pleurisy was the primary trouble, and that from it an interstitial inflammatory 
process attacked the connective tissue of the underlying lung and led to contrac- 
tion and then to the formation of bronchiectases. In our opinion we must indeed 
recognize the manifold anatomical and clinical peculiarities of the combination 
of pulmonary contraction and formation of bronchiectases in question, but aetio- 
logically we are unable to separate it from pulmonary tuberculosis {vide infra), at 
least in the great majority of cases. Only in very rare cases do we find a whole 



152 



DISEASES OF THE RESPIRATORY ORGANS. 



lung filled with saccular bronchiectases, separated from one another by an indu- 
rated tissue which is hardly anywhere normal, without finding somewhere the 
signs of a tubercular process. The origin of these changes is yet quite uncertain. 

The symptoms caused by saccular bronchiectasis alone are derived in part from 
the result of physical examination and in part from definite peculiarities of the 
sputum. If great bronchiectasic cavities lie near the chest-wall, they may give the 
same physical signs that we shall learn to recognize later in the description of 
tubercular cavities. Bronchiectases lying within the lung, however, are often 
devoid of definite physical signs, so that at most we may suspect them from 
other symptoms, like the retention of the sputum. The sputum, as a rule, is 
remarkably abundant, " expectoration by mouthfuls," and is raised in paroxysms ; 
it is of a thin, purulent consistency, it separates on standing, the more purulent 
part sinking to the bottom, and often takes on a foetid character from decompo- 
sition in the readily stagnating secretion. Since bronchiectasis may thus give rise 
to a foetid bonchitis, and since, on the other hand, as we have said, foetid bronchitis 
itself often leads to the formation of bronchiectasis, we can understand the mani- 
fold relations and changes which the two forms of disease described may furnish. 
If ulcerative processes arise in the wall of a bronchiectasis, they may give rise to 
haemoptysis. 

It is not always easy to distinguish between simple bronchiectasic and tuber- 
cular cavities. The presence of tubercle bacilli in the sputum is the only thing 
which is decisive for the latter, while, if they are constantly absent in spite of 
repeated examinations, tuberculosis is very improbable. Beside that, we must 
bear in mind that bronchiectasic cavities are quite frequently situated in the lower 
lobes, while tubercular cavities usually occur in the apices. 

The further course of bronchiectases depends of course upon the nature of the 
primary affection. The cylindrical dilatations which arise after a severe bron- 
chitis, as happens in whooping-cough, measles, or typhoid, may, in many cases, 
gradually get well ; but recovery from saccular bronchiectasis by a process of 
obliteration, if it occurs at all, is extremely rare. Nevertheless, the course of the 
disease may be comparatively benign, since the affection often remains circum- 
scribed and the patient's general strength and nutrition suffer comparatively little 
from it. Finally, of course, severe symptoms arise, either from insufficiency of 
the heart, when there is cyanosis, dyspnoea, or oedema, or as a result of emphy- 
sema, tuberculosis, gangrene, or other complications. 

The treatment is never directed against the bronchial dilatation as such, but 
toward its causes or sequelae. The treatment of bronchiectasis, therefore, coin- 
cides with the treatment of chronic bronchitis, emphysema, foetid bronchitis, 
chronic tuberculosis, etc. 



CHAPTER VII. 
STENOSIS OF THE TRACHEA AND BRONCHL 

1. Tracheal Stenosis. 

iEtiology. — Stenosis of the trachea may be caused either by diseases in the 
vicinity of the trachea, or by diseases of the trachea itself. The first-named 
method of origin is the more frequent. To this method are due all the stenoses 
of the trachea from compression. Enlargements of the thyroid gland from 
simple struma and new growths, aneurisms of the arch of the aorta and of the 
innominate artery, tumors and abscesses in the anterior mediastinum, swelling of 



STENOSIS OF THE TRACHEA AND BRONCHI. 



153 



the lymph-glands at the bifurcation of the trachea, abscesses on the anterior sur- 
face of the cervical vertebrae, etc., may exert so great a pressure on the trachea 
from without that its lumen is made narrower. Beside the direct action of press- 
ure in most cases, a gradual atrophy from the pressure and a softening of the 
rings of cartilage sometimes plays an important part, according to Rose, in the 
occurrence of stenosis. A collapse of the trachea may arise from this "flaccid 
softening," which may come on quite suddenly, and may cause many of the cases 
of sudden "scrofula death." 

Changes in the trachea itself leading to stenosis are quite rare. Cicatricial 
stenosis as a result of syphilitic ulcerations is relatively the most frequent. New 
growths in the trachea are also to be mentioned, such as polypi and carcinomata, 
the latter almost always having invaded the trachea from the adjacent parts. 
Very rarely acute and chronic inflammatory processes like perichondritis lead to 
a swelling of the mucous membrane sufficient to cause stenosis. In conclusion, 
we may mention that stenosis of the trachea may be due to the presence of foreign 
bodies. 

Symptoms. — A slight degree of tracheal stenosis may last for years without 
special symptoms. Marked stenosis, however, leads of course to a most painful 
state of dyspnoea. In many cases breathing is tolerably easy if the patient keeps 
perfectly still, but any physical exertion at once brings on dyspnoea. 

If the stenosis is so extreme that there is a real hindrance to respiration, a very 
striking modification of the breathing occurs. It is diflicult and labored, and is 
performed only by the help of the accessory muscles. Both expiration and inspi- 
ration are protracted, long drawn, and accompanied by a loud stridor. In many 
cases inspiration is more difficult than expiration, so that there is accordingly a 
preponderating inspiratory dyspnoea, and the number of respirations a minute is 
diminished. If the entrance of air into the lungs is incomplete in spite of the 
lengthening of the respirations, we see an inspiratory retraction of the lower part 
of the thorax, and sometimes of the throat and the supra-clavicular fossae. In 
tracheal stenosis the larynx, however, shows little or no to-and-fro movement on 
respiration. This fact is of value in diagnosis in distinguishing tracheal from 
laryngeal stenosis, for in the latter the respiratory movements of the larynx are 
quite well marked. 

"We sometimes notice in the pulse during inspiration a marked fall in tension 
and in the height of the pulse- wave, the pulsus paradoxus. With the sphygmo- 
graph we can show still more plainly the changes in blood-pressure, which vary 
quite markedly with the respiration. The frequency of the pulse is usually a little 
increased, but sometimes it is diminished. 

The symptoms of the disease just described sometimes form so characteristic a 
picture that we can recognize it at the first glance. More precise information 
as to the seat of the stenosis, or the accurate differentiation of tracheal stenosis 
from the very similar picture presented by laryngeal stenosis, demands a direct 
laryngoscopic examination of the larynx and trachea, which of course is hardly 
practicable in a patient with a high degree of dyspnoea. 

2. Bronchial Stenosis. 

Narrowing of a primary bronchus, which is the only form to be mentioned 
here, arises most frequently as a result of the presence of foreign bodies. These 
may enter the air-passages by means of a deep inspiration while eating, or during 
sleep. We know that foreign bodies get into the right bronchus, which is wider, 
somewhat more frequently than they do into the left. Stenosis of the main 
bronchi from pressure also arises from aneurisms of the aorta, mediastinal tumors, 



154 DISEASES OF THE EESPIEATOEY OKGANS. 



enlarged bronchial lymph-glands, etc. Stenosis of the left bronchus from the 
pressure of the greatly dilated left ventricle has been observed in mitral stenosis. 

The symptoms are not equally distinct in all cases, and they depend upon the 
shutting off of the corresponding part of the lung. The dyspnoea is usually very 
evident, especially in acute cases. The respiratory excursions are much less on 
the affected side than on the sound side. The percussion-note, indeed, remains 
clear, but the vesicular respiratory murmur disappears, and instead of it we some- 
times hear over the whole side a loud whistling or humming sound, the vibration 
of which can in some cases be felt by the hand applied to the chest-wall. The 
vocal fremitus is diminished on the affected side. A vicarious emphysema soon 
develops in the other lung. 

Lobular pneumonia frequently develops as a result of the entrance of foreign 
bodies into a bronchus, because the agents of inflammation have entered at the 
same time with these bodies, and, as the expectoration can be evacuated only with 
difficulty, these irritants can readily establish themselves in it. In stenosis from 
pressure the character of the disease may of course be modified in many ways by 
the primary disease. 

The prognosis and treatment of tracheal and bronchial stenosis depend entirely 
upon the nature of the primary disease. General statements as to treatment, there- 
fore, need not be given here. A direct mechanical treatment of tracheal stenosis 
in appropriate cases, such as cicatricial stenosis, may be undertaken according to 
the different methods of dilatation above enumerated. The methods for removing 
foreign bodies from the larger air-passages belong to the domain of surgery. The 
employment of an emetic has met with distinct success in such cases, but it is not 
without danger, for the foreign body may wedge itself into the glottis during the 
act of vomiting and result in the danger of instant suffocation. 



CHAPTER Vin. 

BRONCHIAL ASTHMA. 

(Kervous Asthma.) 

Bronchial asthma is a disease clinically well characterized, but serologically 
it is probably not quite a single affection. Its chief symptom consists of marked 
paroxysmal attacks of dyspnoea. The cause of the dyspnoea is not to be sought in 
any coarse factor that can be demonstrated anatomically, but it is probably due to 
some abnormal condition of nervous irritation. The chief theories as to the origin 
of the asthmatic attacks will be given further on. The disease is decidedly more 
common in men than in women, and it is not very rare even in childhood. 

Symptoms and Course of the Disease.—" Nervous " bronchial asthma consists, 
in its purest form, of attacks of shortness of breath, which come on in people who 
are otherwise quite well, with varying frequency and varying duration, partly 
from some special cause, and partly without any discoverable reason. In the 
intervals between the attacks the patients are completely well and do not show 
the slightest signs of any disease of the respiratory or circulatory organs. 

The asthmatic attack either begins quite suddenly, or it is preceded for a shorter 
or longer period by prodromata. These consist in a general feeling of discomfort, 
in abnormal sensations in the larynx or epigastrium, sometimes in remarkably 
frequent gaping, and often in a marked coryza associated with a good deal of 
secretion and frequent sneezing (compare the relation between many attacks of 
asthma and diseases of the nose given below). The attack begins in most cases 



BEONCHIAL ASTHMA. 



155 



at night. The patient wakes up with an intense feeling of pressure and anxiety. 
Sometimes he complains of a feeling of pain in the chest. He has to sit up 
straight, and in severe cases even to get out of bed. He often hurries to an open 
window in order to "get air." His expression is anxious ; his skin becomes pale 
and cyanotic, and sometimes is covered with a cold sweat. The respiration, too, 
is altered in a very peculiar and characteristic way. Both inspiration and expira- 
tion are almost always accompanied by a high-pitched whistling sound, audible at 
a distance. Both respiratory acts are labored, requiring the aid of the accessory 
muscles. ^On inspiration, only the upper part of the thorax is elevated to any 
extent. We see in the neck the inspiratory contraction of the sterno-cleido- 
mastoids, the scaleni, etc. Still more striking, however, is the labored, panting, 
long-protracted expiration, during which the abdominal muscles are contracted 
to a board-like hardness. We therefore recognize the disturbance of respiration 
in asthma as essentially an expiratory dyspnoea. The frequency of respiration is 
in many cases normal, or even somewhat diminished, yet we have repeatedly 
counted thirty or forty respirations a minute. 

On physical examination of the lungs during the paroxysm, we find the per- 
cussion-note over them normal or even strikingly loud and deep — the "box-tone." 
The lower boundary of the lung is usually found one or two intercostal spaces 
lower than normal. We accordingly have to do with an abnormally low position 
of the diaphragm, with an acute emphysema. On auscultation, whistling and 
creaking sounds, which quite obscure the vesicular murmur, are heard over most 
of the lung, especially during long expirations. In many places, indeed, the 
respiratory murmur is entirely absent, or we hear only a low whistle on expira- 
tion. Toward the end of the paroxysm the noises become deeper and more boom- 
ing, and sometimes we hear a few moist rales. 

Cough and expectoration may be entirely absent in short attacks, but in most 
cases, especially if protracted, a scanty, tough, mucous expectoration is coughed up. 
We usually find in it a few yellowish-green or gray-looking particles, which, on 
closer examination, are made out to be very small twisted threads of mucus. 
These threads, which have been carefully described lately by Ungar and Cursch- 
mann, are of a very tough consistency, and show a striking spiral twisting under 
the microscope. They seem formed of simple fine or coarse spirally twisted 
bands and fibers. We sometimes find in the middle a fine transparent central 
fiber. There is scarcely a doubt that these formations, which we have termed 
" spirals " (Fig. 20), are casts of the finest bronchioles, and they are certainly 
due to the existence of an affection of the last and finest branches of the 
bronchi. 

We see very often under the microscope quite numerous pointed, octahedral 
crystals, especially in the spirals just described. These were first discovered by 
Leyden in the sputum of asthmatics, and are usually termed asthma crystals 
(see Fig. 20). They lie in the midst of swollen and fatty-degenerated pus-corpus- 
cles. When tbe attack ceases, their number quickly diminishes. We often see in 
them, then, the manifest signs of beginning decay. They are identical in their 
chemical relations with the so-called Charcot's crystals found in the leuksemic 
spleen, the marrow of bones, the spermatic fluid, etc. They are composed of the 
phosphate of some peculiar organic base. As we shall see below, Leyden has 
ascribed to these crystals a definite part in the origin of bronchial asthma. 

Among other microscopic constituents of the sputum are calcic oxalate crys- 
tals, found by Ungar in some cases ; and cylindrical and sometimes ciliated epithe- 
lium has also been found. 

The pulse is usually accelerated during the asthmatic paroxysm ; the bodily 
temperature is normal, or sometimes even subnormal. In asthmatic patients who 



156 DISEASES OF THE RESPIRATORY ORGANS. 



have protracted attacks we have repeatedly seen a slight febrile movement up to 
about 102° (39° 0.). 

The duration of the asthmatic paroxysm is very different in individual cases, 
as has already been said. Sometimes it lasts only a few hours, in other cases 
it lasts several days, and even weeks. The cases of protracted asthma are not 
very rare. Marked exacerbations and remissions of the disease usually alter- 
nate in them. The frequency of the attacks in ordinary asthma also varies 




Fig. 20.— Asthma crystals and Curschmann , s spirals (a, central fiber). 



exceedingly. Sometimes they come on almost every night, and then there are 
long pauses of months and years, so that we can not make any general statements 
as to the course of the disease. Definite recoveries are quite rare ; they are most 
frequent in children. 

Although patients with the form of pure essential asthma which we have so 
far described seem perfectly well in the intervals between the attacks, there is 
also a symptomatic asthma. This is seen chiefly in patients with emphysema and 
chronic bronchitis. The term " symptomatic asthma," however, can be used only 
when the attacks actually show the symptoms of pure asthma, and when the dysp- 
noea which occurs in them has no relation to the anatomical lesions present. 
In such cases it is often hard to decide whether the existing emphysema and 
chronic bronchitis are really the primary disease, or the result of the asthma. 
There is no doubt but that a secondary emphysema of the lungs may develop as 
a result of frequent and protracted asthmatic attacks. The attacks of dyspnoea, 
which come on in chronic affections of the heart and blood-vessels, cardiac asthma 
(vide infra), depend upon other causes than the peculiar bronchial asthma, and 
should not be classed with it. 

Theories as to the Origin of Asthma— iEtiology.— The peculiarity of the asth- 
matic symptoms has given rise to numerous theories as to the origin of asthma, yet 
none of them have been able to obtain general recognition up to the present time. 
Many authors, like Weber, Stork, and Frantzel, seek the underlying cause of 
asthma in an acute swelling of the bronchial mucous membrane, as a result either 
of a sudden dilatation of the blood-vessels arising from nervous influences or of a 
very acute catarrh. Wintrich and Bamberger have advanced the theory that 
asthma consists in a tonic spasm of the diaphragm, by which the diaphragm is kept 
motionless in a fixed inspiratory position ; but it is at once plain that such a 
condition can at least not play the chief part in the occurrence of asthma, for we 
can usually feel the respiratory movements of the diaphragm quite plainly during 
the paroxysm. The theory long ago advanced by Trousseau, the chief advocate 
of which of late is Biermer, is the most probable one, and is now generally 



BRONCHIAL ASTHMA. 



157 



accepted — namely, that the spastic nervous element, which is not wholly to be dis- 
regarded in any explanation of bronchial asthma, consists of a tonic spasm of the 
muscles of the smaller bronchi. The tonic contraction of the smaller bronchi 
explains the whistling sounds that are heard. A marked hindrance to respiration 
is set up which can be more easily overcome by the inspiratory suction of the thorax 
than by the expiratory pressure. Since the latter acts not only upon the alveoli, 
but also upon the lesser bronchi themselves, the closure of the bronchi upon expi- 
ration is still more marked. The air which is drawn into the alveoli can conse- 
quently get out again only imperfectly, and this explains the expiratory dysp- 
noea, the emphysema that soon occurs, and the low position of the diaphragm. 
The acceptance of this theory of bronchial spasm also readily explains the often 
sudden onset, and just as sudden cessation of the asthmatic attack. 

If we inquire further, however, into the cause of the occurrence of the bron- 
chial spasm, only a very indefinite answer can be given ; for little is said by 
answering that asthma is a neurosis of the vagus. Many facts make it very prob- 
able that the spasm is of reflex origin, at least in many cases. Leyden has 
expressed the suspicion that the irritation of the mucous membrane by the pointed 
crystals, which he discovered, gives rise to the spasm. It may be said in oppo- 
sition to this, however, that the asthma crystals are sometimes found in the 
sputum of patients with emphysema who have no asthmatic symptoms, and also 
that in asthmatic patients the severity and duration of the attacks stand in no 
constant relation to the number of the crystals. The facts lately corroborated by 
numerous observations by Hack and others, are very important — namely, that the 
asthmatic paroxysm is sometimes of reflex origin, starting from some disease of 
the nasal mucous membrane. We find quite often, for instance, that asthmatic 
patients are suffering from chronic diseases of the nose, like chronic catarrh, nasal 
polypi, and especially the enlargement of the so-called erectile bodies of one or 
more turbinated bones, and that after their removal the asthma disappears. In 
this connection maybe cited the noteworthy fact that many asthmatic patients 
have an attack brought on by certain odors ; for example, at the smell of freshly 
roasted coffee, or of ipecacuanha. Trousseau, who suffered from asthma himself, 
always had an attack on smelling violets. It is doubtful whether a pure bron- 
chial asthma can have a reflex origin from other distant organs. The connection 
between asthma and diseases of the pharynx, or hypertrophy of the tonsils, 
is extremely probable in some cases, but the statements as to the occurrence 
of asthmatic paroxysms in diseases of the stomach ("dyspeptic asthma"), of 
the intestine, or of the female sexual organs, are to be taken only with great 
reserve. We usually have to do here with a confusion between pure asthma 
and other conditions of dyspnoea, nervous dyspnoea, conditions of cardiac weak- 
ness, etc. 

In a large number of cases — which seem to us to be most characteristic — 
the disease can be explained, in our opinion, only by the hypothesis of a peculiar 
primary disease of the bronchial mucous membrane, whose special feature, some- 
what like the spasm of the glottis in whooping-cough, consists in the occurrence 
of a reflex bronchial spasm. The whole type of the disease and the peculiarities 
of the expectoration, the spirals, and crystals, furnish unequivocal testimony for 
this theory of asthma. Curschmann, therefore, claims that the anatomical basis 
of these cases is an exudative bronchiolitis, and many cases of protracted asthma, 
lasting for weeks, deserve the name of asthmatic bronchitis. 

The observation, often made, that many asthmatic patients have attacks only 
when in certain places, and are quite free from them in others, is very remarkable. 
They sometimes have an attack at every change of place. In conclusion, it may 
be mentioned that in some cases a distinct, intimate, hereditary predisposition to 



158 



DISEASES OF THE RESPIRATORY ORGANS. 



asthma has been observed, and that asthma sometimes occurs in families with a 
general neurotic tendency. 

Diagnosis. — This is usually easy if we pay careful attention to all the symp- 
toms and to the whole course of the disease, Other conditions which may lead to 
dyspnoea are of course to be excluded by a careful examination of the chest. 
Attacks of spasm of the glottis and of paralysis of the openers of the glottis are to 
be differentiated from bronchial asthma by the predominance of inspiratory 
dyspnoea as well as by other signs. 

Prognosis. — There is hardly ever any immediate danger to life even in the 
most intense asthmatic paroxysms, but permanent recovery is rare, since even 
after long intervals the attacks may finally return. The chief danger in severe 
and protracted cases lies in the development of a pulmonary emphysema with its 
further consequences. 

Treatment. — In every case of asthma the first thing to be thought of is 
whether there is not a definite cause whose removal may cure the disease. In this 
connection we should examine the nose carefully, since numerous observations 
have recently shown that a previously existing asthma may permanently disap- 
pear after the treatment of some nasal disease which may be present, like the 
removal of polypi, the destruction of the erectile bodies by the galvano-cautery, 
etc. 

If we can not satisfy the causal indication in this way we should always try 
next a remedy which must pass for a direct specific against certain forms of 
asthma — iodide of potassium. In doses of twenty to forty-five grains a day (gnn. 
1* 5-3*0), which can be increased if necessary, this usually causes a rapid improve- 
ment, which of course is not always, although it is frequently, permanent. If 
iodide of potassium has been used in vain, we must turn to the other remedies 
which have been employed against asthma, although their action is often quite 
uncertain. We may mention here the nitrite of sodium (two parts in one hun- 
dred and twenty of water, two to three teaspoonfuls a day), and nitro glycerine, 
which has an analogous action (twenty drops of a one-per-cent. alcoholic solution 
in six and a half ounces (grin. 200) of water, a tablespoonful two or three times a 
day) ; also quinine, bromide of potassium, belladonna, atropine, arsenic, etc. In 
some cases pneumatic treatment, such as the inhalation of compressed air, has- 
been successful, and sometimes, too, electricity (galvanization and faradization of 
the neck), or hydro therapy, has been claimed to give relief. Change of climate 
may be of distinct service. Many patients bear the sea-air well, while with others 
mountain traveling exerts a favorable influence. 

In severe cases a special symptomatic treatment of the attack itself is often 
necessary. Narcotics are without doubt the most effective, especially chloral and 
morphine. In severe attacks we can not avoid injections of morphine, but we 
must always be cautious in order that the patient may not form the habit of 
using this to excess. Inhalations of chloroform and ether are also much em- 
ployed. Among other useful remedies and devices we may mention mustard plas- 
ters to the chest and calves, putting the hands and feet into hot water, inhalations 
of nitrite of amyl, in halations of turpentine or ammonia vapor ; also the often- 
used fumigation with saltpeter paper — unsized paper dipped in a concentrated solu- 
tion of nitrate of potassium and dried. The stramonium cigarettes to be had in 
most drug-stores are much praised. Among internal remedies we may mention 
tincture of lobelia, formerly much used, and also the remedy lately employed by 
Penzoldt, quebracho, in tincture, a tablespoonful pure or in some mucilaginous 
vehicle. 

[The syrup of hydriodic acid can be substituted for the iodide of potassium in 
some cases where the latter does not agree with the patient, Grindelia robusta, 



PULMONARY EMPHYSEMA. 



159 



in fluid or solid extract (TTi xv-xxx, gr. iij-v), seems sometimes to prevent the 
recurrence of attacks. Marked alleviation of the paroxysms is often obtained 
from the inhalation of fifteen to thirty drops of the iodide of ethyl.] 



SECTION" IV. 
Diseases of the Lungs. 
CHAPTER I. 

PULMONARY EMPHYSEMA. 

{Alveolar Eciasis. Increased Volume of the Lungs.) 

Nature of the Disease and iEtiology. — Pulmonary emphysema, the abnormal 
inflation of the lungs, is one of the commonest pulmonary affections. It either 
develops in separate parts of the lung, in which case it is subordinate to other 
pathological changes which co-exist in the lungs, or it involves almost the whole 
extent of both lungs, and then presents the symptoms of a characteristic affection, 
which is usually easy to recognize. 

The essence of pulmonary emphysema, the condition from which most symp- 
toms are immediately derived, is the loss of elasticity in the lungs. If we com- 
pare the sound lung with its normal elastic force to a new and very tense rub- 
ber band, the emphysematous lung must be compared to an old and lax band that 
is stretched and pulled oat. We therefore see why the emphysematous lung takes 
up a greater space than the sound one, for, on account of its lack of elasticity, it 
can no longer contract to its former volume. We may thus call emphysema a 
permanent inspiratory distention of the lung from which it can no longer return 
to its expiratory condition. If we open the thorax of a subject with normal lungs, 
they contract, as is well known, but the emphysematous lungs remain in their 
inflated condition after the thorax has been opened. 

If we inquire into the factors which cause this loss of elasticity in the lung, we 
find that they are the same kind of influences which tend to dimmish the elas- 
ticity of any other elastic body. As a rubber band, by much pulling and stretching, 
gradually gets longer and less elastic, so the lungs, as a result of their abnormally 
frequent and severe distention, gradually become inelastic and emphysematous. 
The normal traction of inspiration, which is continually making new demands on 
the elastic powers of the lungs, finally leads to a loss of elasticity in them. In 
advanced age most lungs become more or less inelastic. The lungs of an old 
man are like an elastic band, which has done its work for years, but which has 
finally become yielding. We therefore class the emphysema of the lungs in old 
age rather among the states of involution such as develop in almost all organs in 
advanced life, than among special pathological changes. We distinguish, more- 
over, most of the lungs with senile emphysema from other emphysematous lungs 
by the fact, that their volume as a whole is not increased, but is rather diminished 
below that of the healthy lung, while at the same time we find in them the exten- 
sive atrophic processes of old age. 

The condition becomes pathological, however, if the elasticity of the lung is 
deficient in earlier years before the lung has been exposed to the action of the 
special injurious influences on the lung which will soon be mentioned. In such 
cases of emphysema, developing in middle life or even in youth, the idea of a 



160 



DISEASES OF THE KESPIKATORY ORGANS. 



congenital weakness of the elastic elements in the lungs can not be set aside. It 
probably consists in a quantitative or a qualitative defect of development of the 
elastic tissue. Some observations seem to corroborate the statement that a dispo- 
sition to emphysema may be present in several members of the same family. 

If a lung whose elasticity is previously subnormal can not persistently satisfy 
the ordinary demands upon it, a normal lung, on the other hand, also loses its 
elasticity if the demands made upon it are greater than it can perform. This is 
the reason why pulmonary emphysema is in part considered a disease arising 
from the occupation. We mean here not only those influences which lead to 
chronic bronchitis and thus later to emphysema {vide infra), but more especially 
the abnormal demands upon the lungs in all those callings which necessitate 
severe physical labor. We must not only regard the deeper and more rapid res- 
pirations, but also the increased pressure on expiration to which the lungs are 
often exposed in the raising of heavy weights, etc. This explains the great fre- 
quency of emphysema in the laboring classes, and also its greater frequency in 
men than in women. Beside this, we must add that in certain callings, like glass- 
blowing, and horn-blowing, the overstraining of the lungs is much more direct. 
In all such cases emphysema may be termed directly a premature exhaustion of 
the lungs. 

In very many cases emphysema develops as a result of other diseases of the 
lung, and especially as a result of chronic bronchitis. Dry catarrh of the middle 
and finer bronchi of long duration leads, as a rule, to pulmonary emphysema. 
The abnormal mechanical influences to which the lungs are thus exposed act 
both in inspiration and in expiration. Since the entrance of air to the alveoli is 
rendered more difficult by the swelling of the mucous membrane in the smaller 
bronchi, abnormally deep and strong inspirations are necessary, with a marked 
expansion of the alveoli, in order to draw a sufficient quantity of air into the 
alveoli. The alveolar walls are therefore exposed to an abnormal traction at each 
inspiration. On expiration a pressure from within, which is, perhaps, even more 
injurious, acts on the alveoli. The ordinary expiration, which usually needs only 
the elastic power of the lungs, is not sufficient in chronic bronchitis to drive the 
air out of the alveoli through the narrowed bronchi. Thus arise the difficulty 
and delay in expiration which are present in chronic bronchitis, and which lead 
to the active participation of the muscles of expiration, the abdominal group of 
muscles. On forced expiration, however, the pressure does not act simply upon 
the contents of the alveoli, but much more upon the smaller bronchi themselves. 
The channel of exit for the air from the alveoli, therefore, becomes still narrower. 
Since the air can not escape, the pressure within the alveoli is raised by the press- 
ure due to efforts at expiration, and the alveolar wall is thus again abnormally 
expanded. The cough, which is often present in chronic bronchitis, is a further 
factor, which acts in a precisely similar injurious fashion. The attacks of cough- 
ing begin with a forced contraction of the muscles of expiration which follows the 
closure of the glottis. Until the glottis opens, therefore, the lower parts of the 
lung especially are put under strong pressure. The air in them, which can not 
escape outward, is driven into the upper parts of the lung, and there leads to 
expansion of the alveoli, and finally to emphysema. 

We accordingly see that a number of injurious influences, working in a like 
manner, are to be considered in the gradual development of emphysema from 
chronic bronchitis, and that, sooner or later, these influences have as their result 
the gradual dilatation of the lungs. Here, too, we must bear in mind the indi- 
vidual differences in the resisting power of the lungs. 

Conditions precisely similar to those in chronic bronchitis occur in other dis- 
eases, and lead in like manner to pulmonary emphysema. We very often see the 



PULMONARY EMPHYSEMA. 



161 



development of emphysema in severe and persistent whooping-cough. The worst 
factor here, beside the existing bronchitis, is the frequent paroxysms of coughing. 
We have already mentioned, in the description of bronchial asthma, both the 
acute emphysema, which occurs during the attacks, and the final development of 
a permanent emphysema. 

In conclusion, we must here consider a theory advanced by Freund, which aims 
to make the development of an emphysema dependent upon a " ; ?imary rigid 
dilatation of the thorax." It is indeed conceivable that from certain pathological 
changes in the costal cartilages, as Freund claims, a thorax, which had become 
rigid in the position of inspiration, might exert a constant abnormal traction on 
the lungs, and so give rise to an emphysema. The occurrence of this hypothetical 
primary disease of the cartilages, however, has, up to the present time, not been 
established. It is rather considered by the majority of authors as a secon- 
dary change, developing as a result of emphysema or else as simultaneous. On 
the other hand, it is certainly remarkable that we sometimes observe in chil- 
dren the " emphysematous habit " of the thorax and neck, which will be more 
fully described further on, and that in fact in such children we can often discover 
early in life a beginning emphysema. 

Beside the already described essential or substantial emphysema, which is a 
special disease attacking both lungs uniformly, we distinguish a so-called vicarious 
or complementary emphysema. If, by any disease, certain portions of the lungs 
are incapacitated in their functions, the parts which remain healthy must then 
assume the whole business of respiration. They become excessively expanded on 
inspiration, and as a result they become emphysematous. Thus we see emphysema 
of the upper lobes in an 3 ections of the lower lobes. Emphysema of one lung is 
most frequently observed clinically when the other lung is extensively diseased, 
especially in unilateral chronic contractions of the lungs and pleurae, usually seen 
in tuberculosis. Vicarious emphysema may also be confined to quite small por- 
tions of the lung, but then it is merely of pathological and not of clinical interest. 

Pathological Anatomy. — As we have seen, the actual abnormality of the lung 
in emphysema is not due to a pathological change, but to a change in its physical 
conditions. The loss of elasticity of the lung is shown in its greater volume, in its 
lack of contractility, and in its persistence in a position of inspiration. 

The single alveoli are of course just as much expanded as the whole lung, but 
their walls show no histological changes. We have here, then, a condition which 
Traube has called " increased volume of the lungs," and has distinguished from 
the " pulmonary emphysema " proper. This distinction is without doubt justified 
anatomically, but clinically it can not well be maintained. As the distention is 
constant, the alveolar walls can not withstand the constant traction and pressure. 
This leads to progressive atrophy of their tissue from pressure. The atrophy 
begins quite gradually — that is, it leads to a real disappearance of the elastic 
elements of the lung. The partition- walls of the alveoli are first perforated, and 
then they partly or wholly break down. The neighboring alveoli run more and 
more into one another, and thus finally arise alveolar ectasis and infundibular 
ectasis, which can be made out with the naked eye, and which may attain a diam- 
eter of five or ten millimetres or more. If single air-bubbles enter the interlobu- 
lar, interstitial, or subpleural connective tissue, which may happen perhaps in 
severe fits of coughing, we speak of an interstitial or interlobular emphysema, in 
distinction from the ordinary vesicular or alveolar emphysema. 

The tissue atrophy in the septa of the alveoli affects not only the elastic tissue, 
however, but it also affects the branches of the pulmonary capillaries in the alveo- 
lar walls. The affection of the elastic tissue adds no new conditions to the dis- 
turbed functions of the emphysematous lung, which we have just described. The 
11 



162 



DISEASES OF THE RESPIRATORY ORGANS. 



destruction and final atrophy of the pulmonary capillaries, however, is the second 
important factor in the pathology of pulmonary emphysema, for, with the destruc- 
tion of so great a part of the vesicular area in the lungs, the outflow from the 
right side of the heart is considerably lessened. There must therefore necessarily 
be a stasis in the pulmonary arteries and the right side of the heart, and the right 
side of the heart can overcome the increased resistance only by increased work, 
and thus in every chronic pulmonary emphysema there finally arise a dilata- 
tion and consecutive hypertrophy of the right ventricle with their further conse- 
quences. 

Symptoms and Course of the Disease. 

General Course of the Disease. — Although a pulmonary emphysema may 
sometimes, as in whooping-cough, develop in a comparatively short time, still its 
course is always very chronic. In most cases the origin of the disease is quite 
gradual, as in all those cases in which an emphysema develops from a chronic 
bronchitis, an asthma, or as a result of some injurious occupation. The symp- 
toms gradually and insidiously associate themselves with those of a chronic 
bronchitis. 

The symptoms of emphysema usually begin in middle or advanced life, but 
marked emphysema may occur in youth and childhood. The disease always lasts 
for years, unless some special intercurrent disease arises. 

The objective and subjective symptoms are due either to the chronic bron- 
chitis, which very often co-exists, or to the emphysema itself. Not only is the 
bronchitis, as we have seen above, very often the cause of emphysema, but, on 
the other hand, the development of a chronic bronchitis is greatly favored by the 
circulatory disturbances in the lung associated with emphysema. Thus emphy- 
sema and chronic bronchitis are two diseases closely connected clinically. 

Bronchitis causes its well-known symptoms — cough, expectoration, moderate 
dyspnoea, and a feeling of pressure in the chest. The bronchiectases, which are 
often gradually formed, especially in the lower lobes, may lend a peculiar stamp 
to the cough and expectoration (see page 152). Emphysema increases the patient's 
dyspnoea to a degree which can never be caused by chronic bronchitis alone. The 
emphysematous lungs soon become incapable of satisfying any extraordinary 
demands of respiration. Many patients are only slightly conscious of the diffi- 
culty in breathing as long as they keep quiet, but as soon as they make a trifling 
physical exertion, go up-stairs, or take a little longer walk than usual, the dyspnoea 
comes on. 

The variations in the intensity and extent of the bronchitis correspond to the 
frequent and quite marked variations in the patient's feelings. These variations 
depend upon the condition of the patient, his external circumstances, and the 
possibility of his taking care of himself ; the change of seasons, too, has an influ- 
ence on him. In pleasant weather many patients live in tolerable comfort, but 
autumn and winter bring an increase of all their symptoms with the increase in 
their bronchitis. 

The last stage of the disease is characterized by the appearance of a disturb- 
ance of compensation in the heart. We have seen above that the cause of the 
impairment of the pulmonary circulation, and of the resulting hypertrophy of 
the right ventricle, is the closure of numerous pulmonary capillaries. A further 
reason for the impairment of the circulation comes from the disturbance of res- 
piration itself, since the influence of the respiratory movements on the circulation 
is well known. The appearance of a marked disturbance of the circulation may 
be deferred for some time by the increased work of the right ventricle. The 
cyanosis of most patients is due solely to incomplete oxidation and to the blood- 



PULMONARY EMPHYSEMA. 



163 



stasis which extends backwards from the right side of the heart into the veins 
of the body. Finally, however, the right ventricle becomes more and more 
feeble, the stasis in the veins increases, oedema of the extremities and transudation 
into the various cavities of the body ensue, and after long suffering the patient 
succumbs to dropsy. 

Emphysema is frequently combined in its later stages with other chronic 
diseases. Pulmonary emphysema with its sequelae is not often found at the 
autopsy as a single lesion, but we often find in the cadaver co-existing disease of 
the heart, the blood-vessels, or the kidneys. Pulmonary tuberculosis is often a 
final development in emphysema, but it is usually of the chronic indurated form, 
and is not very extensive. 

Physical Examination. 1. Inspection. — In many patients we can detect the 
disease with considerable accuracy at the first glance ; we are therefore justified 
in speaking of an emphysematous habit. The patients are usually quite well 
nourished, at least in the early stages of the disease, and are often rather corpulent 
people. They appear of full face, often somewhat bloated, and their faces are con- 
sequently more or less markedly cyanotic. The configuration of the neck and 
thorax is especially characteristic. The neck is usually short and compressed ; 
the sterno-cleido-mastoid muscles, which have to act as auxiliaries in inspira- 
tion, are tense and hypertrophied, especially during inspiration. The inspiratory 
contraction of the scaleni may also be seen and felt. The veins in the neck are 
visibly dilated, and in severe cases are swollen to thick blue cords, and we often 
see in them evident undulating or pulsating movements. The thorax is rather 
short, but broad and strikingly deep — the "barrel-shaped thorax." The inter- 
costal spaces are narrow, and the lower ribs move only a little downwards. 
The epigastric angle is therefore obtuse, and sometimes becomes almost a straight 
line. The respiratory movements are almost always accelerated in severe cases. 
Inspiration becomes short and labored. The excursions of single ribs are there- 
fore slight, and the thorax is raised rigidly and more as a whole. Expiration 
is visibly prolonged. We often see a noticeable retraction of the intercostal 
spaces on inspiration in the lower and lateral portions of the thorax. 

This characteristic form of the thorax in emphysema is regarded as a constant 
inspiratory position of the ribs, and corresponds to the permanent inspiratory 
dilatation of the lungs. The peculiar rigidity of the thorax is probably due to the 
changes in the costal cartilages already described, which, according to Freund, are 
primary. In many cases the emphysematous form of the thorax gradually 
develops in the course of the disease, but in other cases it seems to depend on some 
original predisposition {vide supra) to the disease. 

In conclusion, we must state that the above description corresponds to the typi- 
cal form of emphysema, from which we may have many deviations. In the para- 
lyzed thorax, for instance, we may meet with a high degree of essential emphy- 
sema of the lungs, which has often given rise to errors in diagnosis. 

2. Percussion. — Percussion gives very decided results in the diagnosis of pul- 
monary emphysema. We find the inferior border of the lungs one or two inter- 
costal spaces lower than under normal conditions, corresponding to their perma- 
nent inspiratory inflation. Clear pulmonary resonance on the right front in the 
line of the nipple extends to the lower border of the seventh, and sometimes of the 
eighth rib. On the left front it extends to the fifth or sixth ribs, so that the 
cardiac dullness is lessened. The area of cardiac dullness can often not be made 
out at all ; or at most, on strong percussion, it is made out in a limited extent as 
relative dullness. The pulmonary resonance extends on both sides in the back to 
the first or second lumbar vertebra. This condition on percussion in emphysema, 
however, is often altered, because other conditions, like passive congestion of the 



164 DISEASES OF THE KESPIBATORY OEG-ANS. 



]iver, meteorism, and ascites, may be present at the same time, and push up the 
diaphragm. Thus the detection of emphysema by percussion is often made decid- 
edly more difficult. 

Qualitative changes in the percussion-note may be entirely wanting in emphy- 
sema. The pitch is sometimes remarkably loud and deep — the " box-tone " [tym- 
panitic resonance] ; but in other cases, especially in the back, we find it somewhat 
raised. This may depend in part upon the poor vibratory conditions in the rigid 
chest-walls, but in other cases it is caused by the retention of an abundant secre- 
tion in the lower lobes. 

The detection of dilatation and hypertrophy of the right ventricle by percus- 
sion is in many cases uncertain, because the lungs cover the heart. A positive 
result can be obtained only by carefully defining the relative cardiac dullness. 
The frequent epigastric pulsations in emphysema, and also the marked undulat- 
ing and pulsating movements in the jugular veins, are to be regarded as quite 
certain signs of dilatation of the right side of the heart. 

3. Auscultation. — The characteristic auscultatory sign of emphysema is the 
prolonged expiration. As a flabby rubber band, when it is stretched and then let 
loose, no longer snaps back quickly and strongly, so the emphysematous lung, 
when it has been stretched in inspiration, comes back again only slowly. We hear 
with it a somewhat aspirated, sonorous sound which plainly exceeds the vesicular 
inspiratory sound in duration. The vesicular murmur itself often undergoes a 
modification in pulmonary emphysema. It often sounds exaggerated, and very 
shuffling, but in other cases it is rougher and more indefinite. In a high degree 
of emphysema the vesicular respiration is sometimes very low and obscure, 
because the inspiratory current of air is reduced to a small amount in the lungs, 
which are already excessively dilated. In many cases we hear rhonchi beside 
the respiratory murmur, dry whistling, buzzing, and creaking sounds on inspira- 
tion and expiration. If cylindrical bronchiectases have already formed, we hear, 
especially over the lower lobes, numerous small and medium moist rales, but no 
sonorous rhonchi. The rhonchi may wholly conceal the respiratory sounds. 
With a marked retention of secretion we sometimes hear nothing but a low, sup- 
pressed, rattling sound. 

In the heart the sounds are usually rather low because it is covered by the lung. 
The " accidental systolic sound in emphysema " at the apex, described by some 
writers, we have heard much of tener when the valves were intact than we should 
expect after the statements relating to it. The pulmonic second sound is, as a 
rule, markedly accentuated, as a result of the stasis in the pulmonary circulation. 

The diminution of the expiratory pressure in emphysema may be measured 
with the manometer, or with Waldenburg's " pneumatometer. " The normal expi- 
ratory pressure of 110 to 130 millimetres sinks in emphysema to 100 or 80 milli- 
metres. As we should expect, the spirometer shows a diminution of the vital 
lung capacity, which can be readily explained. The normal lung capacity of 
about 3,500 cubic centimetres falls to 2,000 or 1,000 cubic centimetres. 

Other Symptoms in the Lungs and in Other Organs. 

In regard to the other symptoms in the lungs we have only a little to add to 
what has already been said. The intensity of the cough naturally varies in 
individual cases according to the degree of the existing bronchial catarrh. Many 
patients are troubled by a dry cough, while others have abundant expectoration. 
There is nothing characteristic of emphysema in the composition of the latter. 
All the kinds of sputa which are found in the different forms of chronic bronchitis 
are also found in pulmonary emphysema. The dyspnoea, whose predominant 



PULMONARY EMPHYSEMA. 



165 



expiratory character we have already mentioned, increases in advanced cases to a 
most marked degree. Sometimes the increase shows itself by the appearance of 
distinct asthmatic attacks. These are often really to be regarded as a symptomatic 
bronchial asthma, of nervous origin, but, on the other hand, we must not overlook 
the fact that a temporary increase of the bronchitis, retention of secretion, and 
cardiac failure, may also excite attacks of dyspnoea, which can not properly be 
termed asthma. 

The important changes in the heart resulting from emphysema have already 
been described. The insufficiency of the right ventricle, which finally ensues, can 
no longer overcome the increased resistance in the pulmonary circulation. The 
difficulty of respiration is still greater, from the passive congestion of the pulmo- 
nary vessels. The skin becomes still more cyanotic, and finally oedema and general 
dropsy develop. The failure of compensation is evident by the lessening of the 
pulse, its increased frequency, and often by its irregularity. The difficulty of an 
objective examination of the heart in emphysema has been spoken of above. 

The appearances of blood stasis in the internal organs are shown especially in 
the liver and the kidneys. The liver is swollen, and its increase in size (the liver 
of passive congestion) can often be made out by percussion or palpation. The 
pains in the region of the liver, of which many patients complain, are perhaps 
sometimes due to the stretching of the capsule of the liver, but they are probably 
more often muscular pains excited by the frequent coughing. 

In the kidneys the effect of stasis is first shown by a diminished excretion of 
urine. The urine is more scanty in amount, more concentrated, of a higher specific 
gravity, and of a darker color. It generally gives an abundant sediment of urates, 
and often contains a small amount of albumen. Microscopically, it contains a 
few hyaline casts, and a few red and white blood-corpuscles. It is evident that 
this diminished activity of the kidneys favors the development of dropsy. 

The spleen is not infrequently found congested at the autopsy. The evidence 
of this, however, is often uncertain during life, for percussion of the spleen is diffi- 
cult on account of the emphysema, and palpation is often difficult from the swell- 
ing of the body. 

Gastro-intestinal symptoms are often present in emphysema. The appetite 
seldom remains good throughout the disease. Many patients suffer from chronic 
constipation ; and more rarely there is a tendency to diarrhoea. 

Fever is not present in simple pulmonary emphysema. Every fever which 
exists for a long time depends on other complications, like severe bronchitis, pneu- 
monia, or tuberculosis. 

Complications of emphysema with other chronic diseases are frequent. The 
old opinion that emphysema and tuberculosis, and emphysema and chronic heart 
disease, were antagonistic to each other is entirely false. These complications are 
not very rare. We may also mention the complication with general arterio- 
sclerosis and with chronic nephritis, especially the contracted kidney. Among 
acute diseases we must mention croupous pneumonia, which is not very rare in 
emphysema, where it must always be regarded as a dangerous combination. 

The diagnosis of emphysema can be made directly from the results of the 
physical examination and usually presents no difficulties. It is difficult only 
when the patient is not examined till the final stage of dropsy. Here it is often 
very hard to avoid confusing it with forms of heart disease, like primary hyper- 
trophy, myocarditis, or mitral stenosis, or with contraction of the kidney. 

Prognosis. — Pulmonary emphysema of acute origin, like that resulting from 
whooping-cough and analogous affections, may be recovered from in many cases, 
but otherwise, as regards the final curability of the disease, the prognosis is wholly 
bad. The duration of the disease and the intensity of the symptoms are of course 



166 



DISEASES OF THE RESPIRATORY ORGANS. 



very different in individual cases. Here almost everything depends upon the 
circumstances in which the patient is placed. With sufficient care the disease 
may be tolerably well borne for many years, but otherwise the first symptoms of 
respiratory and cardiac msufiiciency appear much earlier. 

Treatment. — Since emphysema itself is only slightly amenable to treatment, 
most of our therapeutic remedies are directed to that accompanying condition 
upon which the greater part of the symptoms depend — to the chronic bronchitis. 
If we succeed in improving this, or even in wholly removing it, we always obtain 
a distinct improvement in all the patient's symptoms. The therapeutic remedies 
mentioned in the description of chronic bronchitis are therefore of frequent use in 
emphysema. 

In the first place, we must seek the best hygienic conditions for the patient, and 
remove him from all injurious influences, like dust, bad air, and work requiring 
physical exertion. In dry catarrh we should use the alkaline mineral waters, and 
when there is abundant mucous secretion the balsams, such as turpentine inter- 
nally and by inhalation. The most valuable expectorants are apomorphine, liquor 
ammonii anisatus, and senega. Then action, of course, too often fails of the desired 
result, so that we frequently have to change our remedies. When there is a 
troublesome cough, disturbing the sleep, we can not dispense with narcotics, like 
morphine or Dover's powder. If severe dyspnoea comes on, we may try to obtain 
relief by mustard plasters to the chest, or by immersing the hands and feet in hot 
water. With asthmatic attacks we may try iodide of potassium, beside the other 
remedies mentioned for asthma. Here, too, we must finally resort to narcotics. 

We must carefully watch the condition of the heart, and use digitalis when 
there are signs of beginning disturbance of compensation and the appearance of 
a small and irregular pulse, and the use of this drug is often accompanied with 
very good results. If symptoms of dropsy set in, we may sometimes prescribe 
diuretic remedies, like juniper-tea, or acetate of potassium, beside digitalis. We 
also try to strengthen the heart by wine, camphor, benzoic acid, or other stimu- 
lants. 

Beside the purely symptomatic treatment thus described, the attempt has been 
made to meet the causal indications in emphysema, and especially to. aid the 
patient in expiration, and thus to improve the power of the lung to contract where 
it is possible. To this end Gerhardt has recommended assisting expiration 
mechanically by compression of the thorax. This compression must be done 
methodically by another person * about five or ten minutes every day, by the aid 
of both hands laid flat on the lower lateral portions of the thorax. The effect of 
this manipulation in diminishing the dyspnoea and making expectoration easier is 
in many cases very satisfactory. 

The employment of the pneumatic treatment has also become quite general, 
especially since the introduction of Waldenburg's portable apparatus. The expi- 
ration into rarefied air, which meets the causal indication, may procure great relief 
for the patient in many cases, and sometimes, too, result in an improvement of the 
emphysema which can be made out on physical examination. Inhalations of 
compressed air are also employed when there is severe bronchial catarrh. 

* One of my patients al the policlinic in Leipsic, a short time ago, made himself a very simple hut 
very effective apparatus for producing this compression of the thorax on himself by the aid of two 
small boards, which are firmly fastened together at one end by a long cord. These boards, which are 
furnished with a piece of wood at this end fitted to the wall of the chest, are laid flat on the two sides 
of the thorax so that their free ends can project forward some six inches or a foot, and serve as a one- 
armed lever. By pressing them together the patient himself can thus, without any strain, exert a con- 
siderable pressure on his thorax with each expiration. 



PULMONARY ATELECTASIS. 



167 



CHAPTER II. 

PULMONARY ATELECTASIS. 

(Compression of the Lungs. Aplasia of the Lungs in Cases of Kyphoscoliosis.) 

JEtiology. — Atelectasis of the lungs is a condition directly opposed to emphy- 
sema. While in the latter the lungs are abnormally inflated, in the former they 
are abnormally collapsed. The air has disappeared from the alveoli and lesser 
bronchi, and in the most advanced cases even from the larger bronchi. The atelec- 
tatic portions of the lung are not altered histologically, but are changed to a firm 
tissue, deprived of air — the so-called splenization or carnefaction. 

The atelectasis of the new-born is due simply to deficient respiration and to the 
consequent imperfect entrance of air into the lungs. In weak children, who die 
soon after birth, we often find the lower lobes wholly or in part in a foetal, unin- 
flated condition — that is, atelectatic. By artificial inflation we can readily expand 
the lungs to their normal extent. 

Acquired atelectasis occurs in two ways. We may mention, as the first and 
most frequent serological factor, the plugging of the smaller bronchi. If a com- 
plete closure of a bronchus arises from the accumulation of secretion, as may easily 
happen in the narrow bronchi of children, the air can no longer enter, on inspira- 
tion, into that portion of lung supplied by the plugged bronchus. The air which 
is shut up in it is gradually absorbed by the blood. The adjacent parts of the 
lung expand, and the portion that is excluded from respiration collapses, leav- 
ing a circumscribed pulmonary atelectasis, usually rich in blood but devoid of 
air. Such atelectases, in greater or less number and extent, are very often found 
in the bodies of children who have suffered from severe bronchitis, especially after 
measles, whooping-cough, or diphtheria. Beside the direct action of the plugging 
of the bronchus, the weakness of the respiratory movements and the cough, condi- 
tional upon the general state of the disease, play a significant part. 

The second very frequent and important cause of pulmonary atelectasis is com- 
pression of the lung. In all the diseases which diminish the space for the expan- 
sion of the lungs, the lungs are pressed together from without to a greater or 
less extent, whereby the air is pressed out of them. Thus arise the atelectases 
from pressure in pleuritic effusion, hydrothorax, pneumo- thorax, in marked cardiac 
hypertrophy, pericardial effusion, and aneurism of the aorta. Atelectasis of the 
lower lobes also arises in the same way from great upward pressure on the 
diaphragm by ascites, meteorism, abdominal tumors, etc. 

That form of pulmonary atelectasis which arises from deformities of the 
thorax is of great practical importance. In severe kyphoscoliosis, the half of 
the thorax corresponding to the convexity of the vertebral column is much nar- 
rowed. The lungs are materially confined in their expansion, and even in their 
growth, if the deformity occurs in youth. This is called " aplasia of the lungs," a 
condition which may give rise to severe results {vide infra). 

Symptoms. — In the majority of cases the appearances in atelectasis are subordi- 
nate to the symptoms caused by the primary disease. This is especially the case 
in most of the atelectases from pressure, although the most dangerous factor lies 
in the compression of the lung. 

The atelectasis of the lungs developing as a result of diffuse capillary bronchitis, 
especially in children, may of course first be detected by physical examination 
when it is of great extent. The respiration, in extensive formation of atelec- 
tasis, often shows a very striking and characteristic deviation from the ordinary 
type, especially when the atelectasis develops in the lower lobes. It is acceler- 



168 DISEASES OF THE RESPIRATORY ORGANS. 



ated and labored, and is performed chiefly by the upper and anterior portions of 
the thorax. In the lower portions we see marked inspiratory retractions, which 
are caused in part by the external pressure of the air, and in part correspond to 
the forced contraction of the diaphragm. 

Physical examination can, of course, show abnormal conditions, especially 
dullness on percussion, only when the atelectasis is extensive. Dullnesss, however, 
is usually hard to make out in children. Auscultation gives signs of existing 
bronchitis ; and sometimes, too, with more extensive consolidation, there is bron- 
chial respiration. In other cases, as may be easily seen, the respiratory murmur is 
much diminished or wholly absent. As we can perceive, the physical signs of 
atelectasis are not really distinguishable from those of pneumonia, especially of 
lobular pneumonia. In fact, a sharp boundary between atelectatic nodules and 
nodules of lobular pneumonia in the lung can not be drawn clinically. 

Aplasia of the lungs in kyphoscoliosis demands a special description, because 
it is of great practical significance. Many patients with kyphoscoliosis may live 
for years without special respiratory disturbance. More careful observation, of 
course, usually shows a somewhat labored and hurried respiration, but the patients 
have not paid much attention to it. In other cases the difficulty in breathing is 
more noticeable. The person affected is incapable of any severe physical exertion ; 
he always feels short of breath, and often suffers from cough and expectoration. 
In the cases first mentioned, however, which for years have had little or no 
trouble, disturbances in respiration sometimes come on quite suddenly. They 
often develop as a result of a mild bronchial catarrh, and they also frequently 
arise without any special cause, and may attain a very threatening degree. The 
condition may improve, but it often leads to death. Examination of the lungs 
during life usually shows nothing but the signs of an extensive bronchitis. By 
careful percussion we may quite frequently detect an increased area of cardiac 
dullness to the right. Sometimes a moderate oedema develops. In such cases the 
autopsy shows nothing as the cause of death but the changes in the lungs. The 
lungs are abnormally poor in air, small, and compressed, but in circumscribed 
portions, on the contrary, emphysematous and expanded. The right side of the 
heart in the great majority of cases is dilated and hypertrophied. There can 
scarcely be a doubt, therefore, that the cause of the onset of severe symptoms and 
the final cause of death is to be sought in the appearance of a disturbance of com - 
pensation in the heart. 

Finally, it is worthy of mention that there is a frequent form of mild atelectasis 
in the lower lobes, which often occurs in very sick and bed-ridden patients who 
usually keep in one position — on the back — as in typhoid fever. On making such 
patients sit up we hear during the first inspirations exquisite crepitant rales over 
the lower lobes, which sometimes disappear after a few deep inspirations. Here 
we have to do with a mild atelectatic condition, with a temporary adhesion of the 
walls of the alveoli and smallest bronchi. 

The treatment of atelectasis coincides in great measure with the treatment of 
the primary disease, and is therefore to be looked for in the corresponding chap- 
ters. The prophylaxis of atelectasis, by constant attention to the respiration, is of 
great practical importance. We should forbid the patient to lie continually on 
his back if we can, and we should make him take deep inspirations. The timely 
use of tepid baths, with shower-baths, is a special preventive of the development of 
atelectasis, and it may bring about a recovery when atelectasis is already present. 

Tepid baths may also be used with care in the treatment of dyspnoea caused by 
kyphoscoliosis. The condition of the heart, however, deserves especial attention 
(stimulants and digitalis). In other respects the symptomatic treatment by 
expectorants, etc., is the same as in other chronic pulmonary affections. 



PULMONARY (EDEMA. 



169 



CHAPTER III. 
PULMONARY (EDEMA. 

iEtiology and General Pathology.— We have in pulmonary oedema the exuda- 
tion of a highly albuminous fluid, usually somewhat hsemorrhagic, not only into 
the interstitial tissue, but also into the alveoli themselves, corresponding to the 
anatomical structure of the lungs. The danger of the condition is easily under- 
stood from the high degree of dyspnoea which immediately ensues from it. In 
fact, pulmonary oedema is in many cases a terminal symptom, which comes on 
in all forms of acute and chronic disease. Many patients are said to die with 
the signs of pulmonary oedema, especially patients with heart disease, pulmonary 
and renal disease, and also with other affections of the most different varieties. 

In rare cases pulmonary oedema is a transitory symptom. Repeated attacks of 
it may occur, especially in heart disease and chronic renal disease, and at times, at 
least, the patient recovers from them. 

Many erroneous notions formerly prevailed as to the particular cause of 
pulmonary oedema. The theory was especially wide-spread that arterial con- 
gestion in the lungs could excite an oedema, but through the experiments of 
Cohnheim and his pupils we now know that pulmonary oedema is to be con- 
sidered a pure oedema from stasis. It takes place when the outflow of venous blood 
in the lung meets an obstacle which can no longer be overcome by the mechanical 
force of the right ventricle. The obstacle which plays the most significant part 
here, and which may occur in all possible forms of disease — of course more readily 
in those mentioned above than in others — is the paralysis of the left ventricle. 
If the further progress of the blood is much hindered by this, the overfilling of 
the pulmonary circulation and a consequent pulmonary oedema will necessarily 
follow, in spite of the most vigorous action of the right ventricle. Every terminal 
pulmonary oedema depends upon this fact, that the left ventricle is paralyzed in 
its action sooner than the right. 

Inflammatory pulmonary oedema must be distinguished from the pure oedema 
from stasis just described. It is found in the vicinity of portions of lung infiltrated 
with pneumonia, it is usually of limited extent, and therefore it is of subordinate 
importance as a cause of disturbances in respiration compared with the general 
oedema of stasis. 

In very rare cases, as we have seen, an apparently primary acute pulmonary 
oedema, with a speedily fatal termination, develops in men who were apparently 
before that perfectly healthy, and the autopsy gives no further cause for its origin. 
We probably have to do in these cases with the sudden failure of the left ventricle. 

Symptoms. — Marked dyspnoea is the most striking symptom in pulmonary 
oedema. It is subordinate only when the patient is found in the death agony 
and is no longer fully conscious. 

In pulmonary oedema the respiration is hurried, labored, and rattling. All 
the accessory muscles of respiration are called into play. The patient usually sits 
upright in bed. We see on his lips and cheeks a gradually and constantly 
increasing cyanosis, and we often hear at a distance the moist rales in the larger 
bronchi. 

On examination of the lungs, the percussion is essentially normal, if there is 
no other disease of the lungs. Sometimes the percussion-note is a little higher in 
pitch, and often it is slightly tympanitic. On auscultation, we hear everywhere 
many small and medium moist rales. If the patient can still expectorate, he 



170 



DISEASES OF THE RESPIRATORY OEGANS. 



raises a large amount of frothy, sero-hsemorrhagic sputum. The whole picture 
of the disease is so characteristic that the condition can rarely be mistaken. 

Treatment. — Since in most cases pulmonary oedema is not so much the cause 
as a symptom of approaching death, our remedies against it are often power- 
less, but it must always be our duty, at least in all cases that are not abso- 
lutely hopeless, to try to relieve the pulmonary circulation. From the patho- 
genesis of pulmonary oedema it immediately follows that we must pay par- 
ticular attention to the condition of the heart, especially of the left ventricle. 
Hence we should use energetic stimulants, especially subcutaneous injections of 
camphor or ether, every half hour or hour. Internally we give camphor, musk, 
wine, and strong cafe noir. Beside that »we apply strong irritants to the chest, 
such as large mustard plasters, or hot sponges. Sometimes an actual improve- 
ment of the respiration, when it has already stopped, may be obtained by a bath 
with cold douching, where there is marked general cyanosis. If the patient is 
on the whole strong and well nourished, venesection is sometimes of manifest 
effect. Emetics, however, accomplish little, and are even dangerous on account 
of the collapse which may readily come on after them. An energetic "deri- 
vation to the intestines," however, by senna, calomel, or enemata of vinegar, 
seems sometimes to be really of service. Acetate of lead in large doses, one or 
two grains (grm. 0*05-0*10), in powder, every hour, employed empirically by 
Traube, is deserving of trial. 

In this way, especially in acute diseases like typhoid and pneumonia, we in 
fact sometimes succeed in averting the danger of pulmonary oedema by rapid and 
energetic action. In the cases of oedema occurring in incurable chronic diseases 
of the heart and kidneys, the remedies employed are of course unfortunately 
incapable of preventing death. 



CHAPTER IV. 

CATARRHAL PNEUMONIA. 

(Broncho-pneumonia. Lobular Pneumonia.) 

iEtiology. — Catarrhal pneumonia is not, like croupous pneumonia, a distinct 
and independent disease clinically, but in the great majority of cases it is a sec- 
ondary phenomenon, which may develop in the course of acute and chronic dis- 
eases of various kinds. It almost always follows bronchitis. The same proc- 
ess, which produces catarrh of the bronchial mucous membrane, in its further 
course invades the bronchioles and the alveoli, and here leads to catarrhal pneu- 
monia. 

In every acute or chronic disease the conditions are especially favorable for 
the development of an inflammation in the bronchi, and subsequently in the pul- 
monary alveoli. Everywhere in the air-passages, as well as in the cavities of the 
mouth and pharynx, saliva, mucus, etc., readily collect if the patient is very ill. 
Expectoration is imperfect, and the constant dorsal decubitus favors the accumu- 
lation of secretion, especially in the lower lobes. The mouth and pharynx are 
harder to keep clean than under normal conditions. Fungi and bacteria collect 
in the secretion itself, as well as in the epithelium and particles of food which 
are left in the mouth, and these excite and keep up processes of decomposition. 
The inflammatory agents, which are carried into the air-passages with the inspired 
air, find everywhere favorable conditions for settling and further development. 
From the upper portions they are drawn farther downward. From the larger 



CATARRHAL PNEUMONIA. 



171 



bronchi the process invades the finer bronchi, and finally leads to catarrhal pneu- 
monia. We must also bear in mind that many patients who are very ill have 
difficulty in swallowing-. They get choked, and particles of food, with the agents 
of inflammation clinging to them, are carried into the air-passages. That which 
a healthy person could easily cough up again remains there, is decomposed, and 
gives rise to the development of bronchitis and lobular pneumonia. 

This is the explanation of the frequent development of lobular pneumonia in 
the course of diseases which are entirely dissimilar. We observe it especially in 
all patients with stupor, in severe typhoid, in meningitis, and also in cases of nerv- 
ous disease, where coughing and deglutition are impaired, as a result of bulbar 
affections. In all such cases lobular pneumonia is to be considered a complica- 
tion, and with reference to its origin deserves the name of inhalation pneumonia 
or deglutition pneumonia. We shall soon see that this form, under some circum- 
stances, may pass into circumscribed gangrene. 

Although the serological factors just described, which come into notice in the 
development of lobular pneumonia, have nothing to do with the nature of the 
primary disease as such, there are, on the other hand, certain infectious diseases 
which from the beginning are exclusively, or at least mainly, localized in the 
air-passages. Among these are measles, whooping-cough, and also, to a certain 
degree, diphtheria, small-pox, etc. In these diseases we very often see lobular 
pneumonia following bronchitis. In individual cases, of course, it is scarcely 
possible to decide how far the bronchitis is directly dependent upon the specific 
cause of the disease, or whether it is merely a complication such as might also 
occur in any other disease. Lobular pneumonia in diphtheria, and in severe 
small-pox, is probably for the most part a deglutition or an inhalation pneumonia, 
the occurrence of which in this disease may be readily understood. In measles 
and whooping-cough, however, we may consider that the pneumonia is directly 
dependent upon the specific agents of the disease, although here, too, the other 
causes for the development of lobular pneumonia should be borne in mind. 

The development of lobular pneumonia from bronchitis is most frequent, as 
we know, in children and old people. The frequency of catarrhal pneumonia in 
childhood depends in part upon the anatomical relations of the bronchi. Be- 
side that, however, the diseases in which it is especially frequent — namely, mea- 
sles and whooping-cough — are children's diseases. In old people its comparatively 
easy development is due to their imperfect expectoration. 

Primary mild bronchitis only exceptionally leads to lobular pneumonia, since 
it is usually confined to the larger bronchi. Lobular pneumonia is somewhat 
more frequent in the intense bronchitis following the inhalation of chemical irri- 
tants. 

Pathological Anatomy. — It is characteristic of catarrhal pneumonia that the 
inflammation is circumscribed, being limited to the territory of a small bronchus. 
Hence the name of " lobular " pneumonia, in distinction from croupous lobar pneu- 
monia. An atelectasis {vide supra) of the affected lobule, arising from the plugging 
of the bronchus leading to it, often, but not always, precedes the inflammation. 
The inflammatory process itself consists of the exudation of a scanty fluid, which 
does not coagulate, and of numerous pus-corpuscles (white blood-corpuscles) into 
the lumen of the alveoli. The alveoli and smallest bronchi are completely filled 
by the pus-corpuscles. There are also more or less abundant red blood-corpuscles. 
The vessels of the alveolar walls are very hypersemic. The alveolar epithelium 
is much swollen, and is often thrown off in quite large amounts, the " desquama- 
tive pneumonia." It is doubtful whether it also takes an active part in these 
changes by processes of division. 

The inflamed lobules are readily apparent to the eye and the touch by their 



172 



DISEASES OF THE RESPIKATOEY OEGANS. 



firm structure, devoid of air. Their color at first, from the blood contained in the 
inflamed part, is a dark red, but later it becomes more grayish. Their lobular 
boundary is usually easily recognized, but, by confluence of adjacent nodules, large 
portions of the lung, and even whole lobes, may become infiltrated throughout — 
generalized lobular pneumonia. 

Symptomatology. — As has been already mentioned, catarrhal pneumonia almost 
always develops secondarily in the course of other diseases. Hence it happens 
that its symptoms are often subordinate to other prominent symptoms of the dis- 
ease. We often find at the autopsy single lobular nodules in the lower lobes, 
which have caused no clinical symptoms at all. 

In other cases, however, the development of extensive lobular pneumonia is 
of the greatest clinical significance. The disturbance of respiration, during the 
patient's life, forms the most striking symptom of the disease, and lobular 
pneumonia is shown at the autopsy to be the immediate cause of death. The 
largest part of the fatal cases of measles and whooping-cough, and no very small 
part of those of diphtheria, scarlet fever, typhoid, or small-pox, are due, in the 
last instance, to the disturbance of respiration dependent upon lobular pneumonia. 

Since a diffuse bronchitis, extending into the finer bronchi, almost always pre- 
cedes the development of lobular pneumonia, and since it may also give rise in 
itself to marked disturbance in respiration, there is no sharp boundary to be drawn 
clinically between diffuse capillary bronchitis and lobular pneumonia. Only the 
fact, a hundred times repeated, that every extensive capillary bronchitis readily 
leads to lobular pneumonia permits us to suspect the latter, at least with consid- 
erable certainty, even if there is no direct clinical evidence of it. 

The type of lobular pneumonia seen in childhood is the most characteristic and 
the most important clinically. It is observed in measles and whooping-cough, and 
also in weak, atrophic, and rachitic children. The increased frequency of respira- 
tion is most striking. The breathing is superficial, but labored, as is shown by the 
contraction of the auxiliary muscles of inspiration and the play of the nostrils. 
We often notice inspiratory retraction of the lower lateral portions of the thorax 
as a result of the incomplete entrance of air. The number of respirations a 
minute increases in children to sixty or eighty, or even more. In most cases 
the child has a frequent and apparently painful cough. Expectoration is entirely 
absent in small children. When it is present it shows no characteristic peculiari- 
ties different from ordinary catarrhal sputum. The general condition is always 
bad. The child is restless, apathetic, and often stupid. Its face is usually pale, 
but often quite cyanotic. The pulse is very rapid, and in small children often 
attains a frequency of 140 to 180 a minute. Fever is almost always present. It 
shows no typical course, it is now remitting and now intermitting, and toward 
evening it often rises to 104° or 105° (39'o°-±0'5° C). The occurrence of such a 
high rise in temperature is not without value in the diagnosis of catarrhal pneu- 
monia. If in diffuse capillary bronchitis a high fever is present for a long time, 
we may assume, with considerable certainty, that the formation of lobular nod- 
ules has already begun. 

Physical examination furnishes direct evidence of the affection of the lungs, 
but its results are for the most part to be referred to the diffuse bronchitis and 
not to the lobular infiltration. Auscultation gives the most constant signs. We 
hear over the lungs, in a greater or less extent, numerous small and medium 
moist rales, and often quite loud sonorous rhonchi. From these signs, strictly 
interpreted, we can diagnosticate simply bronchitis, but we may suspect pneu- 
monia with the greatest probability. With very confluent broncho-pneumonia 
auscultation sometimes gives bronchial breathing and bronchophony beside the 
rales. 



CATAKKEAL PNEUMONIA. 



173 



It goes without saying that little lobular nodules, surrounded by normal lung- 
tissue containing air, give no special signs on percussion. With numerous nod- 
ules running into one another, the percussion-note is duller, and there is some- 
times tympanitic resonance. The dullness is often first to be made out over a 
stripe extending along the vertebral column — the so-called "stripe-pneumonia." 

Course and Termination. — The course of an extensive lobular pneumonia is 
usually quite protracted. Even in favorable cases the disease rarely lasts less than 
two or three weeks, and often much longer. The chief danger of the disease lies 
in this tendency to a protracted course, extending over weeks and months. Many 
children finally die, not of the lobular pneumonia itself, but from the general 
weakness and emaciation following the tedious febrile disease. We must remem- 
ber, however, that complete recovery may sometimes take place quite late in the 
disease. 

The " transition of catarrhal pneumonia to caseation and tuberculosis " is a 
clinical fact with which physicians have long been conversant. In fact, we often 
find true tubercular changes in the lungs of children who have died after a 
tedious illness, as a result of measles, whooping-cough, etc. There can, of course, be 
no real question, however, of an actual transition from one disease to the other. 
In such cases we have to do either with an acquired tubercular infection, which has 
found a favorable soil in an already diseased lung, or the disease of the lung has 
given -rise to a further development of a previously existing tuberculosis. It is 
usually weak children, with a hereditary predisposition to tubercle, who succumb 
to tuberculosis as a result of the above-named diseases. The diagnosis of a devel- 
oping tuberculosis is not always easy, since it is only rarely that marked phthisical 
changes — like dullness at the apex, cavities, etc. , which can be made out by a physi- 
cal examination — are found in the lungs. We can usually suspect tuberculosis 
only from the general conditions — emaciation, persistent hectic fever, hereditary 
predisposition, or some secondary tubercular disease like meningitis, etc., espe- 
cially as the certain distinction, from the presence of tubercle bacilli in the spu- 
tum, is only rarely possible in children. 

The transition of inflammatory lobular nodules to purulent foci (abscesses), or 
nodules of gangrene, which sometimes happens, especially in small-pox, depends 
upon the specific malignant property of the agents of inflammation which have 
entered the bronchi. 

If the lobular nodules extend to the pleura, a secondary sero-fibrinous or even 
purulent pleurisy may develop. 

Treatment. — Since we have already mentioned the proper treatment, in our 
description of the various diseases in which secondary pneumonia is especially 
prone to develop, we can now be brief. We have also laid repeated stress upon 
the possibility and the great practical importance of prophylaxis, which is self- 
evident from a just comprehension of the origin of lobular pneumonia. Beside 
keeping the cavities of the nose, the mouth, and the pharynx as clean as possible, 
tepid baths, with cool douching later, are the best means of preventing the devel- 
opment of lobular pneumonia, or of checking its further extension if possible. 
Cold packs are often used with advantage, but, in our opinion, they are much more 
disagreeable to the patient than baths. It is an advantage, which is to be considered 
in the second rank in comparison with the desired improvement in respiration, 
that by both of these processes the febrile temperature is at the same time 
reduced. 

In the treatment of lobular pneumonia in children the best remedies are tepid 
baths with effusions, and general wet packs applied several times a day. The 
higher the fever is, the of tener must these be repeated ; with moderate fever, the 
child may stay in the pack for two or three hours. If there is great stupor, and 



174 DISEASES OF THE EESPIEATOEY OKG-ANS. 



the breathing' is feeble, it is very advisable to put a handful of mustard into 
the water of the bath, or into the water in which the towels for the pack are 
dipped — "mustard baths," "mustard packs." The irritation of the skin obtained 
in this way is very considerable. 

Among external applications to the chest, beside mustard plasters, poultices, 
and embrocations, dry cups are to be mentioned, which often do very good service 
in strong, older children, and especially in adults. We never need to use local 
blood-lettings, however, in catarrhal pneumonia. 

Of internal remedies, expectorants are most used. In strong children the 
abundant collection of mucus in the bronchi may sometimes be relieved by the 
administration of an emetic. "We should be cautious in the use of narcotics. 
Stimulants must often be used in severe cases. Inhalations are quite valueless in 
lobular pneumonia, yet it is recommended to keep the air in the sick-chamber 
rather moist by hanging up wet towels, or by sprinkling with water. The room 
should also be as large and as well ventilated as possible. The general hygienic 
treatment is of the greatest importance. One of the most important duties, of 
which the physician must always be conscious, is to keep up the patient's strength 
by sufficient and proper food. When convalescence sets in, complete restoration 
to health may be furthered by a suitable residence in the country. 



CHAPTEE V. 

CROUPOUS PNEUMONIA. 

{Lung Fever. Lobar Pneumonia. Fibrinous Pneumonia. Plenro-pneumonia.) 

Croupous pneumonia is an acute febrile disease of the lungs, very sharply 
defined both anatomically and clinically. It is one of the most important and 
most common of the severe acute diseases. It is generally known among the 
laity by the name of "lung fever." Since secondary pneumonia may develop 
in the course of various other diseases, like typhoid, small-pox, or diphtheria, 
and may anatomically have all the signs of croupous pneumonia, but astiologi- 
cally be quite distinct from it, we speak of this pneumonia as primary, genuine 
pneumonia, in opposition to the other forms. The physical signs and the disturb- 
ances of respiration are, of course, the same in primary pneumonia as in secondary. 
The whole typical picture of the disease, which is so striking, is seen, however, 
only in genuine croupous pneumonia, of which we will make exclusive mention 
in what follows. 

iEtiology. — The majority of pathologists have now become convinced, from a 
series of clinical facts and observations, that the cause of pneumonia is to be 
sought in an infectious agent, which enters the lungs and there gives rise to the 
development of an inflammatory process. This conception of croupous pneu- 
monia as an acute infectious disease, with which conception alone all the patho- 
logical appearances may readily coincide, has, up to the present time, however, not 
always obtained the desired support of facts. Friedlander, indeed, has almost 
invariably found in the pneumonic lung a special kind of micrococcus, which, 
singly or in larger numbers, is inclosed in a characteristic shell or capsule — " cap- 
sule coccus" — and on cultivation shows a peculiar "nail-like" growth in the cult- 
ure gelatine ; but since quite similar cocci are also found under other conditions, 
there is no definite proof at present that they are really the pathogenetic agents in 
pneumonia. 



CROUPOUS PNEUMONIA. 



175 



[Friedlander himself lias now agreed that the capsule is simply accidental, 
probably due to imperfect staining* or decolorization. Talamon has produced 
pneumonia in animals by the injection of the ovoid coccus in pure culture, but 
has obtained also a similar result with round cocci. Thus the question of the 
coccus of pneumonia is still undetermined.] 

Supposing the infectious nature of pneumonia to be correct, all the other 
alleged causes may of course be regarded as at most " predisposing causes." The 
old opinion, which is even now quite wide-spread, that pneumonia is a disease due 
to exposure to cold, is deprived of its foundation It is indeed exceptional that 
we can make out an actual exposure to cold as an setiological factor in a case of 
pneumonia. It is the same with the so-called " traumatic pneumonia." Patients 
from the classes who work hard physically sometimes assert that they were taken 
ill as a result of heavy lifting, or of a blow on the chest, but in such cases the 
subsequent stitch in the side was probably not the result of the injury, but a 
symptom of the disease which had previously begun to develop. 

It is a noteworthy fact in favor of our conception of pneumonia as an acute 
infectious disease that it may be endemic, which sometimes, though rarely, seems 
to be quite certain. Extensive endemics of pneumonia, usually of quite a malig- 
nant character, have been repeatedly observed in single houses, especially in bar- 
racks or prisons, as well as in tenement-houses and other localities. 

Pneumonia does not show a decided epidemic character. In a large population 
sporadic cases occur at any season, but, on the other hand, we may notice a strik- 
ing increase in pneumonia at many seasons. Most attacks occur in the winter or 
spring months, without any necessary relation, however, between the frequency 
of pneumonia and the occurrence of especially bad, wet, or cold weather. 

Individual predisposition plays an unmistakable part in the disease, as we must 
suppose that it does in all infectious diseases. Like facial erysipelas and acute 
articular rheumatism, pneumonia is one of those diseases which attack the same 
person several times, with a certain preference. There are people who have had 
acute pneumonia four or five times in their lives. 

We can not amrm with certainty that the disposition to pneumonia is due to a 
special bodily constitution. The strongest and most robust often fall ill with it, 
and, on the other hand, weak and delicate people, with a tendency to phthisis, are 
frequently attacked. Drunkards seem to have a special predisposition to the dis- 
ease, but of course it is exceedingly hard to give any definite statistics upon this 
point. 

Pneumonia occurs at any time of life, most frequently in youth or middle age ; 
but it is by no means rare in early childhood, and also in more advanced years up 
to sixty or seventy. In general it is observed rather more frequently in men than 
in women. 

[Defective house drainage seems to be a predisposing cause of pneumonia in 
some cases. A careful inspection of the local sanitary conditions is desirable, 
especially where more than one case occurs in a house.] 

Pathological Anatomy. — The anatomical process in croupous pneumonia con- 
sists in the formation of a hsemorrhagic, coagulable " fibrinous " or " croupous " 
exudation into the pulmonary alveoli and the smallest bronchi. The develop- 
ment of the exudation usually extends over one or more lobes to their whole 
extent, and, as the alveoli and fine bronchi are completely filled by the tough 
exudation, the spongy lung, filled with air, is changed to a firm tissue, devoid of 
air, except as it is penetrated by the large bronchi. 

Since Laennec's day we distinguish three stages in the development of the pro- 
cess. In the first stage (stage of inflammatory engorgement, engouement) the 
lung is very hyperaemic, dark red, and the air contained in it is even now much 



176 



DISEASES OF THE RESPIRATORY ORGANS. 



diminished, but not entirely absent. The alveoli are filled with an abundant 
exudation, already hasmorrhagic, but still fluid and not coagulated. 

In the second stage (stage of red hepatization) the coagulation of the exudation 
is complete, and the lung has become throughout of the consistency of the struct- 
ure of the liver. The hepatized lung shows a somewhat increased volume, and is 
strikingly hard. The surface of the section has a red and manifestly granular 
appearand', which, is due to the projection of the numerous little fibrinous plugs 
situated in the alveoli. With the knife we can scrape off a tough, creamy, grayish- 
red fluid from the surface of the section. In the small bronchi, divided by the 
section of the lung, we find characteristic tubular bronchial casts. 

In the third stage (stage of yellow or gray hepatization), which gradually 
develops from the second, the red color of the surface of the section changes to a 
yellowish gray, while the contents of the exudation grow poorer in red but richer 
in white blood-corpuscles. The consistency of the lung is still dense but more 
boggy. The fluid scraped from the surface of the section is more abundant, milky, 
and more like pus. We also speak, therefore, of a " stage of purulent infiltra- 
tion." 

The recovery from the process begins as the exudation becomes fluid. The 
fluid is in part absorbed and in part coughed up. 

It is not necessary for every pneumonia to go through all three stages com- 
pletely. In mild cases the process may stop sooner and go on to recovery. 

Concerning the finer histological processes in croupous pneumonia, the pri- 
mary process is probably to be found in the injury and partial destruction of the 
epithelium in the alveoli and smallest bronchi, produced by inflammation due to 
the specific causes of the disease. In conformity with the processes seen in every 
croupous inflammation of the mucous membrane (see the chapter on diphtheria), a 
coagulable exudation is formed on the surface of the alveoli and smaller bronchi 
after the destruction of the epithelium. With the microscope we see the fibrinous 
net-work of the exudation filling the alveoli. Between its meshes lie numerous 
red blood-corpuscles — red hepatization. Where there is any of the alveolar epi- 
thelium left, we often notice active proliferation — increase and growth of cells. 
Later on the white blood-corpuscles increase, passing from the vessels into the 
exudation — yellow hepatization. The red blood-corpuscles are dissolved where 
they are not removed by the expectoration. The fibrinous exudation is also grad- 
ually dissolved as the result of chemical changes not yet clearly understood 
(peptonization of the albuminous substances ?), and is absorbed like the cells. 
The regeneration of the missing epithelium comes from the epithelium that has 
remained intact, and with that follows a gradual and complete restitutio ad 
integrum. 

The whole process is comparatively brief, usually running its course in a week 
or ten days. The most frequent termination is in complete recovery. The other 
methods of termination, as well as the complications in other organs, will be 
spoken of in connection with the clinical symptoms. We may here mention 
simply that the pleura over the affected portion of the lung takes part in the 
inflammation, without exception, as soon as the disease reaches the periphery, 
and a fibrinous pleurisy, which is not very intense, may then be recognized ; 
hence the former use of the terms " pleuro-pneumonia " and "peripneumonia." 

Croupous pneumonia usually spreads rapidly over a great part of the lung. It 
is very often quite sharply limited to a single lobe — " lobar pneumonia " — so that 
the septum of connective tissue between two lobes also forms a strict boundary 
between pneumonic infiltration and healthy lung tissue ; but this boundary is by 
no means insurmountable, and quite frequently several lobes are wholly or in 
part attacked by pneumonia. According to all statistics, the lower lobes are more 



CROUPOUS PNEUMONIA. 



frequently affected than the upper. Isolated disease of the right middle lobe may 
occur, but it is much rarer than pneumonia of the upper lobes. Of the two lungs, 
the right is attacked with decidedly greater frequency than the left. We have 
ourselves seen, in 244 cases, 137 on the right, 86 on the left, and 21 in which 
both lungs were attacked to a great extent. Simultaneous affection of the lower 
lobe on one side and the upper lobe on the other — quite a rare occurrence — is 
termed "crossed pneumonia." 

General Course of the Disease. — In spite of the numerous modifications which 
the course of pneumonia may offer in individual cases, we can still call pneumonia 
a typical disease, considering the great majority of cases. The subjective and 
objective symptoms dependent upon the local affection of the lung usually, but 
not always, take the chief place among the clinical appearances. In this, pneu- 
monia differs from many other infectious diseases, like typhoid, in which the 
local affection is subordinated to the general infection. 

Pneumonia usually begins quite suddenly. In the majority of cases it begins 
with a pronounced chill of half an hour to an hour's duration, or at least with a 
marked chilliness lasting a longer time. The initial chill may attack the patient 
while in the best of health. It comes on in the day-time, in the evening, or even 
in the middle of the night after a previously quiet sleep. At the same time the 
patient almost always feels as if a severe illness were beginning. 

In other and somewhat rarer cases the beginning of pneumonia is more grad- 
ual. A prodromal stage of a few days, or even longer, precedes the severe illness. 
The symptoms are either of quite a general and indefinite nature, consisting of 
malaise, dullness, loss of appetite, and headache, or the signs of a pulmonary 
affection follow the prodromal symptoms more closely. The patient always com- 
plains, for some days or weeks before the special severe illness, of cough, some 
pain in the chest, or slight trouble with breathing. We can not usually be sure 
whether these prodromata belong to pneumonia or not. A pre-existing simple 
bronchitis may often furnish the most favorable soil for the development of pneu- 
monia. 

In the cases where the disease begins more slowly, the onset of severe symptoms 
is sometimes marked distinctly by a chill or by sudden severe thoracic symptoms. 
In other cases the severe symptoms develop gradually, without any sharp bound- 
ary from the milder prodromal symptoms. 

The subjective symptoms in the chest begin as a rule a short time after the 
onset of the disease, often on the first day or only a little later. The patient feels 
on every deep inspiration a stabbing pain in one side. The breathing is shallow, 
accelerated, and often somewhat irregular. Later on in severe cases there is very 
marked dyspnoea and rapidity of respiration. There is usually an irritating 
cough from the beginning of the disease. The cough is usually painful, and 
hence short, half suppressed, and quite frequent and troublesome. From the sec- 
ond day the expectoration may assume its characteristic tough, rusty, hsemor- 
rhagic appearance. Physical examination gives on percussion and auscultation 
the physical signs to be described more fully below. These are rarely to be found 
on the first day, but more frequently on the second, and sometimes not till later. 

Among the appearances in other organs we may mention, as the most impor- 
tant in diagnosis, the very frequent occurrence of herpes on the lips or on the 
alas of the nose. In severe cases there are sometimes marked symptoms on the 
part of the nervous system : headache, sleeplessness, and delirium. The appetite 
is usually completely lost. Vomiting is not infrequent, especially in the begin- 
ning of the disease. The bowels are usually constipated, but diarrhoea may some- 
times be present. 

Pneumonia is almost always associated with high fever. The typical character 
12 



178 



DISEASES OF THE RESPIRATORY ORGANS. 



of tlie disease may be best demonstrated by the behavior of the temperature curve 
in it. A corresponding increase in the frequency of the pulse is seen with the 
increase of the temperature. 

The course varies greatly according to the previous individual circumstances, 
the severity of the disease, and the existence of complications. In the majority of 
cases, after a comparatively short duration, the disease takes a favorable turn. 
The beginning of improvement is often sudden, like the onset of the disease. 
After the symptoms have lasted for some five to seven days, or in rarer cases a 
shorter or a longer time, at a constant height or with increasing intensity, there 
occurs in the regular course of the disease a critical decline of the fever, often 
associated with quite a copious perspiration, and with that a very rapid improve- 
ment of all the other symptoms. In a short time complete recovery follows. 

In other cases, however, the course is not so favorable. The disease may have 
a fatal term in ation. In a third small class of cases the disease finally takes a pro- 
tracted course, which is usually due to the occurrence of abnormal sequelae in the 
lungs. 

Desceiption of Single Symptoms and Complications. 

1. Symptoms on the Part of the Lungs.— The chief subjective symptom in pneu- 
monic patients is the characteristic painful feeling in the affected side — the " stitch 
in the side." This probably always has its origin in the dry pleurisy which accom- 
panies the pneumonia. It is therefore absent in the cases of central pneumonia 
(vide infra). In pneumonia of the lower and right middle lobes the pain is usu- 
ally more severe than in pneumonia of the upper lobes. One result of the stitch 
in the side is the difficulty, or even the impossibility, of deep inspiration. Hence 
the patient's dyspnoea is considerably increased, and this explains the incongruity 
between the shortness of breath and the relatively slight extent of the pneumonia 
in many cases. The subjective feeling of difficulty of breathing is present in the 
majority of cases, and it may become most distressing. 

Cough is one of the most constant symptoms in pneumonia, and is usually very 
painful ; hence the patient often tries to suppress it. Expectoration is usually 
very difficult at the onset of the disease from the toughness and scanty amount of 
the sputum ; hence very severe and distressing paroxysms of coughing are some- 
times observed. The cause of the cough is probably not to be found in the affec- 
tion of the alveoli, but in the co-existing bronchitis. The irritation of the pleura 
may also set up a reflex cough. In rare cases cough is entirely absent in pneu- 
monia. Except in the cases of limited or late localization (vide infra), we observe 
this absence of cough chiefly in the pneumonia of old or very weak people, and 
also, what is of practical importance, in the drunkard's pneumonia associated with 
delirium tremens. 

The pneumonic expectoration is so characteristic that we can often make the 
diagnosis of croupous pneumonia from this alone. It consists of a very tough 
mucus, which sticks fast to the bottom of the vessel, and is mixed with blood, and 
therefore has a more or less intense red or yellow haemorrhagic color. In indi- 
vidual cases there are numerous gradations. We usually call the pneumonic spu- 
tum "rusty," or "brick-red," or "prune-juice color," etc. Sometimes it has only 
a slight reddish or yellowish tint, and sometimes it consists almost entirely of 
blood. In some cases it assumes a peculiar grass-green color, which is due to a 
change in the blood coloring-matter, or to a mixture with bile pigment in " bilious 
pneumonia." 

The red color of the sputum, as microscopic examination shows, is due to 
numerous red blood-corpuscles, still well preserved, mixed with it. They are, 
however, in part dissolved, and hence cause the uniform red color of the sputum. 



CROUPOUS PNEUMONIA. 



179 



Separate spots containing 1 much blood are often seen in it. Beside the red blood- 
corpuscles, the microscope shows numerous partly swollen or fatty degenerated 
pus-corpuscles. We also see long threads of mucus, sometimes large, round, pig- 
mented cells (alveolar epithelium ?), and finally in rare cases ciliated epithelium 
and crystals of haematoidin. Micrococci always, and capsule-cocci frequently 
{vide supra), are to be found in stained preparations, but these have at present no 
diagnostic value, since nothing certain is known as yet as to their significance. 

We have still to mention the bronchial casts as important constituents of pneu- 
monic sputum. Since they are usually rolled up together, we may not find them 
except by spreading out the sputum in water. They consist of the most beautiful 
casts of the small bronchi, with many dichotomous divisions, and are a product of 
the croupous inflammation extending into the bronchi. The casts of the smallest 
bronchi are sometimes found in the form of " spirals " like those in asthmatic 
bronchitis (see page 155). 

The amount of the pneumonic sputum is, as a rule, not very considerable, but 
it differs a good deal in different cases. The chemical examination of the sputum 
has so far given no remarkable results. The amount of common salt contained in 
it is quite considerable. 

In many cases the pneumonic expectoration is absent. Sometimes it is very 
tough and slimy, but without any admixture of blood ; in other cases the sputum 
is simply catarrhal, when present at all, and then of course it comes, not from the 
parts infiltrated with pneumonia, but from the catarrh of the larger bronchi. We 
often find simple catarrhal sputum, too, beside the characteristic pneumonic 
sputum. 

The pneumonic sputum sometimes occurs in the first or second day of pneu- 
monia, but sometimes not till later. With the beginning of resolution it gradu- 
ally loses its characteristic appearance. The expectoration then becomes less tena- 
cious, and simply muco-purulent, and finally disappears entirely. 

Physical Examination. — Inspection shows no especial anomaly in the general 
contour of the thorax. A marked bulging of the affected side occurs only when 
there is also abundant effusion into the pleural cavity. The action of the thorax 
on respiration is very important. With a limited pneumonia we often notice a 
very marked delay and limitation of motion of the affected side on inspiration. 
This is due in part to the pain in the side, which comes on with every deep inspi- 
ration, and also, in extensive pneumonia, of course, to the physical conditions 
from the anatomical changes. The unaffected portions of the lung act all the 
more forcibly. 

The acceleration of respiration is very striking, its frequency increasing to 
thirty or forty, or even more, a minute. We have repeatedly counted sixty respira- 
tions in adults, even in cases that finally resulted favorably. The breathing is 
shallow, but yet in all severe cases very labored. We see the inspiratory con- 
traction of the sterno-cleido-mastoids and scaleni in the neck, and often in the face 
a marked dilatation of the nostrils on respiration. The patient usually sits with 
the upper half of the body raised up in bed. The cheeks and lips are cyanotic. 
The pale parts about the corners of the mouth are often sharply- contrasted with 
the circumscribed bluish-red coloring of the cheeks. 

The results of percussion are directly dependent upon the changed physical 
condition in the lung, due to the anatomical processes. In the beginning of pneu- 
monia, as long as the total amount of air in the lung remains unaltered, the per- 
cussion-note remains clear, but when the elasticity and tension of the tissue in the 
diseased portion of the lung diminish, the resonance often becomes quite tym- 
panitic. With increased exudation into the alveoli and smallest bronchi the 
amount of air in the lung constantly grows less, and therefore the percussion reso- 



180 DISEASES OF THE RESPIRATORY ORGANS. 



nance becomes very dull, but it usually retains its tympanitic timbre. Since the 
pneumonic lung is only rarely absolutely deprived of air — for a certain amount is 
always left in the larger bronchi — the percussion resonance seldom becomes so 
completely dull — " flat " — as it does, for example, with a large pleuritic effusion. 
As soon as the absorption of the exudation begins, the volume of air in the lung 
increases, and the percussion-note becomes clearer, and remains for some time still 
markedly tympanitic, until the lung has regained its normal tension and elas- 
ticity. We have also to note that the intensity of the dullness in croupous pneu- 
monia is sometimes subject to quite marked variations, since the secretion retained 
in the bronchi is at one time abundant and at another, after expectoration, scanty. 

The extent of the dullness or of the tympanitic resonance is naturally depend- 
ent upon the extent of the anatomical process. Small and central infiltrations 
may entirely escape detection by percussion. 

Auscultation is of greater importance than percussion in the detection of a 
beginning or limited pneumonic infiltration. The auscultatory signs depend in 
part upon the presence of the pneumonic exudation and in part upon the change 
of the lung into a firm tissue containing air only in the larger bronchi. In the 
beginning of the disease we hear over the affected portions large or small rales, 
and very often, too, the characteristic crepitant rale on inspiration discovered by 
Laennec. This arises because the walls of the alveoli and smallest bronchi, which 
are cemented together, are torn apart at each inspiration. The crepitation, how- 
ever, is neither pathognomonic of pneumonia, nor is it heard in every case of 
pneumonia. With increasing infiltration, bronchial breathing replaces the vesi- 
cular. The bronchial breathing in pneumonia is, as a rule, very loud and sharp, 
and sounds close to the ear. Beside this, we may detect more or less numerous 
sonorous rhonchi. We may hear a pure, loud bronchial breathing when there is 
marked infiltration, without any adventitious sounds. With the beginning of 
the " resolution of pneumonia " — that is, as soon as the exudation becomes more 
fluid — abundant, loud, moist rales occur, which are usually rather large, and more 
or less obscure the bronchial breathing. At this time we often hear the charac- 
teristic crepitant rale again — crepitatio redux. The rales gradually disappear, the 
respiratory murmur loses its bronchial character, becomes harsh, and indefinite, 
and finally is normal vesicular again. 

We often hear a few rhonchi over the unaffected portions of the lungs, but 
the respiratory murmur is usually completely normal over them. 

The auscultatory signs just described undergo an important change if the larger 
bronchi leading to the affected portion of the lung are completely plugged by the 
secretion, which often happens. The respiratory murmur may then almost 
entirely disappear, and we hear, perhaps, only here and there a few obscure rales. 
Since such a plugging may be very transitory, we understand why in one day 
over the same portion of the lung we hear first loud bronchial breathing and 
rales, and then quite obscure and diminished breathing. 

Wherever there is bronchial breathing, we hear marked bronchophony. The 
vocal fremitus persists or is somewhat increased over a pneumonic lung as long as 
the large bronchi are open ; but, when they become plugged, the vocal fremitus is 
weakened or wholly absent. 

We have yet to add a few remarks about the parts of the lung in which we 
usually first perceive the physical signs of pneumonia, especially the auscultatory 
signs. 

In the first place, we should never neglect to examine carefully the lateral por- 
tions of the thorax and the axillary region when we suspect a developing pneu- 
monia. We often find the first rales here in pneumonia of the lower lobes. The 
first signs of infiltration are often found in the posterior middle portion cf the 



CROUPOUS PNEUMONIA. 



181 



thorax, and extend downward from this point. Pneumonia of the upper lobes 
begins just as often behind in the apices as in front in the infra-clavicular fossae. 
Isolated pneumonia of the right middle lobe also occurs, to be made out in front, 
on the right, between the fourth and sixth ribs. 

Little that is generally valid can be said of the nature or the rapidity of the 
extension of pneumonia, since in these respects the greatest differences are 
observed. The infiltration often remains confined to a small portion of the lung, 
and again it often spreads over a whole lobe or more in a short time, even in one 
or two days. We call the pneumonia, whose constant extension by continuity 
we can follow from day to day, wandering pneumonia {pneumonia migrans), or, 
from a purely superficial resemblance, which has given rise to many wrong ideas, 
" erysipelatous pneumonia." In these cases all the signs of resolution are present 
in the parts first attacked, while the parts affected later are found still at the height 
of the disease, or in the beginning of infiltration. We also find in the autopsies 
of wandering pneumonia the parts of the lung affected later in a more advanced 
stage (gray hepatization) than the parts first attacked, which are still in the stage 
of red hepatization. Wandering pneumonia is almost always severe and quite 
protracted. 

Pneumonia in rare cases progresses by leaps. Such cases have been termed 
erratic pneumonia. 

2. Symptoms on the Part of the Pleura.— As we have already mentioned, every 
pneumonia which reaches the. periphery of the lung is associated with a fibrinous 
pleurisy, but in many cases this causes no objective symptoms. The stitch in the 
side in pneumonia, however, is often due to the affection of the pleura. In other 
cases the dry pleurisy is marked by a distinctly audible, and often a very loud, 
pleuritic friction-sound, and a rub, which may sometimes be felt by laying the 
hand on the chest-wall. We rarely hear the pleuritic friction-sound in the begin- 
ning of pneumonia, but more frequently in the later stages, and sometimes not till 
many days after the crisis has already taken place. 

The cases in which pleurisy with effusion develops as a sequel to pneumonia, 
which sometimes may occur quite early, are more important. We usually have to 
do with a serous effusion, but in rare cases purulent pleurisy also comes on after 
pneumonia. In one case, which ended fatally, we saw a haemorrhagic pleurisy, 
leading to an abundant effusion of blood into the pleural cavity. 

The diagnosis of pleurisy with effusion, complicating pneumonia, is usually 
d ot difficult. The percussion resonance is duller than we usually find it in pure 
pneumonia {vide supra). The respiratory murmur and the vocal fremitus are 
constantly diminished and finally entirely absent. The symptoms of pressure on 
the neighboring organs and cavities, the heart, the liver, and the semilunar space 
(see page 242), are especially important because they are most unequivocal. An 
exploratory puncture with a Pravaz's [hypodermic] syringe, that has been care- 
fully cleaned and disinfected, gives a very certain and safe method of recognizing 
pleurisy in doubtful cases. 

A moderate degree of pleurisy may somewhat delay the course of the disease, 
but it has no special significance. Large effusions, however, may decidedly 
increase the difficulty in respiration. Otherwise the pneumonia may often 
recover, leaving the pleuritic effusion quite undisturbed. In pneumonia of an 
upper lobe, too, the pleurisy may develop below, and lead to an effusion there, 
while the lower lobe itself remains quite free from pneumonia. 

3. Circulatory Apparatus— The pulse is accelerated from the beginning of the 
disease. In cases of moderate severity its frequency reaches 100 or 120, and, in 
very severe cases, a still higher increase up to 140 or 160 occurs, and is always a 
dangerous symptom. This high rate of the pulse does not have as bad a signifi- 



182 



DISEASES OF THE RESPIRATORY ORGANS. 



cance in children as it does in adults. The consideration of the quality of the 
pulse is important. Smallness, weakness, and irregularity of the pulse are of bad 
omen as symptoms of the onset of cardiac weakness. The attacks of collapse, 
which sometimes come on quite suddenly in severe cases of pneumonia as in 
other acute diseases, are especially dangerous. They consist of sudden attacks 
of weakness of the heart with a very small and frequent pulse. The temperature 
sinks to subnormal, 95° to 93° (35°-34° C). The peripheral parts, the nose and 
extremities, become cool, pale, and somewhat cyanotic. The general weakness is 
extremely marked. The collapse often passes away, especially with timely assist- 
ance, but patients may die in it. 

The pericarditis that sometimes accompanies a fibrinous or sero-fibrinous exu- 
dation is one of the most important anatomical changes in the heart. This can 
always be explained by a direct conduction of the inflammatory process from the 
neighboring pleura, and is therefore somewhat more frequent in left-sided pneu- 
monia than in right. It is a complication to be borne in mind. Its diagnosis is 
usually not difficult if we make a careful physical examination of the heart, but 
with very severe and extensive symptoms in the lungs a complicating pericarditis 
may easily be overlooked. 

A slight fresh endocarditis is sometimes found on autopsy, but it has no clin- 
ical significance. Disease of the cardiac muscle, especially fatty and parenchy- 
matous degeneration, may be discovered post mortem, but they are by no means 
very frequent. In very weak people, drunkards, etc., who die of pneumonia, 
we sometimes, indeed, find the heart remarkably flabby, with the right ventricle 
often dilated, but in many cases of pneumonia we find the muscle of the heart at 
the autopsy perfectly normal. A constant relation between the finer histological 
changes in the cardiac muscle and the condition of the heart's action during life 
is, at any rate, not proven. 

4. Digestive Apparatus. — In severe cases of pneumonia the tongue is usually 
dry, coated, and quite like the tongue in typhoid. In all severe cases the appetite 
is almost wholly lost from the beginning. Vomiting is not infrequent, especially 
in the beginning of pneumonia, and it also occurs later. It is observed with 
especial frequency in the pneumonia of children. Severe symptoms on the part 
of the intestinal canal are rare. The bowels are usually somewhat constipated, 
but quite severe diarrhoea is also observed. 

The complication of pneumonia with jaundice has a certain significance, but 
its causes are not always very clear. It is sometimes due to an accompanying 
catarrh of the duodenum. In other cases the veins of the liver, dilated from stasis, 
may exert a pressure on the bile-ducts. Slight jaundice has no special significance, 
and is often found, even in mild cases ; a marked jaundice, however, is usually seen 
only in severe cases, especially in drunkards' pneumonia. We call such cases, as- 
sociated with jaundice, " bilious pneumonia." They have often other severe gastro- 
intestinal symptoms, like vomiting, diarrhoea, and meteorism, and usually severe 
nervous symptoms, like stupor and delirium. 

The liver sometimes shows the signs of passive congestion. The spleen is 
moderately enlarged, especially in severe cases — acute splenic tumor (as in other 
acute infectious diseases). 

5. Kidneys and Urine. — The infectious character of pneumonia is also shown 
by the occurrence of a genuine acute nephritis, which is not especially common, but 
which still has been repeatedly observed. It begins most frequently on the third 
to the sixth day of the disease. It is recognized by the presence of albumen, casts, 
and blood in the urine. The nephritis usually gets perfectly well, but we have 
once seen it pass into the chronic form. The slight albuminuria which is often 
found in severe pneumonia is, in our opinion, also due to a mild disease of the 



CEOUPOUS PNEUMONIA. 



183 



kidneys, and not to the fever as such (see the section on diseases of the kidney, 
pages 774 and 789). 

Great weight was formerly laid upon the diminution of the chlorides in the 
urine in pneumonia. In fact, the precipitate of chloride of silver, when we put a 
drop of solution of nitrate of silver into the urine, is often very slight or entirely 
absent. The chief cause of this diminution of the chlorides is the small amount 
of nourishment taken by the patient, but we must also bear in mind the large 
amount of chloride of sodium contained in the pneumonic exudation. 

Great significance was also formerly laid upon the abundant sediment of uric 
acid (sedimentum lateritium — brick-dust sediment) which is often noticed on the 
day of the crisis. This is in part due to a real increase in uric acid, but in 
greater part to the fact that the conditions for the deposition of the sediment are 
especially favorable on the day of the crisis. The urine is scanty in amount from 
the abundant perspiration, and is concentrated and relatively very acid. The uric 
acid contained in it can therefore readily be precipitated in the form of a sediment. 

Pneumonia, in common with most of the other acute febrile diseases, is attended 
with an increased secretion of urea during the disease. 

6. Nervous System. — As in every severe febrile disease, nervous symptoms of a 
mild type are very rarely absent in any case of pneumonia. Among the nervous 
symptoms are the general weakness and dullness, and especially the headache, 
which is often very intense, and is usually increased by coughing. The onset of 
more severe cerebral symptoms, especially delirium, is of great importance. We 
see this chiefly in individuals who have a peculiar predisposition to delirium, 
and particularly in drunkards. Delirium gives the drunkard's pneumonia {vide 
infra) its characteristic stamp. 

While no anatomical basis has as yet been discovered for the above-named 
symptoms, nor for the worst form of delirium in drunkards, there is an anatomi- 
cal disease of the brain, which is, to be sure, a rare complication of pneumonia, 
but which yet stands in an undoubted special relation to it. This is purulent 
meningitis. This complication has been repeatedly observed, especially at times 
when an epidemic of cerebro-spinal meningitis was prevailing, and also at other 
times. It is usually hard to make the diagnosis of a complicating meningitis, 
since its appearances are usually hidden under severe symptoms. The chief 
points for diagnosis are intense headache, rigidity of the neck, and a stupor in- 
creasing to deep coma. In many cases these symptoms are very slightly devel- 
oped. The termination of meningitis is probably always fatal. 

7. Skin. — The frequent appearance of herpes in the course of pneumonia is 
characteristic and is sometimes of diagnostic importance. It usually appears from 
the second to the fourth day of the disease, and sometimes later. Its ordinary seat 
is on the lips, especially at the corners of the mouth, also on the alse of the nose, and 
more rarely on the cheeks or the ear (herpes labialis, nasalis, etc.). It has been 
seen only very rarely on other portions of the body beside the face, for example 
on the forearm and the buttock, and in some cases on the mucous membrane of 
the tongue. We once saw two eruptions of herpes separated by an interval of 
several days. In a case under our own observation, herpes labialis, with a fresh 
rise of temperature, appeared some days after the crisis had taken place. The 
especial cause of the development of herpes in pneumonia is unknown to us. It 
is connected, at all events, with the infectious nature of the disease, and it is accord- 
ingly quite analogous to the occurrence of herpes in intermittent and recurrent 
fever, epidemic meningitis, etc. Other affections of the skin are of rare occurrence. 
We have seen urticaria in some cases. The jaundice occurring in pneumonia has 
already been described. 

8. Course of the Fever (see Figs. 21 and 22).— Pneumonia is, almost without 



184 DISEASES OF THE RESPIRATORY ORGANS. 



40-0° 



nsnmBBiiii 



•o° 



37-0' 




Hi«H 

■HHHI 

— 

"iissisasgssas " 



Fig. 21. 



Pseudo-crisis. 

-Example of the temperature-curve in croupous 
pneumonia. (Personal observation.) 



exception, accompanied by a more or less high fever with a very typical course. 
In the beginning of the fever the temperature increases very rapidly to a high 
point. Even during the initial chill the bodily heat increases from normal to 

about 104° (40° C.) and over. 
1234 5 6789 10 There are at present no obser- 
vations to show whether, in 
the cases of pneumonia that 
begin gradually, there is ajso 
a gradual increase of the fever. 
During the course of the dis- 
ease the fever shows on the 
whole a continuous or remit- 
ting character, but there is 
with this a decided tendency 
to single deep falls of tempera- 
ture. Since these at first may 
easily be taken for the actual 
occurrence of crisis, although 
later they are proved by the 
renewed rise in temperature 
to be a mere temporary 
decline in the bodily heat, 
they are termed pseudo-crises. 
Pseudo-crises are usually seen 
in the first days of the disease, 
but in some cases they appear later. They may be repeated once or oftener, so 
that then the fever has a decidedly intermitting course. These intermitting 
pneumonias, so called from the course of the fever, have nothing at all to do with 
malaria, which fact must 
be especially noted because 
of the frequency of erro- 
neous statements. 

The fever may be de- 
cidedly high in pneumonia, 
often reaching 105° or 106° 
(40°-41° C). The highest 
temperature observed by us 
was 107-8° (42-1° C). In 
general there is a parallel 
between the height of the 
fever and the severity of 
the case, but sometimes the 
most severe and even fatal 
cases run their course with 
a comparatively low fever, 
varying between 101° and 
103° (38-5°-39-5° Q). We 
usually see the greatest in- 
crease in temperature in 
the first days of the disease. We have certainly not seen such a special increase 
immediately before the crisis — the so-called perturbatio critica — as many state- 
ments would lead us to expect. We have seen a gradual decline in temperature 
quite frequently in the closing days in fatal cases, but the opposite condition also 



19 ll 



41-0° 



40-0° 



39-0' 



38-0' 



17 0< 



■HI IBinniUHHHHH 

■i nnEHMffiui 

isiiinn 

BmilliH I iM 



us 

■nr 
in 



■SBSSEflliSlli 

ssinSBSaSSaHsS 



Fig. 22. 



-Example of the temperature-curve in " intermitting " 
pneumonia. (Personal observation.) 



CROUPOUS PNEUMONIA. 



185 



obtains. A marked rise before death is not peculiar to pneumonia, but it occurs 
wlien there is a complicating meningitis. 

The beginning of the fever is the most characteristic portion of the pneu- 
monia-curve. The fall in temperature usually comes on in the form of a decided 
crisis. During the night there is generally a sinking of the temperature with a 
more or less abundant perspiration, in which as a rule the temperature may reach 
a subnormal point— 96° to 95° (36-°35°C). The critical decline is often broken by 
new and slight elevations of temperature, so that on the morning of the next day 
there may be a definite increase of fever, the so-called protracted crisis. Only in 
a comparatively small number of cases does the fever end by lysis, in which the 
temperature goes down like steps. The duration of lysis is seldom more than 
three or four days at most. A decline of temperature by lysis is most frequent in 
severe and protracted cases, in so-called typhoid pneumonia {vide infra), or in 
pneumonia migrans. 

Although the pathological process in the lungs by no means ends with the 
crisis, we usually consider the day of the crisis as the last day of the disease. 
The pneumonia makes no advance after that, but resolution and absorption of the 
exudation and the return of the patient's strength still take time. Hippocrates 
knew when the time of the crisis occurs, and that the odd days, especially the 
fifth and the seventh, have a special significance in regard to it. In an infectious 
disease that has a typical course there can be nothing strange in the fact that 
the increase of fever, to a certain degree, is associated with a definite period of 
time ; but Hippocrates's rule has frequent exceptions. The crisis sometimes 
occurs on the ninth, the twelfth, or the thirteenth day, and even later, and, 
on the other hand, there are quite short pneumonias of but one or two days' 
duration. 

In the days following the crisis the temperature, which, as we have said, usu- 
ally falls to subnormal, regains its normal height. The pulse, which usually sinks 
to fifty or sixty during the crisis, when it often shows a slight irregularity, 
reaches its normal frequency again in a few days. We quite often see, in the 
days immediately following the crisis, a slight increase of temperature again, 100° 
to 102° at most (38°-39° C), but this has no special significance. 

The general revolution which the whole character of the disease undergoes after 
the crisis is often astonishing. The rapid decline in the respiratory symptoms is 
especially striking. The return of the affected portion of the lung to normal fol- 
lows in quite a short time. The expectoration is more abundant but less viscid. It 
loses its bloody character and is simply catarrhal. In cases which run their course 
regularly, the signs in the lung on auscultation and percussion become normal 
again in about five to eight days after the crisis. Abnormally delayed resolution 
will be mentioned below. 

Special Peculiarities and Anomalies in the Course of Pneumonia. 

1. Pneumonia in Children. — Beside the common lobular pneumonia there is 
also a pure, lobar, croupous pneumonia in children which is by no means so rare 
as some authors formerly supposed. An initial chill is seen only in older chil- 
dren ; initial vomiting, however, is very common in pneumonia in children. In 
many cases severe cerebral symptoms, like delirium, drowsiness, or convulsions, 
obscure the pulmonary symptoms at first. The further course, the development of 
physical signs, the fever, and the complications are quite analogous to the appear- 
ances in adults. The pneumonic sputum is only exceptionally to be observed in 
children under eight years of age. 

2. Pneumonia in old people is always dangerous. It may begin suddenly, 



186 



DISEASES OF THE RESPIRATORY ORGANS. 



as in pneumonia in people of middle age, but often it begins more slowly and 
insidiously. Its course is marked by the speedy onset of great weakness and 
debility. Nervous symptoms, like delirium, are not infrequent. 

3. Drunkard's Pneumonia. — We see croupous pneumonia in drunkards remark- 
ably often. The clinical course is characterized by the development of symptoms 
of delirium tremens, usually in the first days of the disease. The patient's mind 
is disturbed, he is very restless, constantly tries to get out of bed, and he pretends 
to keep a tavern night and day in his bed with the bed-clothes or articles of cloth- 
ing. The alcoholic character of the delirium is shown by the patient's whole man- 
ner, the tremor of the hands and tongue, and the usually happy character of the 
delirium. The delirium usually refers to his favorite beverages, his previous boon 
companions, etc. He becomes tearful or raving only when forcibly restrained. 
He usually thinks himself involved in the tavern brawls. The alcoholic delir- 
ium is almost always associated with hallucinations. The hallucinations of little 
moving black figures are especially characteristic. They are either animals, rats 
or beetles, or little black men, and they give him much trouble. The subjective 
symptoms of pneumonia are wholly in the background. No delirious patient 
with pneumonia complains of cough, pain in the chest, or dyspnoea. Careful 
objective examination is the only thing that confirms the diagnosis. Very often 
patients with a happy delirium serve to entertain those about them, until sud- 
denly very severe symptoms arise, and they become somnolent and succumb, with 
the symptoms of pulmonary oedema. The prognosis of every case of drunkards' 
pneumonia, therefore, is to be regarded as very unfavorable. 

4. Pneumonia in Pre-existing Chronic Diseases. — Croupous pneumonia is 
occasionally seen in all forms of chronic disease. It is especially dangerous hi 
person? who are already enfeebled, or people with chronic cardiac or pulmonary 
disease, like phthisis or emphysema. The pneumonia which often attacks patients 
with emphysema is clinically important, since emphysema sometimes renders the 
objective evidence of pneumonia very difficult. The croupous exudation does not 
completely fill the dilated alveoli ; hence decided dullness and bronchial breath- 
ing are absent. 

5. Pneumonia with late or slight Localization — Central Pneumonia. — Cases 
are quite often seen whose beginning, course, and subjective symptoms correspond 
throughout to a croupous pneumonia, but in which the objective evidence of pneu- 
monic infiltration is absent in spite of the most careful examination. The disease 
begins with a chill, the fever is high, the patient complains of pain in the chest, 
which is usually slight, there is often herpes, but only on the fourth, fifth, or sixth 
day can we make out anywhere any bronchial breathing or crepitant rales. In 
other cases even crisis may set in before we are able to localize the pneumonia 
with certainty. In most of these cases we probably have to do less with an 
actual late development of the localization than with a central infiltration which 
nowhere approaches the periphery, and hence is made out objectively only late or 
not at all. A careful examination of the sputum is of the greatest diagnostic 
importance, since it sometimes has a perfectly characteristic appearance in spite 
of the absence or the indefinite character of the physical signs. If there is no 
sputum, the diagnosis must of course remain very uncertain. In such a case 
under our own observation a slight pleuritic friction-sound was not heard until 
the day after the crisis, but this, added to the rational signs, made the diagnosis 
of pneumonia certain. 

6. Typhoid Pneumonia — Asthenic Pneumonia. — By typhoid pneumonia we 
mean those cases in which, beside the local pulmonary symptoms, which may be 
either slight or very well marked, there are remarkably severe general symp- 
toms. The cases do not often begin as suddenly as ordinary pneumonia, but 



CEOUPOUS PNEUMONIA. 



187 



more gradually like typhoid. Even at first the general symptoms, like great dull- 
ness, loss of appetite, or headache, predominate over the thoracic symptoms. At 
the height of the disease there is a decided typhoidal state, stupor, delirium, a very 
dry tongue, great general weakness, and also enlargement of the spleen, and fre- 
quently mild jaundice, albuminuria, etc. Such cases are to be regarded as pneu- 
monia with an unusually severe general infection. They sometimes occur in epi- 
demics. It is said that pneumonia of the upper lobes shows a somewhat more 
frequent tendency to severe nervous symptoms than pneumonia of the lower lobes. 
Recovery from this typhoid or asthenic pneumonia, which may last two weeks 
or more, often follows by lysis. Typhoid pneumonia is by no means a sharply 
defined disease. It serves merely for a short name for the severe general type of 
the disease. Clinically it is impossible to distinguish it sharply from pneumonia 
migrans, bilious pneumonia, and other forms. 

The croupous pneumonia which comes on in the course of genuine typhoid 
is serologically quite different, but in diagnosis it is often very hard to distinguish 
it. Here we have typhoid with a secondary localization in the lungs — " pneumo- 
typhoid " (see page 12), which is rare. In the cases first described, however, we had 
a pneumonia with very marked general infection — "typhoid" symptoms. The 
only things which render an accurate differentiation of the two diseases possible 
in such cases are observation of the whole course of the disease, attention to all 
the single symptoms, like the intestinal symptoms, and roseola, and the few setio- 
logical relations. 

7. Pneumonia with Delayed Resolution. — While resolution of pneumonia is 
complete, as a rule, in three days to a week after the occurrence of crisis, there are 
cases in which this process demands a much longer time. The dullness and 
bronchial breathing persist, while the moist rales which are heard on resolution 
do not appear. The delay in resolution is of very different length in different 
cases, but complete resolution may finally set in after three or four weeks, or even 
longer. We would mention particularly a form of delayed resolution in pneu- 
monia which we have observed in four cases which resembled one another very 
closely. The patients remain free from fever for some weeks after the crisis 
appears. During this time the dullness remains and the bronchial breathing, 
usually not very loud, is constant. Then a moderately intermitting fever comes 
on again, with an increase of temperature to about 102° or 103° (39°-39'5° C). 
This fever may last from two to four weeks, or even longer. Only occasionally, 
if ever, do we hear a rale over the affected portion of the lung. A moderate con- 
traction of the affected side gradually appears. Then the resonance slowly becomes 
clearer, and the respiration becomes louder and clearly vesicular again. The fever 
disappears, and complete recovery finally takes place. We have demonstrated, 
by making an exploratory puncture, that we have not to do with a pleurisy in 
these cases, though we do not venture to give a definite opinion as to the histo- 
logical basis of the process under discussion (transformation of the contents of the 
alveoli into connective tissue ?). The course taken by such cases is practically 
important, because at first we feared a transition from pneumonia into a chronic 
tubercular affection, but yet a complete and permanent recovery followed. 

8. Termination of Pneumonia in Phthisis, Contraction of the Lungs, Pul- 
monary Gangrene, or Pulmonary Abscess. — Three terminations of pneumonia 
are ordinarily mentioned as unusual and anomalous : the termination in " chronic 
pneumonia," in gangrene, and in abscess. 

Concerning the termination in chronic pneumonia, we have already mentioned 
a process belonging here, the termination in contraction with ultimate recovery ; 
but in rare cases the contraction is persistent. From the complete lack as yet of 
careful post-mortem examinations, we can not give fuller details as to the anatom- 



188 DISEASES OF THE RESPIRATORY ORGANS. 



ical process in these cases (hyperplasia and retraction of the inter-alveolar con- 
nective tissue ?). 

By the " termination in chronic pneumonia " we usually mean a termination 
in phthisis — that is, tuberculosis. With our present conception of the two diseases 
there can, of course, be no question of an actual transition from one to the other. 
Accordingly, where a clear case of phthisis develops as a sequel to genuine croup- 
ous pneumonia — which, however, is quite rare — either the pneumonia develops 
upon a pre-existing tuberculosis, or tuberculosis develops after the pneumonia in a 
person predisposed to tubercle. 

The transition from pneumonia to pulmonary gangrene is sometimes seen, 
especially in old and weak individuals. Here, too, in our opinion, a new infec- 
tion, with a foul and putrid substance, must always take place, and this excites the 
gangrene. The previous pneumonia furnishes only the occasion for the develop- 
ment of gangrene, and perhaps prepares the soil for the agents of decomposition. 
The development of gangrene is made apparent clinically by the change in the 
sputum. 

The transition from pneumonia to pulmonary abscess is very rare. We can 
not decide whether a special further cause is also needed for this, or whether the 
pneumonic process may exceptionally go on into the formation of abscess. The 
transition to an abscess may be recognized by the constitution of the sputum, 
which contains fragments of pulmonary tissue, such as elastic fibers, beside abun- 
dant pus. Beside that, we find, on microscopic examination of the sputum in 
abscess, sometimes scales of cholesterine (Fig. 23) and hsematoidine crystals ; the 
latter may be so abundant as to give the expectoration a brownish color. Some- 
times we have seen a peculiar greenish color of 
the sputum. The signs of a cavity are found in 
the lungs if the abscess opens externally. 

Diagnosis. — No special remarks on diagnosis 
need to be added to the description we have given 
\ of all the important symptoms which may occur 
\ in croupous pneumonia. We should pay par- 
ticular attention to the sudden onset, the char- 
/ acteristic sputum, the physical signs, the fre- 
/ quent occurrence of herpes on the face, and 
finally to the whole course of the disease, 
especially to the temperature-curve. We will 
discuss the differential diagnosis between pneu- 
monia and pleurisy with effusion more fully 
Fig. 23.— Cholesterine crystals. in the description of the latter affection. 

Prognosis. — Croupous pneumonia belongs 
in general to the benignant infectious diseases. The great majority of cases, 
in previously strong and healthy individuals, run a favorable course, and end in 
complete recovery. On the other hand, pneumonia brings a number of dangers 
with it, the knowledge of which should always make us cautious in giving a 
prognosis. 

A grave danger lies in the extension of the process. If the advance of the 
pneumonia can not be stopped, if the whole of one lung is involved, and, beside 
that, a great portion of the other lung, the diminution of the respiratory surfaces 
forms a factor which may give rise to a fatal termination. 

A further danger lies in the onset of certain complications. An intense pleu- 
risy, with effusion, especially if purulent, causes greater difficulty in respiration, 
and thus increases the danger. Still more dangerous is a sero-fibrinous or puru- 
lent pericarditis, which, in not very rare cases, is revealed at the autopsy as the 




CKOUPOUS PNEUMONIA. 



189 



special cause of death. We must note, however, that recovery sometimes finally 
takes place in spite of an empyema or of a purulent pericarditis. The complica- 
tion with a purulent meningitis, which is fortunately very rare, is probably invari- 
ably fatal. 

The dangers of general infection occupy a subordinate place in pneumonia, on 
the whole, in comparison with other infectious diseases, like typhoid, but general 
infection is important in the so-called typhoid, asthenic pneumonia. Sometimes 
unusually severe and malignant forms of pneumonia, with a high mortality, occur 
in epidemics and endemics, but these cases are often characterized by the extent of 
the local process, or by the development of the dangerous complications mentioned 
above. 

The individual circumstances of the patient play the most important part in the 
prognosis of pneumonia. While a constitution that was previously healthy and 
uninjured usually survives the disease, one that was previously weak and diseased 
readily succumbs. Tn this fact lies the danger of pneumonia in old, weak, badly 
nourished persons, and in persons with a pre-existing emphysema, kyphoscoliosis, 
heart disease, etc. In this, too, lies the great danger of every pneumonia in drunk- 
ards. Since the nervous system is much affected by chronic alcoholism, we very 
often see outbreaks of delirium tremens in pneumonia, which come on very read- 
ily. In like manner the other nerve-centers are weakened and incapable of resist- 
ance, especially the regulatory centers for the heart and respiration. Hence we 
can understand why even moderate drinkers, though previously strong and well 
to all appearance, succumb in pneumonia from insufficiency of the heart and 
lungs. 

If we ask upon what symptoms our prognosis in any given case should depend, 
we must reply that no single factor can be given especial prominence. Chief 
stress must always be laid upon the condition of the lungs and the respiration, but 
attention must also be given to the general condition, the heart's action, the height 
of the fever, etc. The chief dangers of pneumonia have just been mentioned. 

Of the abnormal terminations of pneumonia, contraction gives the best prog- 
nosis, but recovery, or at least a marked subsidence of all the symptoms, may some- 
times take place after gangrene and abscess. 

Treatment. — Many of the milder cases of typical pneumonia need no special 
active treatment when the disease on the whole takes a favorable course. Most 
cases get well under, or, we can almost say, in spite of any treatment. From the 
method of treatment by large bleedings, which was formerly customary, and also 
by certain drugs which are even now occasionally used — we refer especially to 
veratrine— we should expect an injurious effect, and not a favorable one ; and yet 
even with such treatment many cases of pneumonia get well. 

[There is good evidence that large doses of quinine — twenty to forty grains — 
given early in the course of the disease, abort it in some cases ; the precise mode 
of action is not known. 

In robust individuals, with a full, hard pulse and great oppression of breathing, 
venesection affords a prompt relief to be obtained in no other way. 

In general, the main indications for treatment are, as in other acute self -limited 
diseases, to support life until the disease has run its course.] 

We do not know a remedy which can in any way exert a favorable influence 
upon the pneumonic process itself. The treatment of pneumonia must therefore 
be purely hygienic and symptomatic, but in this respect it can accomplish very 
much. 

The symptoms which are usually prominent in every pneumonia, even in the 
milder cases, and of which the patient is especially desirous to be relieved, are the 
pain in the side, the troublesome cough, and the difficulty and distress in breath- 



190 



DISEASES OF THE RESPIRATORY OKGANS. 



ing. Since the respiratory symptoms, as we have seen, are partly due to the pain, 
as this improves the patient's breathing often undergoes a decided improvement. 
To quiet the pain we may first mention a number of external applications to the 
skin on the affected side. An ice-bag sometimes gives marked relief. Many 
patients can not bear this, but prefer warm poultices, or cold wet compresses. The 
application of mustard plasters or dry cups to the skin may be of advantage. Sub- 
cutaneous injections of morphine, however, are the most effective remedy, and 
are often indispensable. There is no reason why we should not use this remedy, 
with care and in moderate doses, for the relief of pain ; and, as the disease is of 
short duration, we need not particularly fear the morphine habit. Small doses 
of morphine, subcutaneously or by the mouth, are often required to alleviate the 
cough. 

Local blood-letting is a remedy, the action of which can not be explained 
physiologically, and yet experience has shown that it is of undoubted advantage. 
The relief which many patients feel after the application of ten or twelve leeches 
to the affected side is very striking ; but we should prescribe them only when 
there are severe symptoms at the beginning of the disease, and in persons who 
were strong and healthy before the attack. Wet cups accomplish the same thing, 
but the effect is somewhat more powerful, and hence they should be used in strong 
and robust people, like laborers. 

The tepid bath serves as the most effective means of improving the respiration, 
of aiding expectoration, and of elevating and refreshing the whole general con- 
dition. We hold it disadvantageous, if not injurious, to give a patient baths if 
the disease is progressing favorably, for almost every bath has some disagreeable 
feature. These disagreeable features, however, are always less, in severe cases, 
than the benefit and improvement which most baths give the patient, and which 
most patients recognize with gratitude. The main point is that the patient should 
make no physical exertion while in the bath, that he should be lifted into it, held 
and supported while in it, and lifted into bed again after it. Since the baths are 
given, primarily, not on account of the fever, but to improve the respiration, and 
on account of their favorable influence on the nervous system, their temperature 
need not be especially low. We usually give them from 85° to 90° (24°-26° R.) ; 
somewhat warmer with sensitive and weak people, and cooler, down to 77° (20° 
R.), with strong people or with very high fever or severe nervous symptoms. We 
need not give more than two or three baths a day, and at night we give them 
only when there are threatening symptoms. The favorable action of the baths 
is especially seen in the great relief and refreshment that the patient feels. The 
respiration is quieter and slower, but deeper. The patient often falls into a quiet 
sleep after the bath. 

Antipyretics are usually useless in pneumonia. Even if the temperature rises 
very high, up to 106° (41° C), cool baths are sufficient to avert the dangers of an 
increase of bodily heat. Only rarely are we led to use quinine, or, better, antipy- 
rine (see page 22) in pneumonia. 

Expectorants are much used, especially since in practice we seldom can avoid 
giving some internal remedy. Among the most useful are an infusion of ipecac- 
uanha, liquor ammonii anisatus, and tartar emetic, once held to be a necessary 
specific against pneumonia (!). Finally, digitalis may be indicated under some 
circumstances with a weak and frequent pulse, in an infusion of about 1*5 to 150. 

We must give the greatest attention in all severe cases to keeping up the pa- 
tient's strength. We must therefore take care to furnish an easily digestible but 
nutritious diet. Small pieces of meat, cut up fine or scraped, may be freely al- 
lowed if the patient has an appetite for it, but during the first days of the disease 
we are usually confined to giving soups, milk, and eggs. As soon as the signs of 



TUBERCULOSIS OF THE LUNGS. 



191 



more marked general weakness appear, and the pulse becomes smaller, we must 
use stimulants, wine, strong cafe noir, or still better, ether, or camphor. The latter 
is best given subcutaneously in severe cases, dissolved in olive-oil, in a ratio of one 
to four. If the patient swallows well, we may give it in powder, two grains (grm. 
O'l) every one or two hours in wine. 

We have yet to make some remarks upon the very extensive use of large 
amounts of alcohol in pneumonia. Without doubt a free use of alcohol is neces- 
sary in drunkards, especially when delirium tremens is beginning or is already 
pronounced. Since the withdrawal of any poison that is taken habitually, like 
nicotine or morphine, may excite the severest symptoms, the sudden withdrawal 
of alcohol from drunkards may have the worst results, while, if we give an abun- 
dant supply of the stimulant to which the nervous system is accustomed, we some- 
times succeed in avoiding the onset of severe nervous symptoms, like collapse and 
failure of the heart and respiration. It is quite a different matter with patients 
who before then illness have not been accustomed to take alcohol at all, or who 
took it only in small amounts. It may be true that in these cases small amounts 
of wine may have a stimulating and exciting action, although we never could 
satisfy ourselves of the often praised influence of alcohol upon the action of the 
heart. We hold it, however, unjustifiable to force large amounts of alcohol indis- 
criminately upon every patient with pneumonia, often in spite of great resistance 
on his part. Why should we expect sick people to bear doses of alcohol which 
have only bad results on healthy men unaccustomed to them ? 

[Few American physicians of any experience will accept the reasoning of the 
author on the use of alcoholic stimulants in those not accustomed to their use. 

The toxic effects of alcohol are as undesirable in pneumonia as in any other 
disease, but there are few affections in which so great tolerance is shown for this 
agent. The chief indications for its use are derived from the pulse and the first 
cardiac sound at the apex. A flagging heart calls for alcohol, the effect of which 
on the symptoms and on the circulation is to be carefully watched ; the quantity 
is to be diminished, increased, maintained, or the agent is to be omitted entirely, 
according to the conditions present in the individual case. I am no advocate of 
indiscriminate alcoholic stimulation ; but I believe that lives have been frequently 
saved in the past, and will be saved in the future, by the judicious and sometimes 
extremely free use of this class of remedies in acute pneumonia.] 

The treatment of complications follows the rules in general use, which have 
been given under the individual affections. We must also mention that, in delir- 
ium tremens, tepid baths with cold douches sometimes have a very good effect. 
Beside this, we may try subcutaneous injections of strychnine, seven to fifteen 
minims of a one-per-cent. solution, once or twice a day. We can not wholly dis- 
pense with narcotics, like morphine and chloral, but we must warn against the 
imprudent use of large doses of chloral, above thirty-five grains (grm. 2 '5). 



CHAPTER VI. 

TUBERCULOSIS OF THE LUNGS. 

{Pulmonary Phthisis. Pulmonary Consumption.) 

General Pathology and ^Etiology of Tuberculosis. 

Ever since Bayle, in 1810, demonstrated the extensive distribution of peculiar 
nodules in the various organs, and their relation to pulmonary consumption, few 
questions have so taxed clinical observers and pathologists as those relating to the 



192 



DISEASES OF THE RESPIRATORY ORGANS. 



cause and nature of tuberculosis. Harmony could not be reached, however, as long 
as the criterion for the decision of the questions was sought in the presence of definite 
anatomical changes, which were regarded as specific of tuberculosis. Laennec 
considered the peculiar change in the tubercular products, which later was named 
caseation by Yirchow, to be characteristic, and called everything tubercular where 
it was found. He distinguished the isolated tubercle from diffuse, tubercular, 
cheesy infiltration. Thus Laennec recognized that many processes were allied 
whose affinity was often disputed afterward, and has only recently been estab- 
lished, such as the affinity between " scrofulous " enlargement of the glands and 
tuberculosis. Another opinion became quite prevalent, after Yirchow discovered 
that precisely the same anatomical process as tubercular caseation was also found 
in mflammatory products, which were certainly not tubercular, and in cancerous 
ulcerations. Hence Virchow made a sharp distinction between tubercle and those 
new growths and inflammatory processes which had become cheesy. The ana- 
tomical criterion of tuberculosis was, in his view, the presence of the miliary 
tubercle, a gray nodule, the size of a millet-seed at the largest, made up of cells 
like lymph-corpuscles. The study of the finer structure of the miliary tubercle 
was now pushed most eagerly by Wagner, Schiippel, Langhans, and others, but 
they were unable to reach perfect harmony regarding its origin and significance. 

As long ago as 1865, however, a discovery was made which pointed unequivo- 
cally to the only way which could lead to a correct knowledge of tuberculosis. It 
was the fact, discovered by Villemin, that tuberculosis can be produced artificially 
by inoculating healthy animals with small amounts of tubercular and cheesy sub- 
stances. Although doubted and misinterpreted at first in various quarters, the fact 
that tuberculosis can be transmitted, and, consequently, the fact of its infectious 
character, must now be regarded as proven beyond a doubt. In the general 
change which our opinions upon the nature of infectious diseases have under- 
gone, especially in the last few years, the existence of a specific, organized cause 
of tuberculosis, too, had to be assumed. Klebs and later Cohnheim had already, 
without reserve, defined tuberculosis as a specific, infectious disease, and, sooner 
than we dared to hope, R. Koch discovered the special carriers of the disease, in 
the shape of the tubercle bacilli, in the year 1881. The definition of tuberculosis 
no longer rests upon any external anatomical character. Every disease is tuber- 
cular which is excited by the pathogenetic action of a specific kind of bacteria, 
the tubercle bacilli discovered by Koch. 

The pathogenetic bacteria of tuberculosis belong to the group of bacilli. The 
tubercle bacilli consist of very small, rod-like bodies, about one fourth or one half 
as long as a red blood-corpuscle. They are detected by then' peculiar property of 
not being affected by the ordinary methods of staining granules and bacteria, but 
by being deeply colored by certain other staining fluids (vide infra). We know 
with certainty that they are always present in all the different forms of pulmo- 
nary tuberculosis, both in the lung itself and in the expectoration (vide infra), and 
also in tubercular diseases of other organs, like the brain, the intestines, the spleen, 
the liver, and the kidneys, and also in " scrofulous lymph-glands," in " fungous " 
diseases of the bones and joints, and in the so-called lupus, which is nothing but a 
local tuberculosis of the skin. Precisely the same bacilli are also found in the 
" spontaneous " tuberculosis of animals, such as monkeys, puppies, and guinea-pigs, 
and in every tuberculosis that is artificially produced in animals by inoculation. 
Finally, by the discovery of tubercle bacilli in the " pearly distemper" of cattle, 
the identity of this disease with tuberculosis — an identity which had already been 
established by experiments in inoculation — was confirmed anew. 

Koch, by his successful " pure cultures " and inoculations with the cultivated 
bacilli, has established the fact that these bodies, known as tubercle bacilli, are to 



TUBEECULOSIS OF THE LUNGS. 



193 



be regarded as organized, and as the special cause of tuberculosis. Bacilli coming 
from any fresb product of tubercular disease may be cultivated at a constant tem- 
perature of 98° to 100° (37°-38° C.) in blood-serum, which has been stiffened by heat- 
ing, or in any other nutritious soil that has been prepared artificially. In this 
cultivation they show certain characteristic properties in their growth, which can 
not be fully described here, and they multiply to an unlimited extent. In this way 
we can keep up perfectly " pure cultures " of tubercle bacilli. Inoculation experi- 
ments tried with them on all sorts of creatures, always give a positive result. The 
animals fall ill, lose flesh, and finally die, and at the autopsy we find undoubted 
tubercular disease of the internal organs, which may be more or less extensive. 
The most instructive inoculations are those into the anterior chamber of the eye 
in puppies or guinea-pigs, which were first tried by Cohnheim and Salomonsen. 
After an incubation of two or three weeks we see here very plainly an eruption of 
the first nodules of tubercle in the iris, and the tuberculosis spreads to the other 
organs of the body later. 

^Etiology of Tuberculosis in Man. 

The distribution of tubercle bacilli must be remarkably extensive, for tuber- 
cular diseases occur in almost every country on earth. The predisposition of man- 
kind to the disease is also very great, and thus we understand the frightful fact, 
which statistics show, that nearly one seventh of all deaths are from tuberculosis ! 
It has neither been proved, nor is it probable, that tubercle bacilli multiply out- 
side of the human body, like the bacilli of splenic fever, since they can develop 
only in a constant and uniformly warm temperature between 85° and 105° (30-40° 
C). We must, therefore, regard them as true parasites, which can live — that is, 
which can propagate and multiply — only in the bodies of animals, but they seem 
to preserve their virulence and their ability to multiply outside of the body for a 
long time. Phthisical sputum may be used for inoculation with success, even if 
it has been dried for several weeks. The tubercle bacilli also resist most chemical 
reagents, like nitric acid, very decidedly. 

If the body becomes infected, then, with tubercle bacilli, they probably always 
come originally from some other individual — man or beast — with tubercular dis- 
ease. "We need not mention how numerous the opportunities for infection may be 
considering the present general distribution of tuberculosis. The chief stress in 
this respect is to be laid upon the sputum of phthisical patients, which contains 
the bacilli, and which is in great part expectorated. This dries on the floor, on 
the linen, and on other objects, and then the smallest particles which contain the 
germs of .infection are carried off by the air. The material which contains the 
bacilli or spores is taken into the body, in the majority of cases, along with the 
inspired air. This is probable because, in most cases, tuberculosis has its starting- 
point in the air-passages, the lungs, or larynx. Inoculation experiments show that 
the first extension of the process depends upon the point of inoculation. If it be 
in the anterior chamber of the eye, the first nodules appear in the iris, as we have 
said ; if it be in the abdominal cavity, we have first a tuberculosis of the perito- 
neum ; if the infectious matter be inhaled, we have first a tuberculosis of the 
lungs. For several years Tappeiner and others have experimented with inhala- 
tions of powdered tubercular sputa at the Munich Pathological Institute. Pulmo- 
nary tuberculosis could always be produced by these inhalations in the animals 
experimented upon. Hence it seems very probable that, in tuberculosis in man, 
the infectious matter is taken directly into the air-passages by the breath. In 
this way it sometimes, though rarely, attacks the upper air-passages, as in primary 
tuberculosis of the nose, the pharynx, and the larynx, but more frequently it 
13 



194 DISEASES OF THE RESPIRATORY ORGANS. 



affects the deeper portions of the respiratory apparatus, as in primary tuberculosis 
of the lungs and bronchi. 

We must also consider other methods of infection, first among which is the 
possibility of infection of the intestinal canal, from swallowing the infectious 
material. The transmission of tuberculosis from domestic animals to man plays 
a part in this connection which, perhaps, is not unimportant. Since the pearly 
distemper in cattle is identical with tuberculosis in man, the use of the flesh 
of such animals as food furnishes a possible means of infection. It is a still 
more important circumstance, however, that, when pearly nodules have been 
shown to be present on the udder, the milk of the diseased animal may be pol- 
luted by tubercle bacilli, and that the use of such milk as food, when it is un- 
cooked, certainly involves the danger of the transmission of tuberculosis. Pri- 
mary tuberculosis of the intestines, however, does not seem to be very frequent, 
probably because the tubercle bacilli, which have been swallowed, are usually 
destroyed in the stomach. 

In some cases the tubercular infection may probably arise from little fissures 
and excoriations of the skin. In this way we get either a local tuberculosis of the 
skin, like lupus, or the bacilli are carried by the lymphatics to the neighboring 
glands of the neck or axilla, establish themselves there, and set up a tubercular 
disease in them. In conclusion, we have still to mention that the apparently 
primary appearance of tuberculosis in the genito-urinary apparatus leads us to 
think of the possibility of an infection of the genital or urinary organs. 

Considering the wide distribution of the tubercle bacilli, and the many chances 
for infection, it seems wonderful that in spite of it so many men escape the dis- 
ease. One factor, which has been already mentioned by Koch, must be borne in 
mind, however, and that is the extremely slow growth of the tubercle bacilli. 
This is the reason why the bacilli do not readily remain in the body, but in many 
cases are eliminated again before they have gained a definite foothold. 

Individual predisposition, however, is another factor, which, perhaps, is still 
more important — a factor which we can not well explain, but which we can not 
get on without, at the present time, in the pathology of many infectious diseases. 
In our conception of most of the other infectious diseases, as well as of tuberculosis, 
we must assume provisionally an unlike predisposition to disease in different 
individuals. Only a part fall ill of all who are exposed to the action of the 
poison, and in these persons the poison may establish itself and extend farther. 

We have long considered people with a generally feeble physical constitution 
as especially liable to tubercular disease. We speak of a "tubercular habit" 
{vide infra). In this connection we must, of course, remember that much that 
we once regarded as merely the signs of a special predisposition to disease is 
really the expression of a disease that already exists. If, for example, we once 
affirmed that " scrofulous " children had a special predisposition to tuberculosis, 
we know now that the so-called scrofulous diseases of the mucous membranes, the 
lymph-glands, and the bones, are the results of an existing tuberculosis ; or, at 
least, that this is so in a large number of cases. 

We now believe that many evil influences, which were once thought to be 
causes of tuberculosis, act only in increasing the disposition to the disease. In- 
sufficient food, bad air, severe illness, childbirth, want and care — these alone, of 
course, can never produce tuberculosis, but we can easily imagine that the body 
which has become weakened affords less resistance to the injurious influence of 
the tubercular poison than does the strong and healthy body. 

People often used to speak of the transition of other affections of the lungs 
into pulmonary consumption — that is, into tuberculosis. It was imagined that 
an old bronchial catarrh, croupous inflammation of the lungs, or catarrhal 



TUBERCULOSIS OF THE LUNGS. 



195 



pneumonia in measles, or whooping-cough, could readily become "tubercular." 
It goes without saying now that such an idea is no longer tenable, after the 
demonstration of the specific, infectious nature of tuberculosis. If we see a 
pulmonary tuberculosis develop as a sequel of any other affection of the lungs, we 
can express the relation between the two diseases only in this way, that the first 
disease furnished a favorable soil for infection with tubercular virus, and that, 
consequently, the tubercle bacilli could more easily take root upon a previously 
diseased mucous membrane than under normal conditions ; moreover, there is no 
doubt that many of the affections, whose " transition into tuberculosis " we once 
frequently assumed, are themselves tubercular. This is the case, as we shall see, 
in many cases of pleurisy. No one will now admit the truth of the theory, 
which Niemeyer once vigorously defended, that a primary pulmonary haemor- 
rhage could be the cause for the development of pulmonary phthisis. Certainly, 
in the cases which apparently support such an opinion, the pulmonary haemor- 
rhage is not the cause, but a symptom of pulmonary tuberculosis. 

No single factor, however, which favors the predisposition to tuberculosis, 
plays so manifest and so visible a part as does hereditary predisposition. The fact 
of the heredity of phthisis meets us with such uncommon frequency that it must 
have previously forced itself upon the notice of the older physcians. In the great 
majority of all cases of phthisis we can make out, by close questioning, that, in 
the family, either among the older members, or among the brothers and sisters, 
one or more cases of tubercular disease have already occurred. The closer we 
investigate, and the more we search for some one of the different forms in which 
tuberculosis can show itself, like pleurisy, or affections of the bones and joints, 
the more frequently we can make out this hereditary predisposition in patients 
with the disease. 

While there can be doubt of the facts themselves, their explanation is by no 
means a simple one. At all events, the question of the heredity of tuberculosis 
now needs to be worked up with renewed care. The hereditary character of 
tuberculosis may very well harmonize with its infectious character. We might 
assume, in that case, a perfect analogy with syphilis — namely, a transition of the 
infectious material from the parent to the child before birth. There is only one 
striking difference between syphilis and tuberculosis — that the children of syphilitic 
parents very often come into the world with definite signs of infection, while 
congenital tuberculosis, in this sense, is an extremely rare occurrence. We must 
accordingly compare tuberculosis to that form of hereditary syphilis (lues heredi- 
taria tarda) in which the first symptoms of the affection come on at a late 
period. 

Since certain considerations, however, constantly oppose such a theory, we are 
of late disposed to assume that, as a rule, tuberculosis in itself is not inherited, 
but only the predisposition to tubercular disease. This opinion agrees with the 
facts that members of a family in which tuberculosis prevails very often show 
the so-called tubercular habit, even without any real tubercular disease ; and that 
they often have " weak lungs " — that is, that they easily get out of breath and 
manifest a distinct tendency to catarrh of the respiratory organs. 

Meanwhile there is a third possibility to be considered with regard to the 
"inheritance of tuberculosis." Many cases of apparently inherited tuberculosis 
are, in all probability, to be explained by the fact that children or relatives who 
are constantly in the company of a patient with phthisis are decidedly more 
exposed to the danger of infection than other people. This is also the reason 
why tuberculosis is very often conveyed from husband to wife, or vice versa, 
of which we might furnish a series of examples from our own experience. 

The age of the patient has an important influence upon the predisposition to 



196 



DISEASES OF THE EESPIRATOEY ORGANS. 



tubercular disease. Pulmonary tuberculosis occurs with special frequency in 
youth, between fifteen and thirty. It is not rare in children. After forty it is 
much rarer in its pronounced forms, but it is seen even in the most advanced age. 

It has not yet been shown that sex has a special influence upon the predisposi- 
tion to the disease. 

Pathological Anatomy of Tuberculosis, especially of Pulmonary Tuber- 
culosis. 

The aetiology of tuberculosis has taught us that the system may be infected 
with a specific kind of pathogenetic micro-organisms which may excite all these 
manif old pathological lesions. These lesions must be brought into harmony with 
the great setiological unity of tubercular disease. In what, then, does the injuri- 
ous action of the tubercle bacilli in the body consist ? 

In the first -place, we must bear in mind that the action of the tubercle bacilli is 
primarily a local one. Tuberculosis does not belong to the " general infectious 
diseases," in which the infection of the whole organism, the " general infection " 
of the body, predominates over the local disturbances. The essence of tubercu- 
losis, at least in the great majority of cases, is the local disease. The tubercle 
bacilli give rise to definite anatomical changes in the organs where they settle, 
and the consequent disturbance of function in the organ has an effect on the rest 
of the body. In many cases the whole body may be so little affected that we may 
be justified in saying that there is a purely "local tuberculosis." 

The danger of tubercular diseases, however, consists in the fact that the local 
affection often attacks the most important organs, like the lungs and the brain, 
and sets up such extensive anatomical changes in them that because of these 
changes alone it becomes impossible for life to continue longer. Beside this, the 
infection, in many cases,, does not always confine itself to one organ, but the infec- 
tious material extends over the body by ways and means which we shall learn to 
recognize in part later on, and attacks one organ after another, or even many at 
once. 

"We can not wholly deny that there is also a general action of the tubercular 
poison beside the local action, and independent of it. Its explanation, however, 
is difficult, and the fact may be in part questionable. We will speak of it further 
in the description of the general symptoms and the fever. 

The entire local action of the tubercle bacilli — that is, the pathological anatomy 
of tuberculosis — is almost wholly dependent upon the organ examined. Tuber- 
culosis belongs to the group of so-called " infectious tumors " — that is, the local 
action of the tubercle bacilli consists chiefly in the production of a proliferation 
and accumulation of cells at their place of settlement, which is termed a tubercular 
infiltration or a tubercular new growth. This new growth is very often developed 
in the form of very small, miliary, or larger nodules — " tubercle " — which has given 
the name to the disease. The tubercle consists histologically of an accumulation 
of round cells, which look just like lymph-corpuscles or white blood-corpuscles. 
Beside these we find a few larger so-called epithelioid cells, and also two or three 
giant-cells, in the middle or near one edge. In these latter especially, but also in the 
others, we find, on employing certain special histological methods, the specific 
tubercle bacilli. It is also characteristic that a tubercular new growth contains 
no vessels. 

The larger nodules arise partly from the confluence of many small miliary 
nodules, but the tubercular new growth may also develop de novo in a more 
extensive and diffuse manner — as the so-called diffuse tubercular new growth or 
diffuse tubercular infiltration. 

The tubercular new growth as such is scarcely to be distinguished histologically 



TUBERCULOSIS OF THE LUNGS. 



197 



from other infectious tumors like syphilis, or lepra, but the further fate of the 
new growth is characteristic of tuberculosis — namely, the caseation and final 
destruction of the new-formed tissue. Both the tubercular infiltration, and also 
the components of the tissue surrounded by it, die, lose their nuclei, and are finally 
destroyed. The sort of death, " caseation," belongs to the group of so-called " coagu- 
lation necroses." Where the necrotic portions of tissue are superficial, they are 
thrown off, giving rise to the tubercular ulcer. 

Beside the tubercular new growths we also find in the diseased organs many 
simple, purulent or hemorrhagic inflammatory processes. We may therefore 
suppose that the tubercle bacilli may also act as agents of inflammation, and yet it 
is very probable that many of the inflammatory processes which develop in pul- 
monary tuberculosis do not belong to tuberculosis particularly, but are rather to 
be regarded as secondary {vide infra). 

As regards the special anatomical processes and appearances in pulmonary 
tuberculosis, the tubercular change usually begins in the walls of the smallest 
bronchi. The disease does not begin, however, in many different parts of the 
lung at once, but probably in one or two circumscribed spots only, and in a great 
majority of cases in one apex. We do not know why the apices are so often the 
starting-point of phthisis, but perhaps it is because of their relatively slighter 
excursion on respiration, which thus affords a favorable lodging-place for the 
tubercle bacilli. 

The tubercular infiltration begins in the bronchial wall and extends gradually 
to the periphery. A tubercular peribronchitis arises as a result of the original 
tubercular bronchitis. The infectious material, as soon as there is any superficial 
ulceration, is readily carried from the original focus of the disease to the other 
bronchi, by means of the current of air, and thus the disease gradually extends. 
Tubercular peribronchitis is usually easily recognized with the naked eye. We 
notice the little lumen of the bronchus in the middle of the "cheesy" nodule, 
which at first is gray and later yellowish. Many of the adjacent nodules run 
together in part and even entirely. The lumen of the bronchus is either wholly 
plugged by the infiltration, or the destruction of the necrotic cells begins in the 
midst of the peri-bronchitis. In the latter case the lumen is enlarged to a little 
irregular hole — the first beginning of the formation of a cavity. 

The alveolar tissue of the lung can not long remain unaffected with such a dis- 
ease of the smaller bronchi. Lobular atelectasis, the necessary result of every 
permanent bronchial obstruction, must arise, but this soon passes into a lobular 
pneumonia, which from its specific nature later becomes caseous. We can not go 
into the histological details here. The alveoli are filled with pus-corpuscles and 
large epithelioid cells, which are considered by many authors to be the offspring 
of the alveolar epithelium. The alveolar walls are also infiltrated. This finally 
results in the destruction of the cheesy and necrotic tissue, and consequently in 
the formation of cavities. At other times the neighboring nodules run together, 
and the tubercular infiltration thus extends, giving rise to a diffuse caseous pneu- 
monia. These processes may all be readily recognized by the naked eye. The 
earlier stages of atelectasis and infiltration correspond to the jelly-like, gray color- 
ing seen in the so-called gelatinous infiltration of Laennec, and the transition to 
caseation is recognized by the eye from the appearance of a yellowish color. 

Although all the processes thus far described are destructive in their nature, 
changes are also found in the lungs in tuberculosis, which seem to have a tendency 
toward circumscribing the disease and toward healing. Prominent among these 
are the chronic interstitial processes. We meet with the formation of new con- 
nective tissue, partly about the tubercular infiltration, but especially where there 
is already destruction of tissue, and this leads to contraction and the formation of 



198 



DISEASES OF THE RESPIRATORY ORGANS, 



a firm cicatrix. This is possible only when the tubercular new growth does not 
break down too rapidly, since otherwise this newly formed connective tissue may 
itself be destroyed before it can contract. We see the cicatricial formation, there- 
fore, more especially in chronic cases ; we find it in places which have been affected 
the longest, and where the tubercular process, perhaps, has finally come to a stand- 
still of its own accord. Macroscopically, this cicatricial connective tissue is com- 
posed of a thick, firm substance, usually pigmented — the so-called pigment indura- 
tion. If the cicatricial formation follows a previous extensive destruction of the 
pulmonary tissue, the affected portion of the lung may thus be diminished to more 
than half its bulk. Cavities and firm cicatricial tissue form the anatomical basis 
of such an extensive "pulmonary contraction." The cavities are either formed 
hi the usual way from the destruction of lung tissue, or they may be simple bron- 
chial dilatations due to the traction of the contracted tissue — bronchiectasic cavities. 

The contractile changes in pulmonary tuberculosis teach us that the tuber- 
cular process is in itself capable of healing. The incurability of most cases of 
phthisis is due to the fact that the infectious material from every existing tuber- 
cular nodule is carried into other bronchi, and there sets up a new tuberculosis. 
Thus the disease is constantly extended. The original tuberculosis, which was 
localized in one apex only, gradually spreads to the lower portion of the lung. 
The infectious material is carried by coughing into the trachea, and from this 
point may be carried by inspiration into the other lung. This becomes diseased, 
and finally there is such an extensive destruction of the lungs as to make the 
further continuance of life impossible. 

Beside the spots of specific tubercular disease, we very often find in phthisical 
lungs simple inflammatory processes, bronchitis, lobular catarrhal pneumonia, and 
sometimes even croupous pneumonia. This, of course, is rarely extensive. These 
changes may be partly due to the peculiarities of the tubercle bacilli themselves in 
exciting inflammation, but it is, of course, easily conceivable that many other 
excitants of inflammation may readily settle in the secretions of the bronchi and 
the cavities, and lead to complicating diseases of the bronchial mucous membrane 
and the alveoli. Thus in pulmonary tuberculosis a local gangrene may occa- 
sionally arise. 

If we consider the list of anatomical processes which are found in tuberculosis 
of the lungs, and which may be combined in the most manifold ways, we can 
understand the great difference in the anatomical picture in different cases. 
Simple bronchitis, tuberculosis of the bronchial wall and tubercular peribron- 
chitis, diffuse cheesy pneumonia, and destruction of the tubercular new growths, 
with the formation of cavities, on the one hand, contracting interstitial pneumo- 
nia, cicatricial formation and pigment induration on the other — these are the 
comparatively simple anatomical changes from which the whole process in its 
different forms is composed. Beside this, as we have still to add, we often find 
here and there one or more miliary tubercles scattered through the lungs which 
are probably due very largely to an extension of the infectious material by means 
of the blood or lymph current. 

The secondary tubercular diseases of the pleura and other organs will receive a 
special description. 

Clinical History of Tuberculosis in General and of Pulmonary Tuber- 
culosis in Particular. 

In judging of the various appearances in the clinical picture of tuberculosis 
we must especially consider the following points : The place of the first infec- 
tion is of the chief importance — that is, the place where a local affection, set 
up by the tubercular poison, first arises. As has been said, the lungs are the 



TUBERCULOSIS OF THE LUNGS. 



199 



organs first attacked, in a large number of cases, and such cases are termed pri- 
mary pulmonary tuberculosis. In other cases, as has already been mentioned, the 
tubercular poison first fixes itself in the larynx, as in primary laryngeal tubercu- 
losis, or it reaches the intestine, as in primary intestinal tuberculosis, or the genito- 
urinary organs, as in primary tuberculosis of the genito-urinary apparatus, etc. 
In other cases still we apparently have to do with a primary tuberculosis of the 
serous membranes {vide infra) or of the lymph-glands ; and finally we very often 
see primary tubercular diseases of the bones and joints, to which a large number 
of the formerly so-called chronic scrofulous and fungous inflammations of the 
bones and joints belong. It is obvious that all these diseases although identical 
setiologically must have a very different clinical appearance. 

Another reason for the great variation in the course of tuberculosis is found in 
the fact that the extension of the local tubercular process may vary very greatly 
as regards time. Tuberculosis in one case may produce the most extensive destruc- 
tion in both lungs in a few months or even weeks, and in another case it may 
remain almost quiescent for years, or advance only very slowly. We do not 
know on what these differences depend, but much is certainly due to the hygienic 
influences under which the patient lives. In the last instance, however, we are 
often led to think of individual differences of disposition, which now check and 
now favor the rapid extension of the disease. 

A third and final reason for the differences in the course of tubercular infec- 
tion is the manner of the further extension of the tubercular poison in the body. 
As we shall see in the description of tuberculosis in single organs, there are differ- 
ent ways in which tuberculosis may pass from one organ to another. Many con- 
tingencies are involved here, and we can easily comprehend how greatly the whole 
clinical course of the disease must be modified by the rapidity and the degree in 
which individual organs are affected. 

After these preliminary remarks, which we have thought necessary to a right 
understanding of tubercular disease in general, we will pass on to the description 
of the clinical course of pulmonary tuberculosis. 

The onset of pulmonary tuberculosis is quite slow and gradual in the majority 
of cases. The patient can give only an approximate idea of the time when he 
began to be ill. The symptoms which he notices are referred directly to the res- 
piratory organs. The cough and its attendant expectoration are the chief things 
which affect him. Beside that, there is often pain in the chest, either the pleuritic 
stitch, or a pain in the sternal region, or pain between the shoulder-blades. The 
patient also often complains of shortness of breath, especially on severe physical 
exertion. 

Beside these symptoms, which point pretty directly to disease of the lungs, 
there are often quite striking general symptoms. The patient's emaciation is 
especially noticeable, which may be partly, though often not wholly, explained 
by his loss of appetite. Beside the emaciation there is often a steadily increasing 
pallor of the skin. The patient also shows a general dullness, weakness, and dis- 
inclination to work. There is often a slight rise of temperature in the first stages 
of the disease, which causes chilliness and subjective feelings of heat. Severe 
night-sweats may also be noticed early. 

All such general symptoms should furnish an urgent reason why the physician 
should not regard the mild thoracic symptoms, which are also present, as insigni- 
ficant, but should think of the possibility of incipient tuberculosis. It is very 
important to remember that the pulmonary symptoms may be entirely subordi- 
nate to the general symptoms mentioned, and that the patient himself often pays 
little or no attention to them. Incipient phthisis is therefore frequently diagnos- 
ticated as simple " chlorosis " or " gastric catarrh " for a long time, and is treated 



200 



DISEASES OF THE RESPIRATORY ORGANS. 



as such. An early and careful physical examination of the lungs is the only pro- 
tection against such an error. 

Both the pulmonary and the general symptoms assume significance, if we have 
to do with a patient in whom we suspect a " tubercular predisposition." We very 
often meet people in whose family, either in the parents, or the brothers and sis- 
ters, several cases of phthisis have occurred. They are persons who are always 
pale and weak, and who have previously shown a special liability to disease, 
particularly to disease of the respiratory organs. They have often had diseases 
before, which our present theories bring into direct relation with tubercular infec- 
tion. We refer to those quite frequent cases of pulmonary tuberculosis in people 
who have previously suffered from " scrofulous diseases," like chronic swelling of 
the lymph-glands, chronic affections of the eye or ear, or fungous diseases of the 
bones and joints. This fact, as we have already said, does not signify that scrofula 
passes into tuberculosis. It is much more probable that many scrofulous diseases 
are really tubercular, as has been proven formerly by the result of inoculations in 
animals, and recently by the discovery of tubercle bacilli in " scrofulous " lymph- 
glands, or in the fungous nodules in the bones and joints. 

As we have said, pulmonary tuberculosis often develops in people who have 
suffered before from diseases of the respiratory mucous membrane, in whom, as we 
express it, the lungs have always been the locus minoris resistentice. The pre- 
disposition to tuberculosis may really perhaps coincide at times with the predispo- 
sition to other pulmonary affections ; thus we often see tubercular patients who 
have previously had several attacks of croupous pneumonia. In other cases, how- 
ever, the predisposition to tuberculosis is probably derived from some disease of 
the respiratory mucous membrane, although sometimes these previous diseases of 
the respiratory organs are themselves of a tubercular nature. This is especially 
true of pleurisy, but we will have to take up its relation to pulmonary tuberculo- 
sis somewhat more in detail in our description of pleurisy. 

Although the first symptoms of pulmonary tuberculosis often develop in peo- 
ple who were not quite well before, this is true in only a part of the cases. We 
often see precisely the same symptoms, both the pulmonary and the general symp- 
toms, occurring in people who previously seemed quite well and strong. No 
physical constitution is perfectly protected against the disease. We have even 
seen the herculean athletes of a circus die of phthisis. 

In distinction from the slow and gradual method of the development of tuber- 
culosis which has just been described, the first symptoms in other cases may be 
more sudden. A definite exposure is often given as a cause, after which the first 
symptoms of the disease have speedily developed. It goes without saying that we 
must consider these noxious exposures — like a chilling of the body, a cold draught, 
over-exertion, or marked mental excitement — at most, as exciting causes. 

Some cases in our own observation seem- to us worthy of note, in which young 
people have fallen ill quite suddenly, with rather severe, general febrile symptoms. 
At first a cause for the fever could not be made out, so that the diagnosis was in 
doubt, or the attack was even falsely regarded as typhoid or some other disease. 
Some time later thoracic symptoms developed, and it became possible to make 
out the physical signs of phthisis. Most of these cases took quite a rapidly pro- 
gressive course. 

In conclusion, those cases are to be mentioned in which the first signs of 
tuberculosis appeared, not in the lungs, but in the larynx. The full description of 
these cases has already been given in the chapter on laryngeal tuberculosis (see 
page 123). 

The further course of pulmonary tuberculosis may differ so much that it is 
impossible to give a complete enumeration of all the varieties. 



TUBEECULOSIS OF THE LUNGS. 



201 



In some cases it advances rapidly. We can make out the extension of the dis- 
ease objectively, almost from week to week. At first the apex of one lung alone 
is attacked, soon after the lower lobe of the same lung, then the other lung, either 
at the apex first or in the lower part. Beside the pulmonary symptoms, there is 
quite a high fever, rapidly increasing emaciation, and general loss of strength. 
Death ensues in a few months. We term such cases florid phthisis, or " galloping 
consumption. " 

In other cases, however, the disease has a remarkably chronic course. Its 
onset is very gradual, or else, after rather an acute onset, there is a comparative 
cessation of all symptoms. The thoracic symptoms do not disappear, but they are 
only trifling, and do not disturb the patient. Physical examination of the lungs 
does not show any advance in the extension of the process for months. The fever 
which accompanies it is slight, or else there is none. The patient remains quite 
well nourished, but in some cases there is a good deal of weakness. He feels bet- 
ter and worse by turns, the changes being largely due to the question of his 
having proper care and good nursing. 

Unilateral contracting phthisis, especially, has this comparatively favorable 
course {vide supra). The affection remains confined to one lung for a long time. 
The occurrence of contraction shows the slight tendency of the tubercular process 
to advance, and with satisfactory care the patient may remain quite well for years. 

In cases, too, which have had severe symptoms for a long time, a temporary 
standstill of the affection may take place, with an actual improvement in all the 
symptoms. At other times, in cases which have made no advance for a long time, 
all the symptoms suddenly grow worse. 

There are all possible stages between the extremes of florid phthisis and the 
very chronic cases which last for years. If we recall the further modifications 
which the whole course of the disease may assume if complications arise, we can 
appreciate the manifold character of the clinical picture of phthisis. 

Most cases terminate fatally. Death ensues, either with the signs of general 
exhaustion, or as a result of the final failure of respiration ; or it is due to the 
occurrence of complications, like tubercular meningitis, miliary tuberculosis, pul- 
monary haemorrhage, or pneumothorax. A recovery from the tubercular pro- 
cess is certainly possible. The comparatively great rarity of recovery in pulmonary 
tuberculosis, however, is due chiefly to the possibility of the continual spread of 
the tubercular poison in the lungs themselves, and also in other organs. From 
clinical and pathological experience, however, we can not deny the possibility of 
definite recovery in pulmonary tuberculosis. We do not, of course, mean a resti- 
tutio ad integrum of the lung-tissue, but a recovery with a cessation of the tuber- 
cular process, and with the formation of a cicatrix, or contraction. Such recov- 
eries, as we have said, are always rare, and they occur only where the changes in 
the lungs are of limited extent. The possibility of recovery depends mainly upon 
the general physical constitution and upon the external circumstances of the 
patient. 

Special Symptoms and Complications. 

1. Symptoms on the Part of the Lungs.— Pain in the Chest— Extensive destruc- 
tion in the lungs may exist without any feeling of pain. Many cases of phthisis 
are painless throughout their course. In other cases, however, the patient's chief 
complaint is of severe pains in the side or in the front of the chest. These are 
probably always due to co-existing affections of the pleura, like pleurisy, or 
pleuritic adhesions. In patients who suffer from severe cough, pains sometimes 
arise in the abdominal muscles, and at the insertion of the diaphragm, due to 
the excessive muscular contraction. Stabbing pains between the shoulder-blades 



202 



DISEASES OF THE RESPIRATORY ORGANS. 



are held by some to be a diagnostic symptom of incipient phthisis, a symptom 
which is not wholly unimportant. 

Cough. — In the majority of cases cough is one of the most distressing symp- 
toms in phthisis, but its severity varies very much in different cases, and at differ- 
ent times in the same patient. We sometimes see cases in which, in spite of 
advancing phthisis, cough is remarkably slight, or entirely absent. In these cases 
we usually have to do with patients who are very slightly sensitive. In cases 
with severe cough, it is often worse at night, but paroxysms of coughing of long 
duration often come on in the morning or evening hours, which are painful and 
very distressing, and unpleasant for the patient. The cough is usually associated 
with a more or less abundant expectoration, but sometimes there is chiefly a dry 
cough. The cough usually becomes very severe if the tubercular affection attacks 
the larynx and trachea (see laryngeal tuberculosis). 

Expectoration. — The amount of expectoration differs very much in different 
cases. It is most abundant where there is extensive formation of cavities in the 
lungs. In such cases it is often evacuated in the morning by persistent coughing. 
The consistency of a great part of the sputum is muco-purulent, and it does not 
differ from that of simple bronchitis ; in fact, a large part of the phthisical expec- 
toration comes from the catarrhal inflammation of the bronchial mucous mem- 
brane. Another part comes from the purulent secretion of the walls of the cavities. 
The sputum has a characteristic tendency to roll itself together in single large 
lumps, into the ball-like, or so-called nummular sputa, which is noticed especially 
where there are cavities. Sometimes the muco-purulent sputum forms partial or 
quite complete casts of the smaller bronchi. 

The admixture of blood with the sputum is of great diagnostic and practical 
importance. Since no other disease so often gives rise to the presence of blood in 
the expectoration, coughing of blood (haemoptoe or haemoptysis) is almost synony- 
mous with consumption among the laity. Little streaks of blood in the expectora- 
tion are quite frequent. They have no great significance, but, of course, they may 
sometimes be the precursors of severe haemorrhages. Severe haemoptysis takes 
place when the wall of a little pulmonary vessel — almost always a branch of the 
pulmonary artery — is pierced, destroyed, and finally eroded, by the tubercular new 
growth. The reason why haemoptysis is not more frequent is because the contents 
of the vessels usually undergo thrombosis. Severe haemorrhages very often have 
their origin in the perforation of little aneurisms of the branches of the pulmonary 
artery, which penetrate into the interior of the cavities. In the cases of fatal 
haemoptysis we very often succeed in finding the little aneurism and its point of 
rupture. 

Pulmonary haemorrhages occur in all stages of phthisis. The amount of blood 
coughed up sometimes amounts to only one or two tablespoonfuls, sometimes to 
one or two pints. The blood is bright-red in color, usually quite frothy, only 
slightly coagulated, and partly mixed with the other constituents of the sputum. 
If the patient recovers from the first severe haemoptysis, the expectoration usually 
contains some blood for several days. Recurrences of severe haemorrhages are 
frequent. The haemoptysis sometimes comes on quite suddenly, often at night, 
without any cause, but it may return from some definite cause, like physical 
exertion, severe paroxysms of coughing, straining at stool, or mental excitement. 
Many cases of phthisis are characterized by a special tendency to haemorrhage, 
while in many others haemoptysis never occurs. Severe haemoptyses are, of 
course, always an undesirable and dangerous complication, since they weaken the 
patient very much, and also depress his spirits. Many patients maintain their 
peculiar, careless indifference, which is almost characteristic of the disease, despite 
the spitting of blood. The haemoptysis may sometimes be the direct cause of 



TUBERCULOSIS OF THE LUNGS. 



203 



death, but, as a rule, the patients survive it. We can not make the general asser- 
tion that the further course of phthisis is materially hastened by haemoptysis. 

A purulent sputum intimately mixed with blood is quite frequent and char- 
acteristic in many cases of phthisis with extensive formation of cavities. This 
arises in the cavities from the mixture of the purulent secretion with little capil- 
lary haemorrhages. In this way the sputum, which is often nummular, assumes 
a greasy character and a reddish-brown, or chocolate color. 

If foetid or gangrenous processes develop in the lungs, the sputum assumes a 
foetid character. In some cases we see temporarily in phthisis the characteristic 
sputum of croupous pneumonia, which comes from portions of the lung attacked 
with pneumonia. 

Microscopic examination of the sputum may show — beside the ordinary ele- 
mentary forms, like pus-corpuscles, red blood-corpuscles, pavement epithelium, 
drops of myeline, arid sometimes, perhaps, pulmonary epithelium — two constitu- 
ents which are of decided diagnostic importance : elastic fibers and tubercle bacilli. 

The positive evidence of elastic fibers in the expectoration permits us to decide 
with certainty that there is a destructive process in the lungs, and thus it usually 
is direct proof of tuberculosis. Elastic fibers are also found in pulmonary gan- 
grene, and in the very rare cases of pulmonary abscess, as well as in tuberculosis, 
but gangrene is easily recognized by the other peculiarities of the sputum. The 
search for elastic fibers in the expectoration of tubercular patients demands a 
certain amount of practice. We are most sure to find them if we look in the 
sputum, when it is spread out, for little lentiform particles, which can easily be 
made out with the naked eye. These consist of necrotic shreds of tissue torn off 
from the walls of cavities. If we press one of these " kernels " under a cover- 
glass we often find, in the midst of the granular detritus, beautifully twisted 
elastic fibers, which often have quite a definite alveolar arrangement (see Fig. 24). 
The elastic tissue is the only one spared in the general destruction. There is a 
special method of looking for elastic fibers, but we 
have found it unnecessary. The sputum is boiled in 
sodic hydrate dissolved in water, and we look for elastic 
fibers in the precipitate which then forms. We are 
never justified, however, in deciding that pulmonary 
tuberculosis is absent because we do not find elastic 
fibers in the sputum. Their presence is the only thing 
that has a sure diagnostic significance. 

The discovery of tubercle bacilli in the expectoration 
of phthisical patients is of much greater importance, 
and often this is of itself decisive (see Fig. 25). They 
were first demonstrated by Koch, but Ehrlich has given 
the first simple method for their discovery. 

The sputum is spread in the thinnest possible film 
on a cover-glass, and permitted to dry on it. The best 
way to do this is to rub some of the sputum between 
two cover-glasses, and to slide one slowly off of the 
other. We pass the cover-glass through the gas-flame 
three times slowly to fix the sputum, and then, after 
cooling it for a little time, we let it float in the stain- 
ing fluid.* After about half an hour or an hour the Fig. 24.— Elastic fibers, 
cover-glass is taken out, rinsed with water, the color 

washed out for a few seconds with nitric acid (one part of officinal nitric acid to 




* The staining fluid is prepared in the following manner : About 5 c. c. of aniline-oil is mixed with 
100 c. c. of distilled water and carefully filtered. To 100 c. c. of this filtrate — " aniline- water " — add 



204 DISEASES OF THE RESPIRATORY ORGANS. 

three parts of distilled water), then rinsed again with distilled water. Then the 
sputum is put into a one- or two-per-cent. aqueous solution of Bismarck-brown for 
half a minute to a minute, rinsed, dried, mounted in water or Canada balsam, and 

examined. The pus-cells and some of the 
other bacteria are stained brown, but the 
tubercle bacilli have taken on a dark-blue or 
red color. 

The number of bacilli varies a good deal 
in different cases and at different times in 
the same case. The more bacilli there are, 
the earlier we can decide that there are ex- 
tensive processes of ulceration. The "ker- 
nels " in the sputum just mentioned give the 
finest picture under the microscope. As we 
have repeatedly convinced ourselves, their 
fine detritus consists in large part of tubercle 
bacilli, which are plainly to be seen with a 
No. 8 Hartnack (330-440 diameters). We can 
find no definite prognostic conclusions in the 
relation of the bacilli, but their presence is of 
the greatest significance in a diagnostic point of view, especially as they can be 
found upon careful examination in incipient cases. At so early a period all the 
other symptoms by themselves could very often not furnish a certain diagnosis. 

Dyspnoea. — A marked subjective feeling of dyspnoea is a symptom which is of 
relatively rare occurrence in phthisis. 

Many patients hardly ever complain of their breathing in spite of extensive 
destruction in the lungs. A patient who is much emaciated manifestly needs 
little oxygen, and the increased frequency of respiration, which is almost constant, 
can satisfy his needs. If there is a greater demand upon the respiration a sub- 
jective feeling of dyspnoea may of course very readily occur, especially on a slight 
bodily exertion. In many cases, however, the patient complains of a difficulty in 
breathing even when quiet, especially if pleuritic pains or adhesions between the 
surfaces of the pleura prevent him from taking a deep breath. 

2. Symptoms on Physical Examination. — In many cases inspection gives us 
that general impression of the patient which we term the "phthisical habit." 
The special signs of this are as follows : A slender, but often quite a tall frame, 
weak muscular development, a thin layer of fat, a pale and often very delicate 
skin with a bluish translucence, sometimes a circumscribed " hectic " flush in the 
cheeks, a long and slender neck, a long and narrow thorax, small, thin hands, etc. 
There are, of course, many variations from this type in individual cases. 

The inspection of the thorax is of special value. The phthisical or " paralytic " 
thorax is generally noticeable by its length, but it is small and flat. Unusual 
width of single intercostal spaces, and acuteness of the epigastric angle, are 
associated with a long thorax. The sternum is also long and small, and the 
sternal angle — Louis's angle — is often prominent. The supra-clavicular and infra- 
clavicular fossae are sunken, the neck is wasted, and the shoulder-blades stand out 
from the thorax. On comparing the two halves of the body, we very often see 
unilateral contractions, most frequently in the upper and anterior portion of the 
thorax, but often in the lower portions. 

11 c. c. of a concentrated alcoholic solution of methyl violet or fuchsin, and 10 c. c. of absolute alcohol. 
The solution must be renewed every ten or twelve days. The longer the cover-glass with the sputum 
is left in the staining fluid, the more certain is the staining. If we warm the staining fluid the process 
is more rapid. 




Fig. 25.— Tubercle bacilli in the sputum. 



TUBERCULOSIS OF THE LUNGS. 



205 



The paralytic form of thorax is very often seen in phthisis, but it may be en- 
tirely absent. 

The respiration is usually somewhat accelerated, and sometimes quite mark- 
edly so in women with disease at the apices. The feminine type of high thoracic 
breathing is largely changed to low thoracic or diaphragmatic breathing. The 
presence of a unilateral impairment of respiration is of greater importance; in 
such a case one apex, or one side, if there be phthisis of the lower lobe, holds back 
in inspiration. The respiration is sometimes irregular, especially if there be pleu- 
ritic pains. 

The results of percussion are, of course, entirely dependent upon the sort of 
anatomical changes in the lungs, and hence differ very greatly in different cases. 
Since the phthisical process begins in the apices in the majority of cases, our chief 
attention is turned to the condition of the upper portions of the lungs on percus- 
sion. Slight changes in percussion may wholly escape discovery. Only when 
the air contained in the lung-tissue in the part affected is replaced to a certain 
degree by the tubercular infiltration does the percussion-note become dull. Uni- 
lateral dullness at the apex is therefore one of the most frequent physical signs 
of phthisis. We can usually make it out most plainly in the upper anterior in- 
tercostal spaces first, and in incipient cases often in the supra-clavicular fossae 
only, but it is also observed sometimes in the back in the supra-scapular fossae. 
As the infiltration advances the dullness becomes more extensive. It very often 
assumes a tympanitic quality, as a result of diminished tension or partial retraction 
of the lung-tissue. 

The formation of cavities in tuberculosis has a great influence on the percus- 
sion-note. The dullness on percussion may thus become decidedly less, the degree 
of resonance depending, of course, upon the fullness of the cavity and the char- 
acter of the surrounding tissue. We often find a decided tympanitic resonance 
or a muffled tympanitic resonance over a cavity. The different modifications of 
the percussion-note in cavities are given below. The " cracked-pot resonance," or 
buckram sound, is often met with in percussing over cavities, but we also find it 
in many other pathological conditions. 

Auscultation, too, of course, gives no special pathognomonic signs of phthisis. 
Varying with the character and extent of the tubercular changes, abnormal respir- 
atory sounds and adventitious sounds are heard in place of the normal vesicular 
murmur. With slighter changes the vesicular breathing is merely modified ; it 
seems remarkably diminished or interrupted, or sometimes exaggerated, with pro- 
longed expiration. When the infiltration of the lungs increases, we find bron- 
chial respiration in place of the vesicular breathing ; but, on the other hand, the 
formation of a cavity is a frequent cause of bronchial respiration. 

The most constant auscultatory signs of phthisis, and the most important for 
diagnosis, are the different kinds of rales, which are due to the accumulation of 
the secretion in the bronchi or in the cavities. They are heard at one apex only, 
or over a larger space, according to the extent of the affection. 

Physical Diagnosis of Incipient Phthisis.— On account of the importance 
of the diagnosis of incipient phthisis, we will here mention connectedly the phys- 
ical signs which are chiefly met with in it. The auscultatory signs in the beginning 
of the disease are generally more certain and easier to recognize than those from 
percussion. He who lays too much weight on the so-called " slight dullness at 
the apex " will often make a false diagnosis. We will mention particularly the 
following symptoms : 1. Constant and evident diminution of the respiratory mur- 
mur at one apex, especially if it is associated with marked deficiency of the respira- 
tory movement on the affected side. In some cases the respiratory murmur on the 
diseased side is not weaker, but it has a more indefinite and harsher character. 



206 



DISEASES OF THE RESPIRATORY ORGANS. 



2. Markedly interrupted respiration at one apex. 3. A prolonged expiratory mur- 
mur, which has a harsh character. 4. The discovery of dry rhonchi or moist 
rales at one apex is most important, since we know by experience that "apex 
catarrhs " are, as a rule, tubercular. 5. Definite dullness, apparent on repeated 
examinations, or tympanitic dullness at one apex. 6. Evident contraction at one 
apex, as revealed by inspection or percussion above the clavicles. 7. Some authors 
lay stress upon a systolic murmur in the subclavian artery, especially loud on 
expiration. This may occur in the beginning of phthisis, if the" caliber of the ves- 
sel is narrowed by processes of contraction in the neighboring apex, but this 
symptom has no great practical importance. 

The chief rule in the diagnosis of incipient phthisis must be held to be this — 
not to give a definite opinion until repeated examinations have been made. The 
other portions of the lungs are to be carefully examined as well as the apices, 
since in rare cases tuberculosis may begin in the lower lobes. We must always 
consider the patient's general symptoms as well as the physical signs. 

Symptoms of Cavities. — The diagnosis of a cavity in the lungs by the physical 
signs is often very difficult. We may mention as the chief symptoms of a cavity : 
1. Loud bronchial respiration, often of an amphoric character, in places where the 
percussion-note is only slightly or not at all dull. Such a condition means that 
the bronchial respiration is not due to an infiltration of lung-tissue. Bronchial 
respiration, however, may of course be heard over cavities which are surrounded 
by thickened lung-tissue, and hence give dullness on percussion. 2. The so-called 
metamorphosing respiration, which begins as vesicular and suddenly becomes 
bronchial, is heard especially over cavities, and hence has a diagnostic value. 3. 
The different kinds of " changes in the percussion-note " over cavities are impor- 
tant signs. Wintrich's change in pitch is when the tympanitic resonance, which 
is retained over the cavity, becomes, on opening the mouth, more decidedly tym- 
panitic, louder, and especially much higher. The respiratory change of pitch of 
Friedreich usually consists of a higher pitch on inspiration, but here there are 
numerous variations. Gerhardt's change of pitch (Weil) consists in a change in 
pitch of the tympanitic resonance when the patient changes his position, the pitch 
usually being higher when the patient sits up than when he was lying down.* 
4. Loud, bubbling rales are one of the most frequent signs of a cavity. They are 
definite indications of the occurrence of rales in a larger space than is normally 
present in the apices of the lungs. 

Contraction of the Lungs [Fibroid Phthisis]. — Unilateral contraction of the 
lungs, more frequent on the left than on the right, is a form of tuberculosis 
which is made apparent both by special physical signs and also by certain clin- 
ical peculiarities. It is usually recognized at once by inspection of the thorax, one 
side of the thorax being remarkably retracted. The upper anterior portions of 
the thorax, and, in all cases of a high degree of disease, the lower lateral and 
posterior portions, are much less tense than the corresponding parts on the other 
healthy side. The fossae and intercostal spaces on the affected side are deeper, 
the shoulder-blade is drawn nearer the vertebral column, and the latter is even 
sometimes drawn over to the contracted side (scoliosis). The resonance is duller, 
to a greater or less degree, over the affected side, which either lags behind, or 
remains almost wholly at rest on respiration. The respiratory murmur is quite 
loud, and bronchial; and we also hear many rales, which are usually bubbling. 
Anatomically, we have to do with a marked process of contraction of ,the inter- 
stitial connective tissue in the lungs, which is almost always associated with 



* Fuller details of the significance of the different fonns of changes in the pitch are found in Weil's 
" Handbuch der topographischen Percussion." Leipzig: Vogel, 1880. 



TUBERCULOSIS OF THE LUNGS. 



207 



extensive formation of cavities, partly of an ulcerative, partly of a bronchiec- 
tasic character. The pleura is involved in the process almost without exception, 
but always secondarily ; it is also thickened and contracted. If there is marked 
pleuritic thickening, the respiratory murmur and the vocal fremitus are decidedly 
weakened. 

The influence of the contraction on the neighboring organs is very decided, and 
usually it is easy to discover. The heart especially, whose external pericardium 
is usually very adherent to the pleura, is drawn well over to the side of the con- 
traction. The apex-beat and the cardiac dullness are correspondingly displaced. 
With left-sided contraction the heart may be drawn over to the line of the left 
axilla, and with right-sided contraction it maybe drawn to the median line, or 
even to the right of the sternum. With contraction of the left upper lobe the 
anterior surface of the heart comes into immediate contact with the anterior chest- 
wall over a larger area than normal. We therefore see the motions of the heart 
over an abnormal extent, and we can often feel very plainly in the second left inter- 
costal space the pulsation and the closure of the valves of the pulmonary artery in 
diastole. The upward traction of the diaphragm may be recognized by the position 
of the liver, or, in left-sided contraction, by the increase of the " semilunar " tym- 
panitic space on the left. We usually find the sound lung on the other side quite 
emphysematous, as shown by the downward displacement of the lower boundary 
of the lung, and also by the drawing over of the anterior median edge of the lung 
to the contracted side. In a part of the cases we can make out by percussion the 
development of consecutive dilatation and hypertrophy of the right ventricle. 

These are the chief physical signs of the so-called unilateral form of chronic 
pulmonary contraction. To these we would add here a few clinical remarks. 
The cases often, but of course not always, run a very chronic course, frequently 
lasting for years. The general condition and the nutrition of the patient may 
thus remain comparatively undisturbed for a long time. The patient very often 
looks somewhat pale and cyanotic, yet he is often so well nourished as to pre- 
sent a very marked contrast to the appearance of the ordinary cases of phthisis. 
The appetite remains good, the fever is entirely absent, or else a slight degree of 
fever may be at times discovered by careful examination. The cough and ex- 
pectoration, too, which are often very severe, are at other times very slight, espe- 
cially when the patient has good care and nourishment. We need not wonder, 
then, that many physicians do not consider that these cases have anything to 
do with phthisis — " consumption " ; and yet we are convinced by many clinical 
and anatomical observations that, aetiologically, they are in great part, if not 
exclusively, tubercular. They represent a very slow form of tuberculosis, which 
has time to develop interstitial processes which lead to contraction — that is, to 
local healing. If such cases come to autopsy, their tubercular character is usually 
definitely confirmed. We find undoubted tubercular changes in the other lung 
and also in the remaining organs, like the intestines. Furthermore, sudden 
changes for the worse may occur in every "pulmonary contraction," even those 
which seem favorable ; the other lung may become highly tubercular, a miliary 
tuberculosis or a tubercular meningitis may develop, etc. On the whole, however, 
the slow course of this form of chronic tuberculosis is characteristic and of prac- 
tical significance, and its prognosis is therefore comparatively favorable. 

We can not absolutely deny that a non-tubercular unilateral contraction of the 
lung may occur, but it has not been demonstrated. As a result of foetid bronchitis 
and pulmonary gangrene, and possibly after croupous pneumonia, processes of 
contraction develop, which are associated with the formation of bronchiectases, 
and certainly have nothing to do with tuberculosis. These processes, however, 
are usually easily recognized by their origin, the peculiarity of the sputum, etc. 



208 



DISEASES OF THE RESPIRATORY ORGANS. 



In conclusion, we must mention that there are very many transitional forms 
between pulmonary contraction and the other varieties of pulmonary tuberculosis. 
We find more or less extensive processes of contraction in one apex in most cases 
of phthisis. 

Disseminated Pulmon ary Tuberculosis. — There is a form of pulmonary 
tuberculosis which is very hard to make out on physical examination. In this 
we have to do with numerous peribronchial nodules disseminated over the whole 
lung. As there is still a good deal of normal tissue, containing air, between these 
nodules, percussion affords no dullness, and auscultation gives at most diffuse 
rhonchi ; hence this form is often confused with chronic bronchitis or pulmonary 
emphysema. The diagnosis can not often be made from the physical signs, but 
only from the other symptoms, like fever, emaciation, striking pallor of the skin, 
and the sputum. 

This form of phthisis sometimes runs a chronic course, but usually it is quite 
rapid. It occurs in elderly people, and also in children. Many forms of " dis- 
seminated, coarse granular " tuberculosis are transitional forms between this and 
genuine acute miliary tuberculosis. 

3. General Symptoms in Pulmonary Tuberculosis.— In the description of the 
general course of pulmonary tuberculosis we have already mentioned the value 
of the general symptoms in diagnosis and prognosis. 

Fever. — Only a few cases of phthisis run their course entirely without fever, 
but it may often be absent for a time, even for weeks and months. This is espe- 
cially the case in the very chronic forms, like unilateral contraction. The more 
carefully we take the temperature, the more frequently will we find a slight even- 
ing rise of temperature up to 100° or 101° (38°-38-5° C), or at least between 99° 
and 100° (37'5°-38° C), even at times when the patient is doing favorably. Such 
subfebrile conditions may last a long time, but many cases of phthisis are associ- 
ated with high fever. 

The fever in tuberculosis is generally noticeable from its very monotonous 
character. For months the temperature-curve may be like this : in the morning a 
normal, or approximately normal temperature, and at evening a rise to 103° or 
104° (39°-40° C), rarely higher. The fever in phthisis, then, shows a decidedly 
intermitting or remitting character, the so-called "hectic fever." 

More rarely we see very irregular temperature-curves, where elevations of 
temperature, which last a shorter or a longer time, alternate in an irregular fash- 
ion with periods that are free from fever. It often happens that toward the end 
of the disease, when the general weakness increases, the curve, that previously 
was regular in its intermissions, becomes irregular. The intermissions then 
become deeper, and we often see genuine temperatures of collapse, 94° to 92° (35°- 
34° C). At other times the fever may temporarily assume a more continuous 
character, probably from an increase of the tubercular process. In some cases 
with an acute onset {vide supra) we have also seen, at the beginning of the dis- 
ease, quite a high and approximately continuous fever, which later went over 
gradually to the ordinary hectic. 

We must probably look for the cause of the fever, not in the tuberculosis itself, 
but in the absorption of septic substances from the decomposition of the secretion 
of the bronchi and cavities. 

Emaciation. — The appearance of great emaciation in the patient is very strik- 
ing in most cases of phthisis. The muscular system and the fatty tissue are 
affected in equal degree. The soft parts of the thorax are often especially 
involved. The emaciation is due in part to the patient's loss of appetite, and to 
the small amount of food which he takes in consequence thereof, but the chief 
cause lies in the persistent fever and the increased metamorphosis of tissue. Quite 



TUBERCULOSIS OF THE LUNGS. 



209 



a high degree of emaciation, however, may appear in the beginning of the disease 
with no fever. This we are wont to ascribe to the "general illness," but the 
special cause of it is unknown. Under favorable external conditions phthisical 
patients may make quite a decided gain in weight, especially at the times when 
they are free from fever. In very chronic cases, which run their course from the 
first without fever, the nutrition of the patient may remain good for a long time. 
Toward the end of the disease the emaciation reaches its highest degree, and many 
phthisical patients die " wasted to a skeleton " in the true sense of the word. 

Ancemia — Color of the Skin. — In most cases anaemia appears in the course of 
the disease, which can be recognized by the pale and sallow color of the skin and 
the visible mucous membrane. The anaemia only rarely reaches that degree of 
peculiar waxy pallor that is found in idiopathic pernicious anaemia. The exist- 
ence of the anaemia is also the reason why the phthisical patient does not look 
cyanotic, in spite of the respiratory disturbance. In the more chronic forms, 
where the general nutrition suffers less, we often see a cyanotic coloring of the 
lips and cheeks. Sometimes the skin of phthisical patients assumes a dirty, dusky 
hue. We have already spoken of the circumscribed " hectic flush of the cheeks " 
seen with the fever. 

General Weakness — Night- Sweats — Nervous Disturbances. — We need not say 
that the general emaciation and anaemia are accompanied by a marked decline in 
the patient's power of endurance. He finally becomes so helpless that he can 
scarcely move alone in the bed. 

The tendency which very many patients have to severe night-sweats is not 
wholly explained. It may have some connection with the fall from the evening 
febrile temperature to the morning remission, and perhaps it is due to the greater 
accumulation of carbonic acid in the blood from the disturbance of respiration. 

The disease has remarkably little influence upon the higher nervous functions, 
especially those of the mind. Most patients have a perfectly clear intellect to 
their latest breath. We all know the contented, hopeful disposition of many 
patients, who often do not recognize their own danger until the last stages of the 
disease. Occasionally the anaemia and the general disturbance of the nutrition of 
the brain lead to mental alterations, such as confusion, distraction, or melancholic 
conditions. 

We find, more frequently, disturbances in the peripheral nerves and muscles. 
Among these are neuralgic pains, and pains of an indefinite character, which have 
their seat in the legs, or sometimes in the arms, especially in the ulnar region, and 
which may be very distressing. Marked hyperaesthesia of the skin and deeper 
parts is also not uncommon. The cause of such disturbances is probably often to 
be looked for in degenerative changes in the peripheral nerves (Vierordt). 

We very often see an increased reaction upon direct mechanical irritation in 
the emaciated muscles, which is shown, for example, on percussing the pectoral 
muscles on the anterior wall of the chest. The phenomena grouped under the 
name of tendon reflexes are also much increased in phthisis. 

4. Symptoms and Complications on the Part of Other Organs.— 1. Pleura.— 
In pulmonary tuberculosis the pleura is also involved as a rule. The affection is 
almost always the result of a direct extension of the process from the lung to the 
pleura. At the autopsy, we find in the pleura a few or many miliary tubercles, 
beside the simple inflammatory process — tubercular pleurisy. 

In many cases, in which we have to do only with an adhesive pleurisy and with 
pleuritic contraction, we can merely suspect the disease of the pleura, but it can 
not be directly made out and differentiated clinically from the pulmonary affec- 
tion. In other cases we can diagnosticate a dry pleurisy in phthisis from the 
occurrence of the pleuritic friction-rub. The symptoms of pleurisy become more 
14 



210 



DISEASES OF THE EESPIEATOEY ORGANS. 



marked, if there is a pleuritic effusion, which is usually readily discovered by a 
physical examination. The patient's symptoms, like pain and dyspnoea, are usu- 
ally much increased by such a complication. Beside a simple sero-fibrinous 
effusion we quite frequently find purulent and even haemorrhagic effusions in 
tuberculosis of the pleura. 

The formation of pneumothorax is an important complication in the pleura in 
phthisis. This is due to the rupture of a superficial cavity into the pleural cavity, 
and the entrance of air into the latter. The different forms of pneumothorax and 
its symptoms will be described under diseases of the pleura. 

2. Larynx, Pharynx, and Trachea. — The symptoms of laryngeal tuberculosis 
and their relation to pulmonary tuberculosis have already been given under dis- 
eases of the larynx. We saw there that, although there is a primary laryngeal 
tuberculosis, most cases are secondary in their development to a pulmonary tuber- 
culosis. The constant passage of tubercular sputa from the lungs, through the 
trachea and larynx, naturally leads to a direct infection of the mucous membrane 
of the parts mentioned. 

The same holds true in regard to the much rarer tuberculosis of the pharynx. 
In some cases this may be of primary origin, but it is usually a result of re-inocu- 
lation with tuberculosis by the sputum, or of a direct extension of the tubercular 
process from the larynx to the pharynx. Tubercular ulcers of the pharynx are 
found most frequently on the soft palate, on the tonsils, on the root of the tongue, 
and on the boundary between the pharynx and the larynx ; they are rare in other 
parts of the pharynx. In exceptional cases tubercular affections are seen in the 
mouth — on the tongue. The local disturbances which all these ulcers cause are 
usually very considerable. Disseminated miliary tubercles, too, have been repeat- 
edly seen in the mucous membrane of the pharynx. 

3. Stomach and Intestinal Canal — Peritoneum. — Tubercular ulcers in the 
mucous membrane of the stomach are exceedingly rare, but we very often notice 
some symptoms on the part of the stomach. Loss of appetite is a particularly 
common symptom in phthisis. Vomiting is quite frequent, both as a result of 
severe paroxysms of coughing and from other causes. This symptom is probably 
caused by a gastric catarrh, set up by the irritation from swallowing tubercular 
sputum, but in some cases the gastric symptoms depend upon the general condi- 
tion, like anaemia. 

Although the tubercle bacilli swallowed with the sputum hardly ever gain a 
footing in the stomach, probably from the acid reaction of its contents, they very 
often settle in the intestinal canal. In the majority of the cases of phthisis we find 
tubercular ulcers, either singly or in considerable numbers, in the vicinity of 
Bauhin's valves [the ileo-caecal valve], in the lower part of the ileum, and the 
upper part of the large intestine. 

Intestinal tuberculosis does not always cause very marked clinical symptoms, 
but as a rule we find diarrhoea in patients with tubercular ulcers of the intestine. 
They may have three or four stools in the twenty-four hours, and even more, but 
the stools have nothing characteristic. We rarely see a slight admixture of pus 
or blood in them. Tubercle bacilli have been repeatedly discovered in them. We 
must call attention, however, to the fact that many patients have diarrhoea during 
life in whom we find at the autopsy no intestinal tuberculosis, but only a simple 
intestinal catarrh, or amyloid of the intestine. On the other hand, we quite fre- 
quently find at the autopsy tubercular ulcers of the intestine, which during life 
caused no diarrhoea. 

In cases of severe intestinal tuberculosis we sometimes meet with meteorism. 
With deep ulcers, extending to the peritoneum, we often see marked tenderness 
of the abdomen. 



TUBERCULOSIS OF THE LUNGS. 



211 



The peritoneum may be affected by the tubercular ulcers of the intestine in a 
twofold manner. Genuine peritonitis from perforation, with a purulent, or even 
a sanious exudation, is quite rare, and is excited by the rupture of an ulcer and the 
entrance of the contents of the intestine into the abdominal cavity. An infection 
of the peritoneum with the tubercular poison is more frequent. This may arise 
from deep-seated ulcers, which do not reach actual perforation, so that we have a 
peritoneal tuberculosis, or a tubercular peritonitis. During" life peritonitis from 
perforation and that from tuberculosis are not always to be distinguished. We 
must also mention that simple ascitic fluid is sometimes found in the abdominal 
cavity in phthisis, which may lead to a false diagnosis of peritoneal tuberculosis. 

Another way in which we may have a peritoneal tuberculosis in the course of 
phthisis is from the extension of the process in a tubercular pleurisy, through the 
diaphragm, to the peritoneum. 

4. Liver and Spleen. — We very often find a few or even many tubercles in the 
liver in phthisis, but they have no clinical significance. The liver is almost always 
infected with the tubercular poison from tubercular ulcers in the intestines, from 
which the poison passes to the branches of the portal vein and then to the liver. 
Fatty liver and amyloid or lardaceous liver are more important clinical changes. 
We can sometimes recognize the former by making out on physical examination 
the increase in the size of the organ, and by feeling its characteristic blunt lower 
edge. 

Amyloid liver is almost always associated with the development of amyloid in 
other organs. In marked cases the liver is evidently enlarged, and its firm, sharp 
lower edge, and often its dense anterior surface, may usually be plainly felt. 

Miliary tubercles or single large tubercular nodules in the spleen have a patho- 
logical interest only. Large tumors, which are obviously splenic, are found in 
amyloid degeneration. 

5. Kidneys, Urinary Passages, and Sexual Organs. — The presence of miliary 
tubercles in the kidneys is the first change to be mentioned in them, but it has no 
clinical significance. Extensive tuberculosis of the genito-urinary apparatus, 
however, may produce marked symptoms, like pyuria, which will be described 
later. In regard to the symptoms of amyloid kidney, which may develop in the 
course of phthisis in connection with amyloid disease in other organs, we will 
refer to the section on renal diseases. 

Genuine cases of nephritis, both acute and chronic, are also found quite fre- 
quently in phthisis, usually combined with amyloid disease. These can not escape 
notice if the urine is carefully examined. Cases of genuine amyloid kidney of 
moderate severity are seen, however, in which the urine remains normal, and in 
particular free from albumen. 

6. Circulatory Organs. — Not only is the frequency of the pulse increased in 
many patients in relation to the existing fever, but even where there is no fever we 
often find it accelerated. The greater or less increase of the pulse, which readily 
comes on from comparatively trifling external causes, is especially noteworthy. 
It may be seen after slight physical exertion, or from mental excitement, as dur- 
ing the physician's visit. 

Anatomical changes in the heart are rare, except that it is often remarkably 
small and flaccid. Moderate fatty degeneration of the heart, slight endocarditis 
of the valves, or occasional tubercles in the heart, cause no symptoms. The occur- 
rence of tubercular pericarditis, however, is important. This almost always arises 
from the extension of the tubercular process from the adjacent pleura, but in 
exceptional cases pericarditis has been seen as a result of rupture of a pulmonary 
cavity into the pericardium. 

7. Lymph-glands. — The lymph-glands are a favorite seat for tubercular 



212 



DISEASES OF THE RESPIRATORY ORGANS. 



changes. We have stated above that the so-called scrofulous, cheesy lymph- 
glands, which are seen chiefly in the neck and the axilla?, are affected with tuber- 
cle in the majority of cases. The tubercular infection probably develops here 
from slight injuries and excoriations of the skin, by which the bacilli enter the 
body and reach the neighboring glands by means of the lymph-current. In 
other cases the infection perhaps comes from the mucous membrane of the phar- 
ynx. In tuberculosis of internal organs, too, we very often find the corresponding 
lymph-glands enlarged and more or less cheesy. The bronchial lymph-glands are 
swollen as a result of pulmonary tuberculosis,* the mesenteric and retro-peritoneal 
glands as a result of intestinal tuberculosis. In children, especially, tuberculosis 
of the bronchial lymph-glands plays quite a part. Pressure from the enlarged 
glands may affect the air-passages, the branches of the pulmonary artery, the 
veins, the recurrent nerve, and even the aorta. Perforation of the cheesy bron- 
chial glands into the oesophagus, the blood-vessels, etc., has also been observed. 
Tuberculosis of the bronchial glands in children does not present any definite 
type of disease, however, and, although we may sometimes suspect it when there 
is pulmonary tuberculosis, we can only rarely diagnosticate it with certainty. 

8. Nervous System. — We have already mentioned various nervous symptoms 
in the description of the general symptoms. We must also add that tubercular 
meningitis is seen in the course of phthisis (see page 663), and also that large 
solitary tubercles may occasionally develop in the central nervous system (see 
page 709). 

9. Skin. — We have spoken of the great tendency which many patients have to 
severe sweats, especially at night. The frequent appearance of pityriasis versi- 
color, especially on the skin over the thorax, is also worthy of note. We often 
see moderate oedema of the legs and ankles, which is due to weakness of the 
heart. More marked oedema of one leg sometimes arises from thrombosis of the 
femoral vein. We must also mention here, in conclusion, the specific tubercular 
disease of the skin — lupus. This occurs alone, as a rule, without a co-existing 
pulmonary tuberculosis ; but, on the other hand, the former bad significance of 
"scrofulous lupus" had reference to the fact that we often find other tubercular 
affections hi lupus beside the disease of the skin. Thus it does not seem strange 
that lupus and phthisis have been repeatedly observed to co-exist. 

Diagnosis. — The diagnosis of pulmonary tuberculosis has become remarkably 
certain, since the discovery of the tubercle bacilli, by the possibility of their pres- 
ence in the sputum (vide supra). In all incipient cases, in which the other symp- 
toms of the disease have not yet made themselves manifest, but where the suspicion 
of incipient phthisis has been aroused by a persistent cough, by marked pallor and 
emaciation, by slight hoarseness, by an evening rise of temperature, by the appear- 
ance of night-sweats, by the presence of a hereditary predisposition, and similar 
symptoms, the presence of tubercle bacilli in the sputum is often the sole deciding 
factor. We must not forget, however, that in most cases the diagnosis may be 
made from the other symptoms alone, and also that we can actually judge of 
the severity of the individual case, and of the exact extension and form of the 
tubercular process, only by considering the other symptoms, and especially by 
considering the data of the physical examination. The latter, therefore, has lost 
none of its importance by the discovery of the tubercle bacilli. Confusion 
between phthisis and other diseases is twofold. Where the constitutional symp- 
toms are predominant, and there are no marked pulmonary symptoms, -an exist- 

* The tubercular virus which reaches the lungs may probably, in some cases, reach the bronchial 
glands through the lymph-channels without remaining in the lungs, and may settle there and set up 
tubercular disease. 



TUBERCULOSIS OF THE LUNGS. 



213 



ing tuberculosis may be overlooked. In the beginning, especially, many cases of 
phthisis are considered to be merely anaemia, chronic gastric catarrh, or simple 
bronchitis. On the other hand, it is by no means rare to consider patients phthis- 
ical who are suffering from some entirely different affection. He who lays too 
great stress on the uncertain results of percussion will often make a false diagnosis. 
Severe latent diseases of the stomach, or certain general diseases, like anaemia, 
diabetes, or chronic nephritis, may falsely be taken for phthisis. Other pulmonary 
affections, too, may be confused with tuberculosis, especially chronic bronchitis, 
emphysema, bronchiectasis, foetid and gangrenous processes, and carcinoma of 
the lungs. A careful, unprejudiced, and complete examination of the patient is 
the only possible protection against such errors. 

Prognosis. — In the condition of our present therapeutic knowledge the prog- 
nosis of phthisis must unfortunately still be regarded as extremely unfavor- 
able. There can be no doubt that the tubercular process in the lungs is in 
itself curable, but, in all cases where we can get certain objective evidence of 
tuberculosis, a definite extinction of the disease is very improbable, because the 
conditions for a further extension of the disease in the lungs are extremely favor- 
able. In individual cases, however, with very favorable external conditions, 
circumscribed tubercular affections of the lungs have been certainly found to heal. 
In advanced cases of phthisis the prognosis, of course, is almost absolutely fatal. 

In individual cases the prognosis with regard to the duration of the disease is 
very difficult. Here we must always be mindful of the great differences in differ- 
ent persons, and hence we must be very cautious in expressing an opinion. How 
many patients with phthisis give us the impression on the first examination that 
they can not live a fortnight longer, and later on we see the disease lasting for 
many months, most of the symptoms improving, and the patient recovering 
again ! In other cases, on the contrary, we think we have to do with an incipient 
case, and give room for great hope — and the patient dies in a few weeks with 
florid phthisis. Disregarding the constant possibility of an unforeseen fatal 
haemoptysis, pneumothorax, or tubercular meningitis, an opinion upon the dura- 
tion of the disease is, therefore, very uncertain in most cases which have not yet 
reached the last stage, and at best can be made only after long observation of the 
patient. Very much, of course, depends upon the circumstances of the patient, 
and upon the possibility of good care, suitable food, and good air. 

Of the single factors which influence the prognosis, our chief attention must be 
paid to the general nutrition, the patient's weight, the extent of the pulmonary 
affection, the fever, and certain complications, especially laryngeal and intestinal 
tuberculosis. We need not refer particularly to the special points which follow 
from these. 

[Flint, especially, has called attention to the fact that phthisis is sometimes self- 
limited ; that recovery or arrest takes place without any special treatment, and in 
spite of relatively unfavorable surroundings. The clinical evidence is greatly 
strengthened by the frequency with which, after death from any cause, the remains 
of an old phthisical affection are found. 

In 1857, 39 "50 deaths from consumption were returned in the State of Massa- 
chusetts for each ten thousand of the population ; in 1883, 29*90. This decrease 
is too large to credit to greater accuracy in diagnosis and to the transference of 
consumptives to other States, and is mainly attributable to the prevention of 
phthisis by improved hygiene. Still, it seems fair to carry some of the improve- 
ment to the account of the arrest and care of actually developed disease through 
early diagnosis and more rational treatment, hygienic as well as medicinal.] 

Treatment. — 1. Prophylaxis. — The question of what prophylactic measures 
may effectually prevent the extension of the disease has entered upon a new 



214 



DISEASES OF THE RESPIKATOBY OBGANS. 



stage since our definite knowledge as to the infectious nature of tuberculosis. 
We can now no longer doubt the contagious character of phthisis, in support of 
which single examples were previously alleged. Even if, according to all experi- 
ence, the danger of contagion is not very great, still it is foolish to ignore it 
entirely. We must therefore lay down this principle, to call the attention of the 
relatives of phthisical patients to the possibility of this danger, and we should 
not permit the children of such patients to be uselessly exposed to it. We should 
take satisfactory precautions for isolation and for disinfection of the sj)utum, 
which can best be done by a strong solution of carbolic acid. The future will 
teach us whether many misfortunes may not be averted by such measures, al- 
though now these measures are almost always neglected. 

The " prophylaxis " at present employed is almost exclusively confined to hard- 
ening and strengthening the threatened individual as much as possible. We 
should try to strengthen the bodies of children of a weak habit, with " scrofulous " 
symptoms, and children from families in which cases of tuberculosis have already 
occurred, and thus to arm them against the enemy that threatens them. Good food, 
fresh air, and a diminution of the sensitiveness of the body by cold sponging and 
cold baths — these are the factors whose favorable influence is generally recognized. 

The removal of certain foci of tubercular disease, already existing, from the 
body may prove of great prophylactic importance. We refer to the timely treat- 
ment or extirpation of scrofulous — that is, tubercular — swellings of the lymph- 
glands, healing or resection of tubercular bones and joints, etc. Although in 
individual cases we can of course never know whether the part removed is the 
sole focus of disease in the body, still we are undoubtedly justified in trying to 
remove at least one possible source for some later general infection. A fuller 
treatment of this important point must be left to the works on surgery. 

2. Treatment. — We do not yet know any actual treatment, corresponding to 
the causal indication, whose point of attack is aimed directly against the tuber- 
cular poison. The inhalations employed with this idea, using very different anti- 
septic substances, like carbolic acid, benzoate of sodium, and lately iodoform, have 
so far all proved unsatisfactory, chiefly because the substances inhaled have not 
reached the bronchi in sufficient amount. Inhalations of iodoform, made by a 
special apparatus invented by Kiissner, have been the most successful in tuber- 
culosis of the larynx. We have already spoken of inhalations with astringents 
and narcotics. 

We must make especial mention of arsenic among the internal remedies to 
which a specific action in tuberculosis has been attributed. Our own experiments, 
which were suggested by quite a number which were made by Biichner, have in 
general given no favorable result. In some cases, however, the remedy seems to 
have a marked therapeutic action, so that we are always justified in trying arsenic 
in incipient cases, the more especially since it has lately been observed to have a 
favorable influence in other tubercular affections, like tuberculosis of the lymph- 
glands, caries, and lupus. It is better not to prescribe arsenic in solution, but in 
pills of a twentieth of a grain (grm. 0*003) of arsenious acid, giving two or three a 
day, and later four or five if possible, always after eating. Good results may be 
obtained only after using the remedy for some months at least. Another internal 
remedy which may be tried is creasote, which sometimes acts favorably, especially 
upon the thoracic symptoms, like cough and expectoration. It may be given in 
pills, or combined with cod-liver oil, as in the following formula : 

5 Creasoti 1 ; 



Olei morrhuag 

Olei menthse piperita? 
Two or three teaspoonf uls daily. 



100 ; 

gtt. 2. M. 



TUBERCULOSIS OF THE LUNGS. 



215 



The hygienic and symptomatic treatment of phthisis is more important than 
the remedies so far mentioned. 

The hygienic treatment, in the broadest sense of the word, aims, on the one 
hand, to increase the power of the resistance of the body to the disease, and, on the 
other, to put the body under conditions which we know can combat the further 
extension of the disease. We try to aid, as far as possible, the process of spon- 
taneous recovery in phthisis. First to be mentioned here is the diet of the patient, 
which must be as nutritious and as abundant as possible. Meat, milk, eggs, farina- 
ceous food, and butter are to be used chiefly, special care being taken that the body 
gets hydrocarbons and fat in sufficient amount, as well as plenty of albumen. 
Many of the special " cures " for phthisis have their only value in the fact that in 
these places the patient takes a large amount of easily assimilated nutriment, like 
milk, and also koumyss, which is, properly speaking, mare's milk fermented in a 
peculiar fashion, although with us it is artificially made from cows' milk — and also 
kefir, which is similar to koumyss. These cures must be judged on this basis 
alone. In ordering milk-cures we must not forget that milk soon becomes repug- 
nant to many patients, and then it can no longer be taken in sufficient amount. 
In such cases we sometimes succeed in making the milk palatable to the patient 
by adding common salt, cognac, or coffee. As regards alcohol, we should chiefly 
prescribe those forms of malt liquor which are relatively rich in nutriment, like 
porter. Small amounts of good wine may aid in improving the appetite and the 
general condition, but alcohol has no specific action. Cod-liver oil, two to four 
tablespoonfuls a day, is a prescription which furthers the patient's nutrition, 
and, if it be well borne, it may be of distinct service, especially in emaciated 
patients. 

We must also pay attention to the patient's manner of living, as well as caring 
for his nutrition. Here we must take care, on the one hand, to remove all the 
injurious influences connected with his occupation, like staying in badly venti- 
lated counting-rooms and work-shops, inhaling dust, or excessive speaking, and, 
on the other hand, to give him such directions as will have a favorable action on 
the whole body, and especially on the respiratory organs — the enjoyment of good 
air, free from dust, sponging the chest with cold water, and baths — but since we 
often can not satisfy all these demands under the patient's ordinary household 
conditions, it has long been the custom to send patients with thoracic diseases to 
certain special health-resorts, where the conditions for a prescribed manner of liv- 
ing may be fulfilled more completely than at home. On this depends the so-called 
climatic treatment of phthisis. Many physicians assert that certain climatic factors, 
like temperature, moisture, and atmospheric pressure, exert a specific therapeutic 
influence ; but this opinion has not yet been confirmed. 

In regard to the choice of a temporary resort for the summer, in many cases we 
must content ourselves with recommending a country residence for the patient, in 
a region as healthy as possible, protected, dry, and well wooded, paying attention 
at the same time to the character of the board and lodging there. A good country 
boarding-place may do just as well as many expensive health-resorts. We may 
mention in particular among the special health-resorts, springs, and places for 
inhalations in Germany (1) the acidulous saline waters at Ems, Gleichenberg, 
Neuenahr, Obersalzbrunn, Reinerz, and others ; (2) the chloride-of -sodium waters 
at Reichenhall, Salzungen, Soden, and others ; (3) the springs containing the earthy 
salts at Inselbad, Lippspringe, and Weissenburg. Beside these we may also men- 
tion some of the well-known high climatic health-resorts in the Alps : Aussee, 
Beatenberg, Berchtesgaden, Engelberg, Gmunden, Heiden, St. Moritz, Seelisberg, 
and others ; and in the Black Forest : Badenweiler, St. Blasien, Rippoldsau, and 
others. 



216 



DISEASES OF THE RESPIRATORY ORGANS. 



The choice of a winter health-resort is, under some circumstances, of still 
greater importance, since the colder season with us brings with it many dangers 
for the patient. The first to be mentioned here are the high health-resorts, where 
the weather is usually clear and sunny. Among these Davos enjoys the greatest 
reputation. This place is especially suited for patients who are still quite strong 
and free from fever, and who do not suffer from laryngeal symptoms. Among 
the winter health-resorts in Germany we must mention first Gorbersdorf, and also 
St. Blasien. The southern climate is better for delicate, "erethistic" patients, and 
also for those with laryngeal affections. Of course only the very distant health- 
resorts in Algiers, Egypt, Malta, and the much-praised Madeira, can furnish a 
certain guarantee of constant mild weather. The Sicilian health-resorts, like 
Catania and Palermo, and also Ajaccio and Pau, afford favorable climatic condi- 
tions, while the health-resorts of the Riviera (see p. 141), Meran, Areo, Lugano, 
and Montreux, are much more uncertain in this respect, and therefore are to be 
used merely as stopping-places by the way during the spring and autumn months. 

We can not go into a more full description here of all the health-resorts men- 
tioned. We can not omit, however, calling special attention to the fact that we 
should always ask ourselves, in choosing a health-resort, whether the expense and 
inconvenience thus imposed upon the patient can be balanced by the possible 
result. It is also blameworthy, from a professional and humane stand-point, to 
send patients in the last stages of phthisis among strangers, to die far from their 
home and relatives. For severe cases, especially, when we wish to send them 
from home, the special institutions are the only suitable places, where the patient 
may at least be under the constant care and attention of the physician. Especial 
asylums for lung patients are Falkenstein on the Taunus, Gorbersdorf, Inselbad 
at Paderborn, and Reiboldsgrun. 

[Our own health-resorts for consumptives are too well known to demand 
extensive consideration here. The prime object is to secure for the patient a 
pure air, with such climatic conditions that he can pass the largest amount of 
time out of doors, at the same time that within doors his comfort is provided 
for, and a sufficiency of suitable and well-cooked food is attainable. In Colo- 
rado large numbers of former consumptives are leading active lives. Florida, 
Aiken, and some other southern resorts are good winter asylums for many cases, 
but patients should not return to New England before June 1st. In general, the 
northern sea-board is much less favorable than the interior, and early cases often 
do well during the winter removed from the dampness of the coast, with its 
alternations of freezing and thawing. A change of climate is a very important 
step, and should receive the most careful consideration of the physician, the cir- 
cumstances of the patient, the stage and character of his disease, his tastes, etc., 
being carefully weighed before a decision is reached.] 

We must also state that, in incipient cases, a residence by the sea, or a long 
sea-voyage, may sometimes be of great help. We have ourselves known several 
young physicians who have become ship-surgeons on account of incipient phthisis, 
and who have returned from the voyage much stronger, and some of them appar- 
ently entirely well. 

The symptomatic treatment of phthisis is directed in the first place against the 
pulmonary symptoms. We use much the same remedies to help the cough as in 
chronic bronchitis. We try inhalations with a solution of common salt, or of the 
alkaline carbonates, or, where there is much secretion, with solutions of tannin 
and the balsams, like turpentine, or balsam of Peru. Where there is severe, spas- 
modic cough, inhalations with narcotic solutions sometimes give some relief, with 
cherry-laurel water, opium, or bromide of potassium. It is doubtful whether the 
inhalation of nitrogen, recommended by many physicians, has any real therapeu- 



TUBERCULOSIS OF THE LUNGS. 



217 



tic value. Pneumatic treatment, by inhalations of compressed air, may some- 
times give good results in cases of incipient phthisis. 

Morphine stands first among the drugs employed to check the cough. We 
should be cautious and sparing in its use at first, but it is an indispensable remedy 
in severe and hopeless cases. It relieves the irritation of coughing, the pain and 
the oppression in the chest, and at least gives the patient for a time the desired 
sleep. In chronic cases, with moderately severe symptoms, we may use for a long 
time the milder narcotics with advantage, like extract of hyoscyamus (extracti 
hyoscyami 1, aquae lauro-cerasi 20, fifteen to twenty drops every two hours), one to 
three grains (grm. 0*05-0 '20) of lactucarium in powder, or half a grain to a grain 
(grm. 0*03-0 *05) of extract of belladonna in powder. 

If the patient complains of difficulty in loosening the expectoration, we pre- 
scribe expectorants, the action of which often fails to meet our desires, but which 
can not be dispensed with in practice. The expectorants most frequently used 
are carbonate of ammonia, ipecacuanha, apomorphine, and sulphuret of anti- 
mony. * We very often combine expectorants with narcotics, as in Dover's powder. 

If severe pain in the chest comes on, we often use local applications : mustard 
plasters, warm poultices and cold compresses, cold wet compresses, painting with 
iodine, or embrocations of chloroform. Narcotics, like morphine, are indispen- 
sable in severe dyspnoea, which usually occurs only in the last stages of the dis- 
ease or as a result of pneumothorax. 

The treatment of haemoptysis is important. As a slight admixture of blood 
in the expectoration often precedes a severe haemoptysis, such an event always 
demands caution. The patient must keep as quiet as possible, and avoid hot 
drinks and alcohol. When there is a severe haemoptysis, absolute rest in bed is 
especially necessary. We should avoid any careful examination of the lungs, 
especially any severe percussion. We should lay a flat and not too heavy ice- 
bag over the lung on the side from which we suspect the haemorrhage ; the cold 
is usually well borne, but sometimes it causes a severer cough, and must then 
be omitted. We would also recommend swallowing bits of cracked ice. Nar- 
cotics, like morphine, are the most suitable internal remedies, since they aid the 
cessation of the haemorrhage by suppressing the attacks of coughing. Among 
the remedies which may be mentioned to check the bleeding are ergotine, two or 
three one-grain pills (grm. 0*05) every hour ; also sclerotic acid, thirty to forty-five 
minims of a four-per-cent. solution subcutaneously in the twenty-four hours ; and 
one or two grains (grm. 0"05-0*10) of acetate of lead in powder every two hours, 
sometimes combined with morphine. The liquor f erri chloridi (a tablespoonful of 
a two-per-cent. solution every one or two hours) is also recommended, but in this 
form it is probably entirely useless. Common salt is a remedy which sometimes 
seems to be of service, and which is almost always at hand. We give one or more 
teaspoonfuls of it in water. Acids, lemonade, and Haller's acid elixir [mixtura 
sulfurica acida (P. G-.)] are favorite household remedies in haemoptysis. 

After the haemorrhage ceases, the patient must be extremely careful for a long 
time, since it often recurs. 

The hectic fever of phthisis is characterized by its great resistance to antipy- 
retic remedies. It is usually utterly useless to try to combat it with large doses of 
quinine or salicylate of sodium. The action of antipyrine, too, is only temporary. 
Cold sponging of the whole body is to be highly recommended at the times of rise 
of temperature. It is usually well borne, and gives the patient visible relief and 
refreshment. 

Cold sponging often diminishes the troublesome sweats in phthisis, but if this 



* We should use tartar emetic instead of the sulphuret. — Trans. 



218 



DISEASES OF THE RESPIRATORY ORGANS. 



does not check them, we may often prescribe atropine to advantage, gr. to ^ 
(grm. 0 '0005-0 "001) at night, but its action does not usually last very long. Lately 
agaricine in T V to ^-grain pills (grm. 0 '005-0 '01) has been recommended for the 
night-sweats in phthisis. Dusting the body with a powder of five parts of sali- 
cylic acid to ninety-five of French chalk is also a good thing. Sage tea is also a 
favorite remedy against night-sweats — two or three cups of it cold at night — and 
so is milk and cognac. 

If there is loss of appetite, small doses of quinine, compound tincture of cin- 
chona, wine of cinchona, and other bitter remedies, like tinctura amara (P. G.), are 
sometimes of service. It is also frequently a good thing to prescribe a little muri- 
atic acid, five to ten drops of the dilute acid, with the meals. It is often very hard 
to treat diarrhoea in phthisis. Opium, combined with tannin or acetate of lead, is 
most effective. This subject will be discussed more fully in the chapter on intes- 
tinal tuberculosis. 

We often prescribe preparations of iron, combined sometimes with quinine or 
arsenic (vide supra), in the beginning of the disease to improve the general con- 
dition and the anaemia, but, as experience shows, iron is contra-indicated in 
patients who are feverish or who have a tendency to haemoptysis. 

The treatment of the diseases complicating phthisis is to be found in the appro- 
priate chapters. 



CHAPTER VII. 
ACUTE GENERAL MILIARY TUBERCULOSIS. 

JEtiology. — Acute miliary tuberculosis is a form of tuberculosis which we are 
justified in describing particularly because of its anatomical relations and of its 
peculiar clinical history. The disease is characterized anatomically by the 
extremely abundant development of miliary tubercles in a comparatively short 
time in many organs of the body. We can not liken this process to anything 
but an overfilling of the body with tubercle bacilli, which in some way reach the 
different organs at the same time, and there give rise to the eruption of tubercles. 
Buhl advanced the hypothesis, a long time ago, that a cheesy focus could be 
found somewhere in the body in every case of acute miliary tuberculosis, and that 
the general infection of the body resulted from the absorption of these cheesy 
masses by the blood. Later investigations, however, have given us a much more 
definite explanation of the nature and manner of this general infection. Ponfick 
first found, in some cases of acute miliary tuberculosis, an extensive tuberculosis 
of the thoracic duct, with destruction of the tubercular new growth. It is easy to 
see how, in this way, a large amount of tubercular material could be brought 
directly into the circulation, from the free communication of the lymph-duct with 
the subclavian vein, and thus be " disseminated " through the different organs in 
a short time. Still more frequently, however, the tuberculosis of the large venous 
trunks, discovered by Weigert, especially the pulmonary veins, seems to be the 
starting-point for an acute general miliary tuberculosis. Usually there are tuber- 
cular lymph-glands, or sometimes other foci of tubercular disease, which unite 
with the wall of a neighboring vein, gradually break through it, and project into 
its lumen. If caseation and ulceration result in this spot, the infectious material 
is of course constantly washed off by the blood-current and carried away, and 
thus it reaches the other organs. 

Since such a tubercular focus, like a tubercular bronchial gland, may remain 
for a long time entirely without symptoms, we can understand how miliary tuber- 



ACUTE GENERAL MILIARY TUBERCULOSIS. 



219 



culosis may break out in an acute form in persons who previously seemed perfectly 
well. In other cases the patient has already suffered from some tubercular affec- 
tion, until suddenly the conditions occur somewhere in the body which lead to 
the development of miliary tuberculosis. Thus we sometimes see it break out in a 
patient who has ordinary phthisis, but acute miliary tuberculosis is one of the 
rarities in advanced phthisis. If we find, at the autopsy of a case of acute general 
miliary tuberculosis, old phthisical changes in the lungs, which is by no means 
very common, they consist of old, partly cicatrized foci, pigment indurations, etc. 
We see miliary tuberculosis rather frequently as a sequel to pleuritic effusion. "We 
have already previously called attention to the fact that in such cases the pleurisy 
itself is a tubercular disease. Miliary tuberculosis is also seen in people with old 
tubercular affections of the bones and joints, like coxitis and vertebral caries, with 
tubercular swellings of the lymph-glands, as in the neck and the axillae, or with 
tuberculosis of the genito-urinary organs. In all such cases, of course, the tuber- 
cular affection, which is discovered during life, need not always be the source of 
the general miliary tuberculosis, but the discovery of the existence of such an 
affection is of the greatest significance in diagnosis, as in this way our attention is 
strongly directed to the possibility of a general tubercular affection. 

In some cases an outbreak of miliary tuberculosis has been seen to follow other 
acute diseases, like typhoid, or measles. 

Pathological Anatomy. — Except for the presence of some old tubercular affec- 
tion' in some organ, and except for the tuberculosis of a vein or of the thoracic 
duct, which are as a rule apparent, and which have been described in the preceding 
chapter, the anatomical lesion in acute miliary tuberculosis consists in the dissemi- 
nation of miliary tubercles through a large number of the organs of the body. 
The lungs, the liver, and the spleen are constantly affected ; almost as constantly 
the kidneys, the thyroid gland, the marrow of the bones, the heart, and the choroid ; 
less constantly, but still quite frequently, the serous membranes and the meninges. 
The miliary nodules may be found in large numbers in all the organs mentioned. 
They may in part be easily recognized by the naked eye, and in the lungs they 
may be very plainly perceived by the touch. In many organs, however, especially 
in the liver and often in the spleen, they are hard to recognize with the naked eye, 
but they are easily discovered by the microscope. In regard to the histological 
structure of miliary tubercles, and the discovery of tubercle bacilli in them, we 
must refer to what has been said in the chapter on pulmonary tuberculosis, but 
we must also mention that, in some of the more chronic cases, some of the nodules 
may grow to be large tubercular foci, from the size of a lentil to that of a pea. 
Less developed cases of miliary tuberculosis are also found, in which only a 
limited number of organs are attacked, and these with less severity. 

Clinical History. — The clinical symptoms of miliary tuberculosis depend upon 
two factors, the first being the general infection of the body, and the second the 
local tubercular affection of certain organs. Although in many organs miliary 
tuberculosis is entirely without symptoms, as in the liver, the kidneys, the heart, 
and the marrow of the bones, in two organs — the lungs, and more especially the 
brain — it leads to the most marked local symptoms. The miliary tuberculosis of 
the choroid, discovered by Cohnheim and Manz, is also without symptoms, but it 
can be made out with the ophthalmoscope, and is therefore of great diagnostic 
value. 

Miliary tuberculosis affords quite different pictures, according to the predom- 
inance of one or the other of the groups of symptoms mentioned. We distin- 
guish the four following forms : 

1. Miliary Tuberculosis, with Predominant Symptoms of General Infection : 
the so-called Typhoid Form. — This form may in part greatly resemble typhoid 



220 



DISEASES OF THE RESPIRATORY ORGANS. 



fever. The patient, who previously seemed quite well, or in whom some local 
manifestation of tuberculosis was suspected, falls ill with gradually increasing 
general symptoms, dullness, loss of appetite, headache, and fever. Since there is 
no local affection to be discovered to explain the symptoms, the disease at first 
may well be taken for typhoid. The general condition grows worse constantly, 
the fever is high and continually rises, and cerebral symptoms appear. In some 
cases an exanthematous eruption, like roseola, may increase the resemblance to 
typhoid. With careful observation, however, symptoms are almost always detected 
later in the disease, which are, to a certain degree, characteristic of miliary tuber- 
culosis, and are due to the existence of that disease either in the lungs or in the 
brain. The patient's complexion assumes a peculiar pallor, and with it a definite 
cyanotic hue. The respiration becomes remarkably deep, and there is dyspnoea, or 
signs of a tubercular meningitis arise, like rigidity of the neck, loss of conscious- 
ness, disturbances in the innervation of the ocular muscles, etc., and death follows 
with these symptoms. These cases last from ten days to three weeks, reckoning 
from the beginning of the severe symptoms. 

2. Miliary Tuberculosis with Predominant Pulmonary Symptoms. — These 
cases, too, may begin quite suddenly, almost like an acute croupous pneumonia, 
or they may develop gradually with quite a long prodromal stage. From the 
onset the symptoms point especially to disease of the lungs or the pleura. The 
patient complains of a stitch in the side, cough, and dyspnoea, and there is also 
usually much general weakness and fever. Later on, the pulmonary symptoms 
constantly increase. The patient has extreme dyspnoea, and we can often make 
out an intense diffuse bronchitis on examining the lungs. The patient's face is 
pale, cyanotic, and anxious. Death ensues with all the signs of insufficiency of 
respiration. The course is usually somewhat more protracted than in the typhoid 
form, lasting for three or four weeks and more. 

3. Miliary Tuberculosis with Predominant Cerebral Symptoms, due to Tuber- 
cular Meningitis. — Tuberculosis of the meninges does not belong among the regular 
lesions of general miliary tuberculosis. It develops in about half the cases, accord- 
ing to our estimation ; but where it occurs it almost always gives the whole type 
of the disease the characteristic imprint of tubercular meningitis, by which the 
other symptoms are entirely concealed. The predominant symptoms are head- 
ache, fever, stupor, increasing to deep coma, rigidity of the back and neck, and dis- 
turbances in the innervation of the ocular muscles. In such cases the tubercular 
meningitis is often the only thing diagnosticated, and the general miliary tuber- 
culosis is not made out at all. In the cases of this sort which we have seen, a 
remarkable, peculiarly deep and accelerated respiration, even in the deepest coma, 
was the only symptom which pointed to a co-existing miliary tuberculosis of the 
lungs. 

The symptoms of tubercular meningitis in many cases predominate in this type 
of the disease from the onset, but in other cases they come on during the attack 
and form its final period. The whole duration of the disease varies accordingly. 

4. Miliary Tuberculosis with a Protracted Course and Indefinite Symptoms 
for a Long Time — Intermitting Form. — Beside the forms already mentioned, 
cases occur which usually take quite a protracted course, lasting for eight or ten 
weeks, and having such indefinite symptoms that a definite diagnosis is for a long 
time, or even throughout the disease, quite impossible. The patient complains of 
a number of general symptoms, like headache and dullness, and also of thoracic 
symptoms, for which, however, we can find no sufficient basis on examination. 
There is almost always fever, usually not very high, and with a very irregular 
course, but we have seen a regular daily rise of temperature for a time in some 
cases, and attacks of fever with quite a severe chill, so that at first we thought of 



ACUTE GENERAL MILIARY TUBERCULOSIS. 



221 



an irregular intermittent fever — the intermitting form. Later on the symptoms 
gradually increase. The apparently inexplicable loss of strength, and the patient's 
anaemia and emaciation, are marked and they are important in diagnosis. Finally, 
either severe pulmonary symptoms or the signs of tubercular meningitis set in, to 
which the patient succumbs. 

We must mention particularly that the four forms of miliary tuberculosis just 
described are only the types of the disease. In individual cases we often meet 
with variations and transitional forms between these types. 

Single Symptoms. — 1. General Symptoms. — In all cases of acute miliary tuber- 
culosis the general condition of the patient is very serious. Most patients 
have a subjective feeling of severe illness, although they make little special com- 
plaint of it from the painless character of the disease. As the disease increases, 
there is often a marked feeling of anxiety and oppression beside the dyspnoea. 
There is, especially in the face, quite a peculiar pallor, characteristic of the disease, 
and associated with a marked cyanosis of the lips and cheeks. 

2. Fever. — Acute miliary tuberculosis almost always runs its course with a 
more or less high fever, a course without fever having been observed in only 
a few cases. It often happens, in more protracted cases, that the temperature 
may be nearly normal for a time, or only slightly elevated. There is nothing 
characteristic or typical in the course of the fever. In the cases with typhoid 
symptoms the fever is usually quite high, between 103° and 105° (39'5°-40'5° C), 
and rises continually, so that the temperature-curve may be exactly like that of 
typhoid. In other cases the fever is irregular and is broken by many remissions, 
remitting or intermitting quite regularly for some time. Death ensues with a 
moderately high temperature or in collapse. In cases with tubercular menin- 
gitis there is also a marked rise of temperature at the close, up to 108° (42° C.) 
and over. 

3. Respiratory Apparatus. — It goes without saying that physical examination 
of the lungs may give no definite results. Almost every positive evidence is 
often wanting, and the contrast between the labored breathing and dyspnoea and 
the insignificance of the physical signs in the lungs is an important feature in 
diagnosis. Auscultation, as a rule, gives the signs of an intense bronchial 
catarrh ; we hear rhonchi or numerous small and medium moist rales all over 
both lungs. The respiratory murmur itself is usually higher in pitch than normal, 
and in many cases it is obscure, rough, or harsh. In one of our cases there was 
heard, over a circumscribed area of the lung, a wholly peculiar, sharp, " lapping " 
sound on inspiration, which we have never heard anywhere else. Jiirgensen 
describes a soft friction sound, due to miliary tuberculosis of the pleura. Per- 
cussion usually gives no objective changes. At times the resonance is rather 
tympanitic, or slightly dull in some places. 

In some cases circumscribed pneumonic infiltration has been observed in the 
lungs in acute miliary tuberculosis, which may give rise to a confusion between 
miliary tuberculosis and croupous pneumonia, from the presence of more marked 
dullness, crepitant rales, and bronchial respiration. 

We must mention, finally, that in some of the cases physical examination of 
the lungs shows old changes in them, a phthisical affection of the apex, a former 
pleurisy, and the like. Positive evidence of such old tubercular affections may 
be of great diagnostic value in doubtful cases. 

Dyspnoea has been repeatedly mentioned among the symptoms in the lungs. 
The respiration is usually very much accelerated, especially during the more 
advanced stage of the disease, so that we see in adults forty, sixty, and even 
seventy respirations a minute. The respiration is also very deep, and is sometimes 
associated with a loud noise. As a rule there is cough, but it is usually trouble- 



222 



DISEASES OF THE KESPIRATORY OKGANS. 



some only in the cases with severe bronchitis. It is often very slight. The 
expectoration is usually scanty, and it is not characteristic. Special mention must 
be made of the fact that tubercle bacilli are absent in it, unless old ulcerated tuber- 
cular foci are present at the same time in the lungs. 

4. Circulatory Apparatus. — The pulse is frequent, about 100 to 120 a minute, 
often weak and small, and sometimes irregular, especially if tubercular menin- 
gitis co-exists. The miliary tubercles, which anatomically are almost always to 
be made out in the heart, especially in the endocardium, cause no symptoms. 
The presence of tubercle bacilli in the blood will be mentioned below. 

5. Digestive Apparatus. — Vomiting is frequent at the onset of the disease. 
The bowels are usually constipated, but in many cases there is a moderate diar- 
rhoea. The loss of appetite, the thirst, and the dry tongue are due to the general 
disease and the fever. The spleen is usually somewhat, but not very much, 
enlarged. 

6. Nervous System. — In many cases where the pulmonary symptoms pre- 
dominate the intellect remains quite clear until the last, but in other cases cere- 
bral symptoms, like headache, dizziness, stupor, and delirium, come on quite early, 
and are a part of the general infection. As has already been said, the nervous 
symptoms in the cases combined with tubercular meningitis become quite promi- 
nent, but in individual cases it may be hard to decide whether they are due to such 
a complication, or are merely severe general symptoms. 

7. Eyes. — The ophthalmoscopic examination of the retina is of special diag- 
nostic importance, since the diagnosis may be made absolutely certain by finding 
miliary tubercles in the choroid. A negative result, however, is never decisive 
against the diagnosis, since the tubercles are sometimes absent, or at least are 
present in very small numbers. Their discovery is almost always difficult, and 
demands much practice in the method of examination. In cases with tubercular 
meningitis we sometimes find an optic neuritis. 

Diagnosis. — The diagnosis of acute general miliary tuberculosis is ordinarily 
and justly considered very difficult. It quite often happens that at the autopsy a 
miliary tuberculosis is found, which was not even suspected during life. We can 
of course say, subsequently, in such cases, that we might very well have thought 
of acute tuberculosis. If, therefore, the possibility of acute miliary tuberculosis 
is brought to our attention during the patient's life, we can make quite a certain 
diagnosis in a number of cases. 

The severe general condition, usually associated with fever, is most important, 
and for this no local cause can be found. Then come the pulmonary symptoms, 
especially the peculiar dyspnoea, for which there is also no adequate corresponding 
physical change to be discovered. It gives decided support to our suspicion if we 
can make out a distinct predisposition to tuberculosis, either hereditary or consti- 
tutional, or the history of a previous tubercular affection, especially pleurisy, and 
also chronic affections of the bones. The peculiar cyanotic pallor of the patient 
is very characteristic. 

On these factors rests the differential diagnosis between the " typhoid " form of 
miliary tuberculosis and typhoid fever. Marked roseola is a distinct argument 
for typhoid, although it sometimes occurs in miliary tuberculosis, and so are the 
characteristic intestinal symptoms of typhoid, like meteorism and the stools ; but 
we must not forget that both the roseola and the intestinal symptoms may be 
absent in typhoid. The course of the fever must always be considered in the 
differential diagnosis. It is much more frequently irregular and atypical in 
tuberculosis than in typhoid. Of course, the temperature-curve is not an abso- 
lutely decisive factor. The occasional decisive evidence of the ophthalmoscopic 
appearances has already been mentioned. 



GANGEENE OF THE LUNGS. 



223 



In many cases the onset of meningeal symptoms may aid the diagnosis. Of 
course, if the patient is not seen until the last stages of meningitis, especially where 
there is an incomplete history, the diagnosis is often impossible. 

Acute tuberculosis is often confounded with severe bronchitis, especially in old 
people Avho were considered emphysematous. The very severe general condition, 
the pallor, the rapid loss of strength, and the fever, are the only things here which 
can call our attention to acute tuberculosis, and render the diagnosis possible. 

Finally, the discovery of tubercle bacilli in the blood is of the greatest diag- 
nostic significance. This was first successfully achieved by Weichselbaum in some 
cases of acute miliary tuberculosis, so that further investigations in this direction 
will probably be attended with success. 

Prognosis. — The cases described in literature as " cured miliary tuberculosis " 
are so uncertain in their diagnosis that they can not be regarded as convincing. 
We must therefore consider the prognosis as absolutely fatal. The differences in 
the course of the disease have been mentioned above. 

Treatment. — Although treatment is absolutely powerless, still the case in hand 
must always receive treatment, since the diagnosis often can not be made out with 
absolute certainty. The treatment is purely symptomatic. The cases with a 
typhoid course are to be treated just like typhoid, with baths, stimulants, etc. 
Tepid baths, and also local applications to the chest, expectorants, and narcotics, 
are indicated when the thoracic symptoms predominate. If meningeal symptoms 
set in, we may try ice, and also local blood-letting, with iodide of potassium inter- 
nally. 



CHAPTEE VIII. 
GANGRENE OF THE LUNGS. 

iEtiology. — The sole cause of pulmonary gangrene — that is, the death and putrid 
decomposition of the lung-tissue — is the entrance of the bacteria of putrefaction 
into the lungs. The opportunity for inhaling them is certainly very frequent, but 
the normal organism apparently possesses the property of nullifying them and 
making them powerless. Under certain conditions, however, they take root in 
the lung, and cause the death of the lung-tissue, which then, as a result of the 
presence of these specific bacteria of putrefaction, succumbs to that peculiar form 
of putrid decomposition known as " moist gangrene." 

The factor which most frequently gives rise to the development of pulmonary 
gangrene is the entrance of organic foreign substances, especially bits of food, into 
the lungs. The bacteria of putrefaction either enter the lungs with the foreign 
substance, or they settle there later and set up a putrid decomposition, first in that 
portion of the lungs, and then in the neighboring lung-tissue. The entrance of 
organic foreign substances into the lungs occurs in different ways. It often hap- 
pens from swallowing the wrong way, or from an accidental inhalation. In this 
way pulmonary gangrene may arise in previously healthy people, but it occurs 
especially in patients who are very low, very stupid, and soporose, and also in the 
insane, in patients who can not swallow or cough well, and in patients with paralysis 
of deglutition, as in bulbar paralysis. Bits of food may also reach the lungs from 
eructations and vomiting. Thus are explained the cases of pulmonary gangrene 
which occur in patients with cancer of the stomach, and, still more frequently, 
with cancer of the oesophagus. Putrid organic material may also reach the lungs 
from ulcerative and ichorous processes in the mouth, the pharynx, and the larynx. 



224 



DISEASES OF THE RESPIRATORY ORGANS. 



In cancer of the tongue, the pharynx, and the larynx, in other ulcerative pre* 
cesses, and in injuries or wounds from operations in the mouth and pharynx that 
have become septic, pulmonary gangrene may develop quite readily. Finally, 
septic foci in the vicinity may extend to the lungs or perforate into a bronchus. 
In this way a pulmonary gangrene may arise from perforation through the pleura 
into the lungs of an ulcerated cancer of the stomach or a gastric ulcer, or in rare 
cases from vertebral caries, or from sanious lymph-glands. 

In some cases the cause of the pulmonary gangrene can not always be made 
out, since the entrance of a foreign substance has perhaps been wholly unnoticed, 
as may happen in children, or during sleep. We had a grown-up young woman 
under observation for a long time with pulmonary gangrene, and one day she 
coughed up several fragments of chicken-bones, but she could give no account of 
how they entered the lungs. 

Experience teaches us that pulmonary gangrene is more apt to develop in 
persons with a general weak nutrition, in old, marantic people and drunkards, 
than in those who are healthy. The tendency of patients with diabetes mellitus 
to pulmonary gangrene is remarkable. 

Pulmonary gangrene often develops secondarily to some other pulmonary 
affection. We have already spoken of the relations between it and foetid bron- 
chitis. Foetid bronchitis, on the one hand, often leads to pulmonary gangrene 
through an extension of the process to the alveoli, and, on the other hand, where 
there is a gangrenous focus in the lungs, the bronchi are often infected to a 
wide extent by the putrid secretion coming from it, and then there arises foetid 
bronchitis. Both diseases often run into each other without any sharp boundary, 
but gangrene may develop secondarily in other affections of the lungs. A neAv 
infection with putrid material, however, is always requisite, and the affection of 
the lungs that already exists furnishes merely a favorable soil. This is the only 
explanation of the process when croupous pneumonia " runs into gangrene," or 
when gangrene develops in catarrhal pneumonia, in bronchiectasis, or in phthisis. 

Although the agents of putrefaction enter the lungs through the bronchi in 
most of the methods of origin of pulmonary gangrene that have been mentioned, 
they may also be transported into the lungs by the blood-current. We call these 
forms embolic gangrene. We find such gangrenous nodules in the lungs in 
extensive gangrenous bed-sores, in puerperal processes, in suppurative caries of 
the bones, etc. In these cases the putrid material enters a vein from the seat of 
the primary process, and is brought to the lungs, and here we find, as a result of 
the putrid character of the embolus, not a simple infarction, but an embolic 
gangrene. 

Pathological Anatomy. — We more frequently find pulmonary gangrene in the 
lower lobes than in the upper, corresponding to its mode of origin. Either both 
lungs are affected or only one, and the right somewhat more frequently than the 
left. We distinguish a diffuse and a circumscribed form, according to the extent 
of the gangrene. Embolic gangrene belongs to the latter form, and its nodules, 
by preference, lie near the pleural surface. 

We can easily recognize the anatomical changes in gangrene. The lung-tissue 
is changed to a discolored, dirty, greenish-gray mass, which gradually and pro- 
gressively becomes dissolved, forming a most foul-smelling ichor. We find, left 
in it, necrotic fragments of tissue and vessels. Gangrene cavities, with irregular, 
ragged walls, are formed from the partial expectoration of the softened gangre- 
nous nodule. The lung-tissue in the vicinity of the peculiar nodule is to a greater 
or less extent inflamed, partly in the form of catarrhal pneumonia, partly in the 
form of circumscribed croupous pneumonia. The inflamed parts in the vicinity 
are gradually involved in the gangrene, as long as the process extends, but finally 



GANGRENE OF THE LUNGS. 



225 



a suppurating line of demarkation may be formed about the gangrene, the whole 
gangrenous fragment is in a measure sequestrated, encapsuled, and gradually 
expelled, and so healing becomes possible. We have already stated that a foetid 
bronchitis may arise from a gangrenous nodule. 

Whenever a gangrenous nodule reaches the pleura, a purulent and usually a 
sanious pleurisy arises from direct infection. Pneumothorax may arise from per- 
foration of a gangrenous cavity. 

Clinical History, — The symptoms of gangrene depend for the most part upon 
the local affection in the lung. The condition of the expectoration is characteris- 
tic, and it alone may decide the diagnosis. 

In many of its conditions the expectoration greatly resembles that of foetid 
bronchitis, and indeed a great part of it does not come directly from the gangre- 
nous nodule, but is the secretion of the diseased bronchi. The penetrating stench 
of the sputum, a most repulsive, putrid odor, is very striking. The patient's breath 
and cough also have this bad smell, which infects the whole vicinity. The amount 
of the sputum is usually large ; it may reach ten or twenty ounces (200-500 c. c.) 
in twenty-four hours. If the sputum is collected in a glass it forms three layers, 
as in the sputum of foetid bronchitis — an upper layer, muco-purulent, greasy, con- 
sisting in part of nummular sputa, and covered with much froth ; a middle serous 
layer, in which some firm masses from the upper layer float ; and a lower layer, 
almost wholly of pus, but greasy and greenish-yellow, which usually contains many 
large and small plugs and shreds of tissue. We find in these plugs, on microscopic 
examination, beautifully twisted needles of the fat acids (see Fig. 19, p. 143) im- 
bedded in countless bacteria, fat drops, and detritus, and often collected in large 
bundles ; but beside these we find in it the constituents of the parenchyma of the 
lungs, and this alone is the decisive factor in distinguishing between pulmonary 
gangrene and simple foetid bronchitis. Traube's theory — that elastic fibers are not 
found in the expectoration in pulmonary gangrene, or that they are rare, because 
the elastic tissue also is destroyed by the gangrene — is untrue. We have almost 
always found elastic tissue in abundance in the expectoration, and also other frag- 
ments of parenchyma, lung-pigment, etc. Which of the coarse, rod-like bacteria, 
described by Leyden and Jaffe as leptothrix pulmonalis, are the special bacteria 
of gangrene is not decided. The chemical examination of the sputum shows the 
presence of those substances which may always be found in the putrefaction of 
organic matter — tyrosine, leucine, ammonia, sulphuretted hydrogen, butyric acid, 
valerianic acid, caprylic acid, etc. The fresh sputum usually has an alkaline reac- 
tion, but, on standing longer, it becomes acid. 

Many cases of gangrene lead to erosion of the vessels and severe haemoptysis. 
Slight admixtures of blood in the sputum are not infrequent. 

The other symptoms on the part of the lungs are not especially characteristic 
of gangrene. Most patients complain of cough, pain in the side, and more or less 
severe dyspnoea. Physical examination, as a rule, permits us to make out the seat 
of the nodule, but not always, since the physical signs, of course, depend upon 
the situation and extent of the gangrene. Small nodules, situated centrally, often 
give no objective evidence of their presence. Every extensive infiltration, how- 
ever, must cause dullness on percussion. Over the area of dullness we hear bron- 
chial respiration, and usually quite numerous moist rales. If a gangrenous cavity 
is formed, the physical examination may show plain symptoms of a cavity — tym- 
panitic resonance on percussion, amphoric respiration, large moist rales, etc. 

The physical signs are sometimes due to the accompanying pleurisy ; the dull- 
ness is more intense, the respiratory murmur and the vocal fremitus are dimin- 
ished, and the adjacent organs are displaced by the abundant effusion ; but an 
absolute diagnosis of an accompanying pleurisy is often to be made only by an 
15 



226 



DISEASES OF THE RESPIRATORY OEG-ANS. 



exploratory puncture. "We have already spoken of the occasional development 
of pneumo-thorax. 

In many cases there is fever, of quite an irregular character and of. very vary- 
ing intensity. In the cases where the gangrenous nodule is sequestrated, and 
where the secretion can be freely emptied through the bronchi, and where, accord- 
ingly, there is no absorption of septic material into the blood, the fever also may 
be entirely absent. 

We often see gastric and intestinal symptoms in pulmonary gangrene, the dis- 
turbance being without doubt due to swallowing some of the foetid sputum. Many 
patients complain of loss of appetite, and sometimes of vomiting, or diarrhoea. 
We also see rheumatic pains in the joints and muscles, as in foetid bronchitis. It 
is also worthy of note that secondary abscess of the brain has been repeatedly 
observed in pulmonary gangrene (see page 701). We must bear this in mind if 
very severe cerebral symptoms, like somnolence, or paralysis, develop in the course 
of a gangrene. 

The general course of the disease shows very great variations. In all cases 
where the pulmonary gangrene is secondary to some other disease, the course and 
the general type of the disease depend very largely upon the primary affection, 
but the cases of idiopathic gangrene also present great variations. The onset is 
either quite gradual and slow, or quite acute, and associated with fever and tho- 
racic symptoms. The stinking expectoration and the bad odor from the patient's 
mouth first direct the attention to the existence of putrid processes in the lungs. 
The disease is usually very chronic, lasting for months or even years. Many 
remissions and intermissions occur. With proper care and treatment we may see 
a clear improvement, and often apparently a complete cessation of the disease. 
The bad odor ceases, the expectoration diminishes or disappears entirely, and the 
patient's strength and nutrition become almost normal ; but relapses may occur 
after long intervals. Where the affection is of slight extent we may even see a 
complete recovery. 

Pulmonary gangrene always takes a worse course in previously weak and 
marantic people, and an unfavorable termination may follow in a comparatively 
short time. Death ensues either from a general loss of strength, as a result of the 
disease, or from complications, like pulmonary haemorrhage, ichorous pleurisy, 
pneumothorax, or abscess of the brain. Rupture of an ichorous empyema out- 
wardly, or into the peritoneum, or into other cavities, is rare. 

Special mention must also be made of the fact that the symptoms of pulmonary 
gangrene are not always so very pronounced. In people who are weak and run 
down we often see pulmonary gangrene at the autopsy, although during life there 
have been no marked symptoms, not even offensive sputum nor the fcetor from 
the mouth. 

Diagnosis. — The diagnosis can be made with certainty only when the charac- 
teristic sputum is present. We can decide whether the sputum comes from a 
foetid bronchitis or from the foetid contents of a bronchiectasis, or from actual 
gangrene, only by finding under the microscope the remains of lung-tissue in the 
expectoration. Physical examination in gangrene, at least in part of the cases, 
also gives the signs of infiltration or of cavity formation in the lungs. 

Prognosis. — The prognosis depends first upon the nature of the underlying 
disease, and then upon the extent of the affection, the strength of the patient, and 
the possibility of sufficient care and proper treatment. If the process in the lung 
becomes sequestrated, marked improvement may follow, even in the severest con- 
ditions ; but we must always remember that a relapse is possible. We have 
already mentioned the dangers which may cause a fatal termination in pulmo- 
nary gangrene. 



DISEASES FKOM THE INHALATION OF DUST. 



227 



Treatment. — Prophylaxis plays an important part in those cases where there 
is danger of the entrance of bits of food into the air-passages from defective deglu- 
tition. We must think of the possibility of this with all patients who show great 
stupor, and also with patients who have paralysis of deglutition, in order to watch 
them while taking food, and eventually to try artificial feeding with the oesopha- 
geal tube. 

The treatment of already existing pulmonary gangrene has, as its chief aim, to 
check the putrid processes of decomposition in the lungs. Unfortunately, the 
remedies at our command are not in all cases sufficient for this. The different 
disinfecting inhalations are the most effective. They are used in the same way as 
in foetid bronchitis {vide supra). Turpentine deserves the most confidence, and 
it may also be given internally with good results. We may also call attention to 
inhalations with carbolic acid, Curschmann's carbolic mask, inhalations with 
salicylic and boracic acids (4 parts of salicylic and 20 of boracic acids to 1200 of 
distilled water), bromine (bromine and bromide of potassium, 2 parts of each to 
1000 of water), and similar substances. 

Beside oil of turpentine other internal remedies are recommended: half a grain 
to a grain (grm. 0 '03-0*06) of acetate of lead every two hours, creasote, carbolic 
acid, etc. Their action is uncertain. 

The general treatment of the patient is very important — he should have good 
food and live in as good air as possible. We must treat the pain in the chest and 
the cough symptomatically, local applications and morphine being most useful . 
The fever seldom gives occasion for direct interference. In general, cold spong- 
ing, or, under some circumstances, tepid baths may suffice, so that quinine is only 
rarely to be used. We may try to relieve the gastric and intestinal symptoms by 
giving antiseptics internally, especially by small doses of muriatic acid, salicylic 
acid, or creasote, as well as by the ordinary remedies, like bitter tincture (tinctura 
amara, P. G.) and opium. 

If a secondary ichorous pleurisy develops, with or without pneumothorax, 
removal of the fluid by operation is necessary, if the patient has sufficient strength 
to bear it. 



CHAPTER IX. 

DISEASES FROM THE INHALATION OF DUST. 

(Pneicmoiioconiosis.) 

Although there are a number of important contrivances in the respiratory 
apparatus to impede the entrance of foreign substances contained in the air into 
the lungs, still, if a person remains in a dusty atmosphere, so many particles of 
dust may be inhaled that they are not without effect on the lung-tissue. The dis- 
eases from the inhalation of dust are usually purely professional diseases, which 
occur especially in workmen whose occupation brings with it the continual inhala- 
tion of some kind of dust. Since we do not have to deal with a specific influence, 
as in the inhalation of infectious substances, but usually only with a mechanical 
effect, all the conditions of disease excited by the different sorts of dust may be 
treated in common. 

We must first mention, however, a condition of the lungs which can scarcely 
be regarded as pathological, although it has its origin in the constant inhalation 
of dust, especially of coal-dust — the ordinary black pigmentation of the lungs. 
There can now no longer be any doubt, although there was once a long dispute 



228 DISEASES OF THE RESPIRATORY ORGANS. 



about it, that the black pigment in the lung comes, in large part at least, from the 
inhalation of carbon. The particles of carbon pass into the lungs themselves, and 
thence into the bronchial glands by means of the lymphatics. Only a part of the 
coal-dust inhaled is removed with the expectoration, and it may easily be found 
in it microscopically, and often by the naked eye, as we see it in the well-known 
black expectoration which we often have in the morning, if we have spent the 
previous evening in a room filled with smoke. In Germany, Traube was the first 
to discover the particles of carbon in the expectoration of a charcoal-burner. In 
the man's lungs,- after death, the vegetable formation of these particles could be 
recognized, and Traube gave the correct explanation of them. In workmen who 
inhale large amounts of charcoal-dust, anthracite coal-dust, soot, or graphite, the 
" normal " pigmentation of the lung passes into a pathological condition, anthra- 
cosis pulmonum. 

Zenker first obtained a clear idea of the fact of the entrance of the different 
sorts of dust into the lungs, and their consequent results. Beside the anthracosis 
already mentioned, the pulmonary disease from inhaling the dust of flint and 
other stones is of especial importance, the so-called stone-cutter's lung — chalicosis 
pulmonum — and also that from inhaling metallic dust, especially oxide of iron — 
siderosis pulmonum. The " stone-lungs " have been observed in workmen in the 
stamping-rooms of glass-factories, in mill-stone cutters, stone-polishers, stone- 
hammerers, plasterers, workers in porcelain, masons, slate-quarrymen, potters, 
etc. " Metal-dust lungs " occur in file-cutters, iron-workers, mirror-polishers, and 
especially in grinders, who inhale a mixture of stone- and iron-dust. The first case 
of a " red iron lung " was observed by Zenker, in a girl who had inhaled a thick 
dust of iron for ten or twelve hours a day. Her work was to color blotting-paper 
with a powder of red oxide of iron. Among the other forms of dust which may 
give rise to pulmonary disease we may mention tobacco-dust, cotton-dust, saw- 
dust, and flour-dust. 

The anatomical changes in the " dust-lungs " consist of a chronic bronchitis, 
and especially a chronic interstitial inflammation, leading to the formation of 
connective tissue, and caused by the mechanical irritation of the foreign body. 
The lungs are studded with nodules, which feel hard to the touch, and which 
grate on section with a knife. All of these nodules consist of firm connective 
tissue, in which the particles of stone or iron are encapsuled. By the union of 
single nodules we may get more extensive induration and cicatricial formation. 
Chemical examination of such lungs gives, as might be supposed, a large amount 
of silicic acid, iron, etc. 

In most of the cases which come to autopsy we find further changes in the 
lungs, which are not the immediate result of the inhalation of dust, but consist of 
sequelae and complications. Chronic diffuse bronchitis in the worker in dust, 
like any other chronic bronchitis, may give rise to pulmonary emphysema, and 
later to cardiac hypertrophy, etc. We very often find in the lungs co-existing 
and prouounced tubercular changes. It need not be stated more fully that these 
changes are not the direct result of the inhalation of dust, but that the changes in 
the lungs set up by such an inhalation furnish merely a favorable soil for infec- 
tion with tuberculosis. In most cases, too, the " dust-lungs " acquire a marked 
clinical significance from the sequelae mentioned — namely, emphysema and tuber- 
culosis. The circumscribed nodules of interstitial pneumonia have no very marked 
symptoms following them. In all cases where there is a fatal termination, with 
pulmonary symptoms, we should regard the immediate action of the dust as much 
less the cause of death than are the diseases that follow its inhalation. 

The actual points to be considered in judging of the clinical symptoms of the 
diseases from inhaling dust are contained in what has been said. The symptoms 



EMBOLIC PROCESSES IN THE LUNGS. 



229 



are those of common chronic bronchitis, or pulmonary emphysema, or phthisis, 
and attention to the injurious influences associated with the patient's calling- is 
the only possible way of making a diagnosis, but in individual cases it may always 
be a matter of doubt how far other accidental causes of disease may come into play. 

The prognosis depends, in the first place, upon whether the patient can be 
removed from the action of these injurious influences or not, but we must also 
mention the fact, that has been often observed, that many people get somewhat 
used to the dust. After they have once recovered from the initial bronchitis, such 
people can live in an atmosphere of dust for a long time without any noticeable 
injury. 

The prophylaxis of diseases from inhaling dust forms an extended chapter in 
the hygiene of occupations, which we can not dwell upon here. The workman 
must be taught the danger to which he is exposed, and the danger itself must be 
diminished as much as possible by sufficient ventilation of the work-rooms, by 
cleanliness, and, under some circumstances, by a change in the technicalities of 
the business. 

We need not give any special data regarding the treatment of diseases from 
inhaling dust. They are founded on the same principles as are given for the treat- 
ment of chronic bronchitis, emphysema, and chronic pulmonary tuberculosis. 



CHAPTER X. 

EMBOLIC PROCESSES IN THE LUNGS. 

{Hcemorrhagic Infarction of the Lungs ) 

iEtiology. — The sources from which the material for an embolic plugging of 
branches of the pulmonary artery comes lie either in the right side of the heart or 
in the veins of the body. Pathological anatomy teaches us how often thrombi are 
formed in the veins, especially in the veins of the lower extremities and in the 
pelvic veins, and in the right side of the heart, in the recesses between the trabe- 
cule, in the auricles, on the valves and the chordae tendinese, and at the apex of 
the ventricle. The particles, torn loose from thrombi so situated, are carried on 
by the blood-current, reach the lungs, plug a larger or a smaller branch of the 
pulmonary artery, according to the size of the particles, and thus cause further 
changes in the lung-tissue. Since the branches of the pulmonary artery are " ter- 
minal arteries," and since thus the vascular territory belonging to each branch 
can not be supplied, or can be supplied only to a small amount, with blood by 
collateral circulation from other vessels, by the closure of a branch of the artery 
the territory supplied by it is shut out of the circulation. The pressure, in the 
part of the vessel lying peripherally to the point of plugging, becomes almost nil, 
and, as a result, there is a backward current into the region shut off from the 
capillaries in the vicinity, and even from the veins belonging to it. Thus we get 
a typical "engorgement." The walls of the capillaries and veins, in which the 
normal blood-current has ceased, lose their natural consistency as a result of this. 
The vascular walls become abnormally pervious. The fluid of the blood, the 
white blood-corpuscles, and also very many red blood-corpuscles, penetrate through 
the walls of the vessels into the surrounding tissue, and change it into the so-called 
heemorrhagic infarction. 

Every embolic closure of a branch of the pulmonary artery does not necessarily 
result in the formation of an infarction. In the sudden plugging of a main trunk, 



230 % DISEASES OF THE RESPIRATORY ORGANS. 



or of several large branches of the pulmonary artery, death may ensue at once, so 
that naturally all further changes in the lung-tissue cease. We also find quite 
frequently, especially in central portions of the lung, embolism of single branches 
of the pulmonary artery, without the formation of an infarction. In such cases 
there must necessarily be a little circulation in the vascular territory which has 
been shut off, either by the presence of anastomoses between the territory of the 
pulmonary artery and that of the bronchial or mediastinal artery, or by the 
neighboring capillaries, whose arteries of supply remain open. 

The changes thus far described are the result of a purely mechanical closure of 
a pulmonary artery. We have noticed this especially where simple fibrinous 
plugs have given the occasion for the embolic process. Pulmonary infarctions 
are most frequent in chronic heart disease, in all forms of primary and secondary 
dilatation of the heart, but especially in disease at the mitral orifice, and in mitral 
stenosis. Thrombus formation is frequent in the dilated right side of the heart, 
and furnishes material for pulmonary emboli ; but these emboli are seen in all 
other possible conditions of disease, in which thrombosis in the right side of the 
heart or in the veins may occur. 

The changes in the lungs assume quite a different appearance if the embolic 
material is not simple fibrine, but if it contains at the same time some specific 
infectious matter. If emboli reach the lungs from an acute malignant endocar- 
ditis in the right side of the heart, or, as is most frequently the case, from a puru- 
lent (septic) phlebitis anywhere in the body, giving rise to a puriform, liquefying 
thrombus, the specific factors in inflammation — that is, bacteria — get into the 
lungs. Thus arise embolic abscesses and embolic gangrenous nodules in the lungs. 
We have already spoken of the latter, and the former are among the most constant 
lesions in every typical pyaemia. 

The fundamental facts as to the occurrence and significance of embolic pro- 
cesses in general, and those located in the lungs in particular, were discovered by 
Virchow. For the fuller understanding of the results of embolic closure of the 
vessels we must thank chiefly the labors of Cohnheim. 

Pathological Anatomy. — Haemorrhagic infarctions may involve one or more 
lobules, or almost a whole lobe of the lung, according to the situation of the 
embolus. Most infarctions are situated at the periphery of the lung, and have 
approximately a conical shape, corresponding to the extent of the region of the 
vessel. The base of the cone lies against the surface of the pleura. It generally 
projects a little above the surface of the pleura, and its dark color can usually be 
plainly recognized through the pleura. The pleura itself is the seat of a fibrinous 
pleurisy at the point to which the infarction reaches, and sometimes for a large 
space around it. The conical shape of the infarction is plainly recognized on sec- 
tion. The lung-tissue is changed to a firm, fragile, uniformly black-red tissue, 
devoid of air. The embolus can usually be readily found in the branch of the pul- 
monary artery leading to the infarction. Under the microscope we see a diffuse 
infiltration of tissue, with red blood-corpuscles in the infarcted portion. The 
alveoli and finer bronchi are also filled with coagulated blood. Under favorable 
circumstances, in cases of longer standing, the blood may be reabsorbed in part. 
The lung again contains air, but it remains much pigmented in' that place, and 
more or less indurated from the development of interstitial connective tissue. 

Hsemorrhagic infarctions are usually situated on the lower lobes, and more 
frequently on the right side than on the left. 

The smaller embolic abscesses are sometimes very numerous, and are dissemi- 
nated over the whole lung. In larger abscesses the conical shape may often be 
plainly recognized. Where an abscess extends to the pleura, a purulent pleurisy 
arises from direct infection. Combinations and transitional forms between the 



EMBOLIC PROCESSES IN THE LUNGS. 



231 



ordinary hemorrhagic infarction and embolic abscesses are occasionally found in 
the lungs. 

Symptoms. — We often find at the autopsy embolism of single branches of the 
pulmonary artery, with or without infarction, which have caused no symptoms at 
all during life. 

Embolism of the main trunk, or of a large branch of the pulmonary artery, 
may cause sudden death, as has been repeatedly observed in patients with heart 
disease, or with venous thrombosis. If death be not immediate, sudden severe 
dyspnoea and oppression arise. The diagnosis may at least be suspected in such a 
case if we know of a possible source for an embolus. In some cases, where an 
embolus is situated in a large branch of the pulmonary artery, but has not com- 
pletely filled it, we can hear a systolic vascular murmur over the affected spot, as 
has been observed by Litten. The diagnosis, however, becomes certain if the 
further signs of infarction appear later. 

The most characteristic symptom of infarction in the lungs is the bloody 
expectoration. If we see quite suddenly bloody sputum in a patient with mitral 
stenosis, we are usually right in assuming a haemorrhagic infarction of the lung. 
Either the sputum consists almost entirely of dark blood, or the blood is mixed 
with more or less mucus ; but there is never much air in it. The bloody expecto- 
ration often lasts for several days. 

We try to learn more of the size and situation of the infarction by a physical 
examination of the lungs. Of course this often gives a negative, or at least a 
doubtful result. It goes without saying that small infarctions, and also all central 
infarctions, can not be made out by physical examination. Large peripheral 
infarctions may give rise in many cases to dullness on percussion, crepitant rales, 
and harsh or bronchial respiration, but it is often hard to decide in an individual 
case whether the physical signs which we meet with are not due to other patho- 
logical changes in the lungs, like bronchitis or hydrothorax. We sometimes hear 
a pleuritic friction-sound in some part of the chest a few days after we suspect 
that an infarction has occurred, by which the diagnosis gains additional certainty. 
We have already mentioned the subjective symptoms in embolism of a large pul- 
monary vessel — sudden dyspnoea and oppression. Small infarctions often cause 
no special symptoms, but in other cases the patient feels a severe pleuritic pain, 
due to irritation of the pleura. 

Fever may be wholly absent, though we sometimes see a moderate rise of tem- 
perature at the onset of a pulmonary infarction. 

The embolic abscesses in the lungs hardly ever give rise directly to clinical 
symptoms. They form a part of the general picture of pyaemia and similar gen- 
eral infectious processes. Marked symptoms on the part of the respiratory appa- 
ratus are seen only when the abscesses are present in very large number. If an 
empyema develops from a focus which extends to the pleura, it sometimes gives 
rise to definite physical signs. 

It follows from all that has been said before, that in the diagnosis of embolic 
processes the chief stress must always be laid on the presence of an etiological 
factor. We must regard the bloody sputum as the main direct symptom in 
haemorrhagic infarction. Embolic abscesses in the lungs may often be suspected 
in pyaemic diseases, but they can hardly ever be made out directly. 

The prognosis is entirely dependent upon the underlying disease. In heart 
disease the occurrence of a haemorrhagic infarction is usually on the whole an 
unfavorable sign, since it points to weakness of the right ventricle, and hence to 
the formation of a thrombus in it ; yet it often happens that the symptoms of a 
pulmonary infarction may pass away entirely. 

We need not give special directions for treatment. It is in part purely symp- 



232 DISEASES OF THE EESPIEATOEY ORGANS. 



tomatic, and in part coincides with the treatment of the underlying- affection. As 
regards prophylaxis, we must bear in mind the absolute necessity of as perfect rest 
as possible in those patients in whom the presence of venous thrombi, as in the 
femoral veins, suggests the possibility of pulmonary embolism. 



CHAPTER XI. 

BROWN INDURATION OF THE LUNGS. 

{Lungs of Heart Disease.) 

In heart disease, especially in mitral stenosis, we often find a peculiar change 
in the lungs, whose origin must be sought in the long-persisting engorgement of 
the pulmonary circulation. The lungs are hard and dense, and show on a fresh 
section an abnormal brownish-yellow color. In the larger pulmonary vessels, the 
arteries and veins, there is a thickening and cloudiness of the intima as a result of 
the stasis. We see here and there on the surface of the section, and beneath the 
pleura, little dark spots of pigment and fresh haemorrhages. We term this condi- 
tion brown induration of the lungs. 

Microscopic examination shows that the capillaries are evidently dilated and 
twisted as a result of the persistent stasis. They even extend a good way into the 
alveoli, whose lumina is thus actually diminished. The interstitial connective tis- 
sue seems somewhat thickened, and we find in it many pigment granules, the 
remains of the extra vasated and decomposed red blood- corpuscles. According to 
Rindfleisch, the muscular constituents of the parenchyma of the lung, the smooth 
muscular fibers at the entrance and in the walls of the alveoli, show a distinct 
hypertrophy. In the intima of the larger vessels we often find fatty degeneration 
of the endothelium, and sometimes even fatty degeneration of the muscular coat. 

As regards the clinical significance of brown induration of the lungs, it is 
possible that the extensive (hminution of the lumina of the alveoli through the 
whole lung may contribute somewhat to the increase of the dyspnoea in heart 
disease, but in practice this factor can not be separated from the other causes 
which produce dyspnoea. 

We have no certain factors by which to diagnosticate brown induration of the 
lungs during life. The anatomical lesions, too, show a certain difference, not 
always to be explained, in that, under apparently the same conditions, the brown 
induration is often very marked, and often only extremely slight. In cases where 
we find this induration in the cadaver we sometimes hear, during the patient's 
life, a very sharp, puerile respiratory murmur, which seems to be characteristic 
of many cases of the "heart-disease lung." We might lay still more stress upon 
the presence of large, characteristic cells in the expectoration, which are thickly 
filled with large and small pigment-granules. These large pigmented cells are in 
all probability white blood-corpuscles, which have taken up the pigment from 
the red blood-corpuscles destroyed within the alveoli. At the autopsy we also 
find these cells lying within the alveoli. Beside these pigment-cells we also fre- 
quently see the still intact red blood-corpuscles in the expectoration of patients 
with heart disease. 

The prognosis and treatment coincide with those of the underlying cardiac 
disease. 



TUMORS OF THE LUNGS. — PULMONARY SYPHILIS. 233 



CHAPTER XII. 

TUMORS OF THE LUNGS. CANCER OF THE LUNGS. ECHINOCOCCUS 
OF THE LUNGS. PULMONARY SYPHILIS. 

1. New Growths in the Lungs. Cancer of the Lungs. — Most of the new 
growths which are met with in the lungs are of a secondary nature. Secondary 
cancers are sometimes found in the lungs, with carcinoma of other organs, whose 
origin may always be explained by supposing a growth of the primary tumor into 
a vein, and the consequent carriage of the germs of the growth to the lungs. 
These secondary nodules in the lungs usually cause no special clinical symptoms, 
unless they are very numerous and extensive, when they give rise to dyspnoea, and 
physical signs. Several years ago there came to the clinic here in Leipsic a case 
of secondary, and very extensive, miliary carcinosis of the lungs, which ran a brief 
and fatal course, simulating acute miliary tuberculosis with predominant pul- 
monary symptoms. 

We must mention enchondroma among the other secondary new growths, but 
it may also occur primarily in the lungs in very rare cases. Secondary sarcomata 
of the lungs are also very rare. "We have seen a very extensive form of it after 
primary sarcoma of the bronchial glands, and also in a case of lympho-sarcoma of 
the cervical lymph-glands, where the sarcoma had grown into the jugular vein, 
and, finally, we have seen it repeatedly in congenital primary sarcoma of the 
kidneys, to the chapter on which we will refer. 

Among the primary new growths in the lung, pulmonary cancer is the only 
one which has much clinical significance. In its clinical relations we can also 
rank with it certain malignant, metastatic forms of alveolar sarcoma. The typical 
cancer of the lungs is always a cylindrical-celled carcinoma, which undoubtedly 
arises from the bronchial epithelium. It is especially common in elderly people, 
over forty, and seems to be found somewhat more frequently in the right lung 
than in the left, and in the upper lobes than in the lower. By its diffusion the 
lung-tissue in the parts affected by cancer is changed to a yellowish-gray and 
quite soft and crumbling mass, devoid of air. We can usually scrape away from 
the section the characteristic cancer-juice, in which the microscope shows the 
typical cancerous elements. The pleura is very often involved. The new growth 
has either grown directly into it, or .single, and more circumscribed, secondary 
nodules have formed in it. The lymph-glands are almost invariably affected, 
especially the bronchial glands, and also the axillary and cervical glands. Sec- 
ondary carcinoma of other organs is rare, but it is found in some cases in the 
other lung, the liver, the brain, and elsewhere. 

It is almost always difficult to interpret correctly the clinical symptoms of 
cancer of the lungs at the beginning of the disease. They are referred to some 
other, more frequent chronic pulmonary disease, like chronic bronchitis, phthisis, 
or pleurisy, but in the further course of the disease we succeed, at least in a num- 
ber of cases, in making a correct diagnosis. In other cases, especially in old people, 
the disease may remain latent. 

The general symptoms in the lungs have, in part, nothing characteristic. 
The patient complains of gradually increasing difficulty in respiration, and of 
pressure and distress in the chest, which may finally increase to the most intense 
dyspnoea. Most patients suffer very much from the labored, frequent, and spas- 
modic cough. The expectoration in some cases has no peculiarity, but it often 
assumes, at least for a time, a characteristic consistency which is extremely impor- 



234 



DISEASES OF THE KESPIEATOEY ORGANS. 



tant for diagnosis. It contains blood, and also has a peculiar " currant- jelly-like " 
appearance. Under the microscope we can sometimes make out the character- 
istic elements of the tumor in it. Severe hsemoptyses are also seen in cancer of 
the lungs. 

Physical examination of the lungs gives a positive result in many cases, such 
as dullness, bronchial respiration, diminished respiration, rales, and sometimes 
pleuritic friction-sounds, all of which have nothing characteristic in themselves, 
but, of course, are of distinct significance in making out the seat and the extent of 
the new growth. Special mention must be made of the often-noticed diffuse pro- 
jection and swelling of the diseased side. 

The occurrence of certain sequelse is of great diagnostic significance. The 
chief one is the discovery of swelling in the lymph-glands in the neck or axilla, 
and also a number of symptoms of compression, which are produced either directly 
by the new growth, or are due to the secondary enlargement of the lymph-glands. 
Pressure on the superior vena cava, or a large branch of it, produces oedema in the 
face, neck, over the wall of the chest, or in one arm. The subcutaneous veins in 
the regions named appear dilated and tortuous. Pressure on the oesophagus 
causes difficulty in deglutition ; pressure on the brachial plexus, intense neuralgic 
pains and paresis of one arm ; pressure on the recurrent nerve, paralysis of the 
vocal cords and hoarseness ; pressure on the trachea or a primary bronchus, the 
symptoms of tracheal or bronchial stenosis. 

Beside the symptoms already mentioned we must consider the general symp- 
toms. As in carcinoma in general, so in pulmonary carcinoma, the well-known 
cancerous cachexia gradually develops. The patient grows dull, loses his appetite 
more and more, disturbances of digestion and sometimes moderate elevations of 
temperature develop, until he finally succumbs to general marasmus. 

The whole duration of the disease is from six months to two years. The prog- 
nosis is fatal. The treatment can be only purely symptomatic, and we employ the 
same remedies as in other pulmonary affections. 

We must still briefly consider a new growth in the lungs which is extremely 
interesting from a theoretical point of view. In workmen in the cobalt mines of 
Schneeberg, in the Saxon Voigtland, the development of malignant lympho- 
sarcomata in the lungs, with the occasional formation of metastases in the glands, 
the liver, the spleen, etc. , is of frequent occurrence. The disease runs its course 
under the type of a chronic pulmonary affection, and almost always ends fatally. 
The endemic occurrence seems to point to an infectious origin for the tumor. 

2. ECHINOCOCCUS OF THE Lungs. — Primary echinococcus in the lungs is very 
rare. In most cases the echinococci are brought to the lungs secondarily from other 
organs, either by way of the blood-current, or, as is far of tener the case, by perfora- 
tion of an echinococcus of the liver through the diaphragm. 

The symptoms of echinococcus of the lungs are manifold. The parasite some- 
times remains entirely concealed. In other cases the type of a more or less severe, 
and often febrile, affection of the lungs is developed, with pain in the chest, cough, 
and sometimes bloody expectoration, and dyspnoea. Physical examination of the 
lungs gives in some cases dullness, absence of respiratory murmur, and diminished 
vocal fremitus, while after the expectoration of the echinococcus (vide infra) 
symptoms of a cavity may ensue. A correct interpretation of all these symptoms 
is possible only when, as has often been observed, the echinococcus cysts are 
coughed up, or at least when parts of them, like the membranes or the booklets, are 
found in the expectoration. 

The termination of the disease may be favorable if the echinococci are expec- 
torated, or if we succeed in removing them by operative means. We can hardly 
hope to be able to kill the parasite by inhalations of turpentine, or benzine. Some- 



PLEURISY. 



235 



times the echinococcus cyst becomes gangrenous or suppurates. Rupture into the 
pleura, into the peritoneum, into the pericardium, and externally has also been 
observed. The latter termination is the most favorable, since, if the affection 
progresses, a fatal result may be caused by the sequela?, or rarely by the occurrence 
of suffocation. The details of the natural history of the echinococcus are given in 
the chapter on echinococcus of the liver. 

3. Pulmonary Syphilis. — This would also be the place to speak of syphilitic 
new growths in the lungs, but, in our opinion, in spite of the quite abundant litera- 
ture of this subject in recent times, no decisive statement as to pulmonary syphilis 
can be given. Those physicians who are disposed to consider every pulmonary 
disease in a previously syphilitic subject to be of a syphilitic nature, certainly 
regard many things as pulmonary syphilis which have nothing at all to do with 
syphilis. At least in the cases of supposed pulmonary syphilis (" syphilitic phthi- 
sis ! ") which we have seen, an ordinary tuberculosis was always found at the 
autopsy. The only form of pulmonary syphilis that has been established patho- 
logically is syphilis of the larger and medium-sized bronchi, which is recognized 
at the autopsy by extensive radiated* cicatrices in the bronchial mucous mem- 
brane, which sometimes lead to stenosis. Single gummatous nodules in the lungs 
are of the greatest rarity. We sometimes find in the pleura peculiar radiated 
cicatrices, which perhaps are of syphilitic origin. Practically we are always justi- 
fied, if severe and otherwise inexplicable pulmonary symptoms occur in a pre- 
viously syphilitic subject, in trying specific treatment ; but only in rare cases do 
we get any good result from it. The pulmonary syphilis of the new-born, which 
occurs in the form of single nodules or as a diffuse syphilitic infiltration, the 
so-called pneumonia alba, has only a pathological interest. 



SECTION V. • 
Diseases of the Pleura, 
CHAPTER I. 

PLEURISY. 

(Pleuritis.) 

iEtiology. — We make the general distinction of a primary and a secondary 
pleurisy. 

By primary pleurisy we mean those cases where previously healthy people are 
attacked with an inflammation of the pleura. We have no doubt that such cases 
occur, but they are much rarer than is generally believed, for many cases of 
secondary pleurisy give one the impression of a primary disease, either because 
the primary affection has caused no symptoms up to that time, or because it gen- 
erally is not detected. Taking cold is one of the chief exciting causes of primary 
pleurisy, and mechanical injury may also sometimes act as a cause. 

[American would seem to differ from German experience as to the frequency 
of primary pleurisy. There can be no question that with us the primary affec- 
tion, followed by lasting recovery, either absolute or relative, is common enough.] 

Secondary pleurisy arises, in a great majority of cases, from a direct invasion 
of the pleura by an inflammatory process originating in some neighboring organ. 
We have already had to point out repeatedly, in the description of pulmonary 



236 DISEASES OF THE RESPIRATORY ORGANS. 



diseases, how the different pathological changes in the lung likewise involve the 
pleura if they reach that organ. Thus arises the pleurisy in croupous pneumonia, 
in lobular catarrhal pneumonia, in pulmonary gangrene, in hasmorrhagic infarc- 
tion, and in embolic abscess. Since many of these affections often develop in the 
course of the most diverse diseases, we can easily understand that pleurisy is a 
not infrequent complication of all possible severe diseases. 

By far the most important secondary form is tubercular pleurisy. The teach- 
ing of daily clinical and pathological experience is that the ordinary chronic 
pulmonary tuberculosis is almost constantly complicated with pleurisy. The 
latter is often entirely subordinate to the phthisis, but in many cases certain sub- 
jective symptoms, like pain, and also physical signs, are certainly to be referred 
to the pleurisy. Of much greater practical importance, however, are those cases 
of tubercular pleurisy which arise as an apparently primary pleurisy. Among 
these are certainly the larger part of all ordinary " pleuritic effusions." The type 
of the disease is wholly dominated by the pleurisy. This may improve decidedly, 
as often happens, or even in many cases be completely cured {vide infra), but, if 
we keep the patient long enough under observation, marked signs of tuberculosis 
usually arise later on (see the general course of the disease), whence it follows 
that the initial pleurisy must be regarded, in an setiological sense, as tubercular. 
The special origin of tuberculosis in these cases is not always quite clear. There 
is certainly a small tubercular focus often present in the lungs, which has 
caused no symptoms in itself, but which became the point of origin for a pleurisy. 
In other cases the pleurisy probably comes from a tubercular bronchial gland, 
and in still other cases the way of infection is not evident to us. 

Other organs beside the lungs may be the point of origin for a pleurisy. 
Thus pleurisy arises from affections of the ribs, or of the vertebrae, like caries, 
from perforation of an oesophageal cancer, etc. Inflammations of other serous 
membranes are especially apt to invade the pleura. Thus it arises as a result of a 
pericarditis or peritonitis. Since the pleural and peritoneal cavities are in direct 
communication with each other by the lymphatics of the diaphragm, we can con- 
ceive that both a purulent and a tubercular peritonitis may result in a secondary 
pleurisy. 

Secondary pleurisy sometimes arises in the course of certain diseases in another 
way. In acute rheumatism, in rare cases, a pleurisy develops, which must be 
considered due to the specific causes of the disease. In chronic nephritis and in 
genuine gout we sometimes see pleurisy of which the precise origin is as yet not 
certainly known. Perhaps in these conditions the abnormal accumulation of the 
products of tissue-metamorphosis in the blood and the tissues is the cause of the 
development of inflammation. 

Pathological Anatomy. — The inflamed pleura is markedly injected, it has lost 
its normal luster, and instead it has a dull surface. This dullness is due to the 
coagulated fibrinous exudation upon the pleura ; the exudation, in mild cases, 
forming only a thin layer. In more advanced cases, however, the surface of the 
pleura is* covered with thick, rough, and shaggy masses of fibrine. As long as the 
fluid in the pleura is little or not at all increased, we speak of a simple fibrinous 
or dry pleurisy (pleuritis fibrinosa vel sicca). 

In other cases, however, beside the layer of fibrine there is an abundant exuda- 
tion of fluid from the capillaries of the pleura, forming a pleuritic effusion. This 
is ordinarily of a simple serous character — serous and sero-fibrinous effusions. 
The fluid collects between the surfaces of the pleura, or, if there is at the same 
time an abundant coating of fibrine, between the gaps and in the meshes of the 
fibrinous exudation. In such cases there are often many flakes of fibrine floating 
in the fluid. 



PLEURISY. 



237 



. In every serous effusion we also find a number of pus-corpuscles, which give 
to it a slight cloudiness, but, if the number of pus-corpuscles increases very much, 
we have a fibrino-purulent or a purely purulent exudation. This is always due 
to the presence of a specific infecting agent. The pleurisies which come from 
embolic abscesses, from gangrenous foci in the lungs, and from carious ribs, and 
those which arise from the rupture of tubercular cavities into the pleura, are 
almost always of a purulent character. We call the purulent pleuritic effusion 
empyema. If putrefactive agencies enter the pleural cavity at the same time with 
the pus poison, as in the pleurisies which develop in pulmonary gangrene, the 
purulent exudation assumes an ichorous, putrid character — ichorous effusion. 

Under certain circumstances the effusion assumes a haemorrhagic character — 
haemorrhagic effusion — especially if haemorrhages arise from the old or newly- 
formed capillaries dilated by the inflammation. They arise partly by diapedesis 
and partly from rupture of the walls of the vessels. The exact cause of the haemor- 
rhages is usually unknown. We know by experience that haemorrhagic effusions 
are most frequent in tubercular pleurisy, a fact which is of diagnostic importance. 
Haemorrhagic pleurisy is also a frequent complication of septic— especially puer- 
peral—diseases, as a result of embolic affections of the lungs. We can often refer 
the onset of a haemorrhagic pleurisy, too, to a general haemorrhagic diathesis, as 
in scurvy. 

The amount of fluid collected in one pleural cavity is, in the majority of cases, 
somewhere between a pint and a quart (500-1000 cubic centimetres), but it may 
reach three or four quarts. Every large effusion must influence the position of 
the yielding walls of the pleural cavity, the chest-wall, the lungs, the mediasti- 
num, and the diaphragm, through the consequent increase of pressure in the 
affected pleural cavity ; and the resultant symptoms of pressure in the neighboring 
organs are of the greatest clinical significance. Attention is first called to the 
lungs themselves. Since the normal lung is expanded in the thorax beyond its 
elastic equilibrium, it will retract as soon as a part of the pleural cavity is occu- 
pied with fluid. Until it has reached its position of elastic equilibrium there can 
be no question of a positive pressure on the lung. The lung floats on the effusion, 
in a certain way, if there be no adhesions, but, as soon as the amount of the fluid 
increases, compression of the lung follows. With a very large effusion the lung 
is pushed wholly up and back against the vertebral column, and is changed to an 
almost bloodless, airless, flat mass. It is, however, possible that the atelectasis of 
the lung is not caused exclusively by compression from without, but that, after 
the normal respiratory movements have ceased, a part of the air in the lung may 
be absorbed by the vessels, or even by the effusion. 

We also see the results of the pressure exerted by the pleuritic effusion in the 
mediastinum and diaphragm, as well as in the lungs. Displacements of the heart 
arise from the lateral pressure on the mediastinum, which must take place if the 
pressure in the diseased pleural cavity is equal to that of the atmosphere, for a 
greater and positive pressure is unnecessary, since a negative pressure prevails on 
the healthy side. 

The downward pressure of the diaphragm, which usually affects both halves of 
it, although in unequal degree, makes itself manifest on the right by the low posi- 
tion of the liver, and on the left by the downward displacement of the stomach 
and large intestine. It must be particularly noticed, however, that adhesions may 
prevent all the symptoms from pressure which we have mentioned, both in the 
lungs and in the neighboring organs. 

As regards the further changes and terminations of the pleuritic processes, they 
depend upon the amount and character of the effusion. Favorable cases may 
result in complete recovery and absorption of the effusion. The fluid contents 



238 



DISEASES OF THE RESPIRATORY ORGANS. 



are taken up directly by the lymphatics of the pleura, and the solid constituents, 
the fibrine and the white blood-corpuscles, are decomposed, dissolved, and absorbed. 

In most of the severe cases, however, an extensive new formation of connective 
tissue and vessels takes place. The fluid effusion is mostly absorbed, but the 
pleura itself is thickened and changed — the so-called pleuritic thickening. Very 
commonly extensive loose or firm adhesions form between the two layers of the 
pleura — adhesive pleurisy. Spaces may be left between the adhesions, in which 
the remains of the fluid effusion may be encapsuled — " sacculated pleuritic effu- 
sion." In protracted cases, and especially in relapses of inflammation, as a result 
of phthisis, the pleural thickening may finally reach a thickness of one or two 
centimetres. 

Even in cases with marked thickening final recovery is possible. This always 
is attended with marked cicatricial contraction of the pleura, in which the whole 
chest- wall is involved. The normal expansion of the lungs and thorax returns 
after months if it can return at all. 

It is largely owing to the nature of the primary disease that large pleuritic 
effusions so seldom fully recover. Hence we often notice that, after temporary 
improvements, new returns of the pleurisy occur, or more extensive and usually 
tubercular diseases of the lungs. 

In old pleural thickenings we sometimes see a deposit of lime-salts, the so-called 
"pleuritic ossification." 

In purulent effusion, too, a final absorption is also possible ; but this demands 
much time, and thick, cheesy masses of pus are often left in the pleural sac. In 
most cases of empyema, if there is not timely operative interference, the pus seeks 
an outlet for itself. It may break through the visceral pleura into a bronchus, 
and is emptied externally, thus giving rise to a pyo-pneumothorax ; but in many 
cases the pleura seems to be destroyed only superficially, and the pus is pressed 
into the alveoli as into a sponge, especially by the movements of coughing, and 
thence reaches the bronchi, without letting the air enter the pleural cavity 
(Traube). In other cases the empyema breaks externally through the chest-wall 
— empyema necessitatis. The point of rupture is usually found in the vicinity of 
the sternum, where the chest-wall is thinnest. In very rare cases the empyema 
breaks into the deeper parts of the body, or into the abdominal cavity. 

Course of the Disease. — We will speak in what follows especially of the course 
and symptoms of ordinary, apparently primary (vide supra), fibrinous or sero- 
fibrinous pleurisy, the so-called simple pleuritic effusion. What is said of it 
obtains in large measure in the other forms of pleurisy also. The physical signs, 
of course, are almost wholly independent of the character of the effusion. As far 
as the different forms of pleurisy differ clinically, we will mention their peculiari- 
ties below. 

Only rarely is the onset of pleurisy quite acute and sudden, beginning with a 
rigor. In such cases we must guard against confusing it with croupous pneu- 
monia. Pleurisy usually begins slowly and gradually. The symptoms, which 
the patient himself feels, are in many cases to be referred directly to the disease of 
the pleura. One of the most constant is the pleuritic pain, the stitch in the side. 
A more or less severe pain comes on in the side at every deep breath, and hence 
upon any physical exertion ; also upon movements of the body, in stooping, 
coughing, or gaping. Shortness of breath is soon added, and constantly increases. 
There is often much irritation and a dry cough. Beside that, severe general 
symptoms almost always appear ; the patient feels dull, looks pale, and has no 
appetite. Patients who can endure a good deal often keep at work for a long 
time, until, after feeling miserable for three or four weeks, they are forced to stay 
at home and summon a physician. It is very important to know that in not a 



PLEURISY. 



239 



few cases the general symptoms are much more prominent at the beginning of 
pleurisy than the local ones. The patient comes to the physician complaining 
only of weakness, loss of appetite, or headache, and the physical examination is 
the first thing that shows the presence of what is sometimes a large pleuritic 
effusion. 

In most of the severe cases the further course is slow like the beginning, but 
sometimes the severest symptoms, most intense dyspnoea, marked cyanosis, etc., 
may come on in a short time owing to a sudden increase of the effusion. On the 
other hand, in mild cases the symptoms may disappear again in a few weeks, but 
the objective changes in such cases are generally to be made out for a longer time. 
The disease ordinarily lasts for at least five or six weeks, and often much longer. 
Gradually apparent cure follows, or the onset of new disease, usually tubercular 
{vide infra). 

Single Symptoms. — The pleuritic pain, the stitch in the side, is one of the most 
frequent subjective symptoms. We have previously mentioned that in primary 
diseases of the lungs, too, as in croupous pneumonia, the stitch in the side is due to 
the accompanying pleurisy. It is remarkable that the intensity of the pain in no 
way corresponds to the apparent intensity of the disease. There is often the sever- 
est pain in the side when the physical examination shows almost no change. On 
the other hand, we often hear a decided pleuritic rub without the patient's com- 
plaining of any special pain. Pressure on the chest-wall on the affected side is 
often very painful. With severe pain we may consider the possibility of an inva- 
sion of the intercostal nerves by the inflammation. We have never observed 
cases, like those described by some authors, of " pleuritic pain on the other side " — 
that is, cases where the pain is localized on the side not affected. 

Cough and Expectoration. — The cough is probably directly excited by the dis- 
ease of the pleura. We often see the pain in the side, and also the irritation of 
coughing, brought on by a deep inspiration. Expectoration is entirely absent in 
uncomplicated pleurisy, or it is scanty, and consists simply of mucus. Much 
expectoration always means a pulmonary complication. A large amount of 
purulent sputum is evacuated if a purulent effusion breaks into the lungs {vide 
supra). 

Dyspnoea. — The respiration is usually shallow, and consequently more fre- 
quent, because of the pleuritic pain. In every large effusion which prevents 
respiration in one lung the dyspnoea becomes more severe, and may, with large 
effusions, reach the highest degree of orthopncea. The stronger the patient was 
before the disease, and the more rapidly the effusion develops, the more severe, as 
a rule, is the dyspnoea. 

Fever. — Most severe pleurisies are associated with fever, but its height is not 
very great, so that it quite rarely reaches 104° (40° C). The fever has no typical 
course. In cases with an acute beginning it is sometimes quite continuous, or 
slightly remitting at first. If improvement takes place, the fever goes down in 
about two or three weeks by lysis, so that this part of the temperature-curve may 
be precisely like the period of defervescence in typhoid. 

In the more protracted cases the fever gradually becomes more remitting, vary- 
ing between 100° and 101° (38 0 -38"5° C), and it assumes more and more the form 
of hectic fever. The longer the evening rise of temperature lasts, the more we are 
justified in suspecting tuberculosis. In empyema we see a higher, irregular fever, 
sometimes associated with severe chills. 

The pulse is constantly rapid, up to 100 and over. In all severe cases the 
strength and tension of the pulse are much diminished. Irregularity of the pulse 
is not infrequent. All these changes are probably due in great part to the press- 
ure of the effusion on the heart and large vessels. Lichtheim has discovered 



240 



DISEASES OF THE RESPIRATORY ORGANS. 



experimentally that the compression of the vessels in the compressed lung does 
not lower the arterial pressure. 

General Symptoms. — Pleurisy is almost always associated with a pronounced 
general malaise, muscular weakness, and dullness. The patient is pale, and often 
markedly cyanotic in cases with much disturbance of respiration. There is 
marked emaciation if the disease is of long duration. 

The appetite declines from the outset. There is often occasional vomiting, 
especially in the first period of the disease. The bowels are usually constipated. 
Many patients complain of headache. 

The condition of the urinary secretion is very important. In every pleuritic 
effusion the amount of urine is decidedly diminished as long as the effusion 
increases or remains at the same height. The daily amount is sometimes only 
eight or ten ounces (200-400 c. c). The urine is also concentrated, its specific grav- 
ity being about 1020-1028. Sediments of urates often form. This diminution of 
the excretion of water by the kidneys is largely the result of the diminished arte- 
rial pressure. An increase of the amount of urine is always a favorable symp- 
tom, often the first sign of beginning absorption of the effusion. If a large effu- 
sion is rapidly absorbed, the amount of urine may increase to eighty or a hundred 
ounces (2500-3000 c. c.) daily. The urine, then, of course, is abnormally clear and 
of low specific gravity. 

Physical Signs. 

1. Fibrinous Pleurisy— Pie uritis Sicca.— Simple fibrinous pleurisy sometimes 
gives rise to no physical signs at all. If it develops as a result of some pulmonary 
affection, the physical signs present are often dependent upon this alone. 

In many cases, however, dry pleurisy may cause marked objective signs. On 
inspection, we are struck by the impaired mobility of the affected side on respira- 
tion, which is due to the pain caused by breathing. For the same reason the 
patient at first often lies on the sound side. Percussion gives no qualitative 
change of resonance as yet. With the beginning of exudation slight dullness 
appears, at first almost always in the lower posterior portion of the lungs. Some- 
times the resonance becomes tympanitic as a result of retraction of the lung. We 
can almost constantly make out, especially in the back, that the lower edge of the 
lung moves less than usual on respiration. Auscultation gives a respiratory mur- 
mur that is either qualitatively unchanged, or indefinite, but it is always dimin- 
ished. The peculiar pathognomonic sign of dry pleurisy, however, is the pleuritic 
friction-rub, that characteristic rubbing, grating, creaking sound, which arises 
from the sliding of the rough pleural surfaces over each other, and is detected 
especially in the lateral portions of the thorax. We can hear it both on inspira- 
tion and on expiration. It is often jerky, one rub following another after a con- 
siderable interval. If we are sure we hear a pleuritic rub, it is direct evidence of 
the existence of a dry pleurisy, but its absence will not let us exclude pleurisy. 
The friction-sound must be absent if there are pleuritic adhesions. We can often 
feel a marked rub by laying the hand on the chest. Sometimes the patient feels 
it himself, but in other cases he has no sensation from it. We may confound a low 
rub with fine crepitant rales. Repeated examinations before and after the patient 
has coughed usually confirm the diagnosis, since the rales at least are often 
changed by coughing. 

2. Pleuritic Effusion. — Small amounts of fluid in one pleural cavity escape dis- 
covery. Physical signs first appear when the amount of effusion reaches eight or 
ten ounces (200-300 c. c). 

Inspection shows first the more or less marked impairment of mobility on the 



PLEURISY. 241 

affected side on respiration. If the amount of the effusion is large, there is a 
marked expansion of the affected side in the lower posterior and lateral portions 
of the thorax. The intercostal spaces are stretched or even a little protruding. 
The nipples and shoulder-blades are farther removed from the median line on the 
affected side than on the healthy side. The hypochondrium on the affected side 
is more prominent. In an extraordinarily large effusion on the left side we have 
seen and felt, in the left hypochondrium, the lower surface of the diaphragm, 
which was actually arched downward. By direct measurement in severe cases we 
can make out accurately that the affected side is expanded several centimetres. 

In every large effusion there is marked dyspnoea and accelerated respiration. 
The slight excursions of the affected side on respiration are usually very striking, 
while the sound side moves so much the more. In this stage of pleurisy the 
patient often lies upon the affected side, in order to breathe with the healthy lung 
with as little restraint as possible. "With large effusions complete orthopnoea may 
develop. 

The signs due to displacement of the neighboring organs, which strike one on 
inspection, will be mentioned below in the appropriate connection. 

Everywhere that a layer of fluid comes between the lung and the chest-wall 
there is a loss of clearness in the percussion-note. If the thickness of the layer 
of effusion is five or six centimetres, the resonance seems completely dull or flat. 
The pleuritic dullness is almost always first made out in the lower posterior por- 
tions of the thorax, more rarely in the lower lateral portions. With a slight 
effusion the height of the dullness is only a few centimetres, but, with much 
effusion, it rises higher in the back and the lateral portions of the thorax. The 
resonance also gradually grows dull on the right, anteriorly and inferiorly, above 
the liver. With very large effusions the dullness may begin in front at the second 
or third rib, or in rare cases even the whole half of the chest, front and back, may 
give a totally flat percussion-note. Pleuritic dullness is always attended with a 
marked feeling of resistance on percussion. 

With medium-sized effusions, where the dullness does not extend over the 
whole back, the upper boundary of the dullness usually forms an oblique line, 
highest at the vertebral column and thence running obliquely downward to the 
side of the thorax. We can no more confirm the opposite opinion, which some 
authors hold, than can Weil and others, yet of course no one can establish a 
schematic rule. The lower boundary of the effusion can not be distinguished on 
the right by percussion from the liver dullness. On the left in front and on the 
side, however, we can often distinguish the dullness of the effusion from the tym- 
panitic resonance of the stomach, and this is often of diagnostic value (see the 
displacement of organs, as given below). 

[In moderate effusion without adhesions or pneumonic complications, the line 
of flatness in the back, the patient being in the vertical position, is lowest near 
the spinal column and rises in a curve like the letter S as it passes outward toward 
the axillary region. The experiments by Dr. Garland, of Boston, with reference 
to this point are well known. Before attempting to mark out this line the patient 
should be told to take several deep inspirations, in order to inflate the triangular 
portion of lung which dips down near the vertebras.] 

The percussion-note above a pleuritic effusion deserves attention. The begin- 
ning of pleuritic dullness is almost always relative, gradually passing to an abso- 
lute flatness. The pulmonary resonance above the beginning of dullness is usually 
tympanitic, from retraction of the lung-tissue. We find the tympanitic resonance 
beautifully distinct in large effusions in the first and second intercostal spaces 
in front. It is loud and deep, and remains unchanged with the mouth open— 
Scoda's resonance. With very large effusions, which cause an actual compression 
16 



242 DISEASES OF THE RESPIRATORY ORGANS. 



of the lung, we sometimes find, in the second intercostal space, a dull tympanitic 
resonance, which becomes higher on opening the mouth. This resonance arises 
from the vibrations of ah' in a large bronchus surrounded by compressed lung — 
" Williams's tracheal tone. " With large effusions we sometimes hear over the 
retracted lung, in the upper anterior intercostal spaces, a distinct buckram sound 
— the "cracked-pot sound." 

Displacement of the neighboring organs, which is made out chiefly by percus- 
sion, forms one of the most important physical signs in pleurisy with effusion. 

In right-sided effusions the liver, especially the right lobe, is displaced down- 
ward. We find the lower border of the liver dullness extending several centi- 
metres below the ribs. In very large effusions the liver may be pushed down to 
the level of the umbilicus. The pushing of the mediastinum to the left hi large 
effusions may be recognized by dullness over the upper part of the sternum, reach- 
ing to or beyond the left border of the sternum. The displacement of the heart 
to the left in the majority of well-marked cases is associated with a displacement 
of the apex of the heart upward. This is easily explained by the position of 
the heart and by the direction of the pressure, which first acts from below. We 
recognize the displacement of the heart chiefly by the j>osition of the apex-beat, 
which is seen and felt at or outside the left mammillary line in the fifth space, or 
often higher, as we have said — in the fourth. Percussion gives a displacement of 
the left boundary of the cardiac dullness to the left. 

In left-sided effusions the displacement of the heart to the right, which can usu- 
ally be made out in moderate effusions, is especially noticeable. Resonance over the 
lower part of the sternum is diminished, the heart's dullness extends to the right 
border of the sternum or several centimetres beyond it. In the most marked cases 
the heart is pushed to the right mammillary line. The displacement of the medi- 
astinum is also to be made out over the upper part of the sternum, the dullness 
reaching to the right border of the sternum or beyond. The low position of the 
diaphragm is made out by a depression of the left, and in marked cases of the 
right, lobe of the liver. It is an especially important sign, however, that dullness 
occurs in the place of a zone, about a hand-breadth wide, of normal tympanitic 
resonance above the left border of the ribs — the " semilunar space " of Traube. 
The normal tympanitic resonance here comes from the stomach or large intestine. 
As the diaphragm is pressed downward the pleuritic effusion presses on the posi- 
tion of these organs. The semilunar space is therefore diminished, and finally, 
with large effusions, its place is completely filled by the dullness up to the edge of 
the ribs. 

Changes in dullness in pleuritic effusions may occur with a change of the 
patient's position, but they may often be absent on account of adhesions. The 
respiratory displacement of the lower border of the lung is almost always absent. 

Auscultation always gives a diminished respiratory murmur over the pleuritic 
effusion. With a beginning effusion it may sound approximately vesicular, but 
later it becomes indefinite, hoarse, and finally bronchial, if the larger bronchi only 
are open for the respiratory current of air. The bronchial respiration sounds 
distant and low, and has the character of the sharp German ch, but in rare cases 
it also assumes a distinct amphoric tone, so that it sounds almost like a cavernous 
respiration. The respiratory murmur may finally disappear entirely over very 
large effusions. Above the upper boundary of the effusion the respiration almost 
always sounds harsh. Among the adventitious sounds we must mention the 
pleuritic friction-sound, which of course can be heard only at the upper boundary 
of the effusion, where the two pleural surfaces meet. Moist rales and rhonchi 
signify a co-existing disease in the lungs. With slight effusions we often hear, 
on deep breathing, pure crepitant rales on inspiration, since the walls of the 



PLEUEISY. 



243 



alveoli and bronchioles in the atelectatic lung-, which were stuck together, are torn 
apart. 

On auscultation of the voice we sometimes hear bronchophony, and sometimes 
that bleating, nasal sound of the voice known as aegophony. Baccelli advanced 
the theory that auscultation of the whispered voice might be of service in diagnos- 
ticating the character of the effusion. With a serous effusion we can understand 
a whisper distinctly through the thorax, but not with a purulent effusion, since 
theoretically the cell-elements destroy the waves of resonance. This theory 
holds true in many cases, but by no means in all. 

On auscultation of the heart we notice, as a result of its displacement, an abnor- 
mal extension of the region over which the heart-sounds are audible. If the inflam- 
mation spreads from the pleura to the outer surface of the pericardium, we can 
sometimes hear an extra-pericardial friction-rub, due both to the respiration and 
the action of the heart. 

The vocal fremitus is always diminished over the pleuritic effusion, and in 
marked cases is entirely absent. 

3. Absorption of the Effusion— Pleuritic Contraction.— The beginning absorp- 
tion of the effusion is usually first made evident by the fact that the percussion- 
note in the upper part of the dullness becomes clearer and sometimes tympanitic. 
The respiratory murmur is also plainer. Where it was bronchial it becomes 
indefinite and gradually vesicular again. The vocal fremitus is again to be felt. 
All these improvements gradually but slowly increase, but it is usually a very long 
time before the percussion-note resumes its normal clearness. 

The changes in the form of the thorax are especially striking. Only in pleu- 
risies with slight effusion does the somewhat expanded thorax resume its old form 
without further change. After every severe pleurisy with large effusion there is, 
during its absorption, a marked and easily recognized contraction of the affected 
half of the chest. In cases of moderate intensity the contraction affects only the 
lower lateral portions of the thorax, in severe cases the upper and anterior portions 
as well. We find the most marked contractions in children and young persons 
with a yielding thorax. The circumference of the affected side is much less than 
that of the sound side. The ribs are pressed together and the intercostal spaces 
become very narrow. The fossae are deepened and the nipples and shoulder- 
blades are drawn nearer the vertebral column, which takes on an abnormal lat- 
eral curvature, in which its convexity is directed toward the affected side, but some- 
times to the sound side. Dullness and diminution of the respiratory murmur and 
the vocal fremitus continue with the contraction of the pleura, but they no longer 
depend upon the presence of a fluid effusion, but are due to the pleuritic thickening. 

The process of marked contraction always lasts for months, or even longer. 
In favorable cases the contraction of the thorax may be readjusted very much 
later, often after years. The thickening is absorbed, and the lungs and thorax 
gradually expand, but in other cases there are extensive adhesions between the 
pleural surfaces, especially over the lower lobe, which result in a permanent dis- 
turbance of respiration. In almost all cases of pleurisy with contractions there 
arises a vicarious emphysema in the lung on the sound side. 

Complications. — Peculiar complications of pleurisy are rare. Where such occur 
they are due either to the primary disease which has led to the pleurisy, or the 
simultaneous action of the same cause of disease, like tuberculosis. Hence it 
happens that we speak of the frequent " complication " of pleurisy with chronic 
bronchitis or with tuberculosis of the lungs or other organs. It is important to 
bear in mind that, by a direct advance of the inflammation, the pleurisy may also 
invade the pericardium, and rarely the peritoneum, through the diaphragm ; but 
we see this extension of the process almost solely in tubercular and purulent pleu- 



24:4: 



DISEASES OF THE RESPIRATORY ORGANS. 



risies. We must mention, finally, that we have lately seen two cases with a large 
serous effusion, in which an acute hsemorrhagic nephritis occurred. For the 
paralysis of the arm on the corresponding side observed in some cases of empy- 
ema, compare, page 506. 

Different Forms of Pleurisy. 

1. The simple fibrinous or exudative pleurisy, as a result of croupous or 
extensive lobular pneumonia, often causes but few symptoms in comparison with 
the primary disease. It usually is completely healed, but sometimes the recovery 
may be much delayed, as may happen in croupous pneumonia. 

The so-called primary simple fibrinous or sero-fibrinous pleurisy, which we 
must regard as a distinctly rare affection, contrary to the generally prevailing 
opinion, has a like favorable course. 

2. Tubsrcular Pleurisy.— In an setiological sense we must declare the larger 
part of the ordinary " pleuritic effusions," which clinically seem to be primary, 
to be tubercular. We do not know how far at first the specific anatomical changes 
of tuberculosis are present, or whether there is always some previous tubercular 
affection in the lungs or bronchial glands, but the further course of the cases, if 
we can watch them for years, almost always permits us finally to recognize the 
tubercular nature of the disease ; yet we can not say that phthisis is always the 
immediate sequel of the pleurisy. In a comparatively small number of cases do 
the symptoms of acute tuberculosis, or more frequently of chronic phthisis, appear 
as an immediate result of the pleurisy, which at that time usually continues or is in 
the contracting stage. The objective changes of phthisis are evident either in the 
apex or in the lower lobe of the affected side. The fever continues, the pulmonary 
affection advances, the other lung is also attacked, and the disease takes a fatal 
course under the type of an ordinary phthisis, now more acute and now more 
chronic. In other cases acute tubercular affections arise sooner or later as a 
result of the pleurisy — tubercular meningitis, or general miliary tuberculosis. In 
other cases still the disease develops under the form of tuberculosis of the serous 
membranes, to which we will return again in the description of tubercular pericar- 
ditis and tubercular peritonitis. We often have to do with a double pleurisy, 
with no evident complication in the lungs. In varying succession are added the 
symptoms of chronic tubercular peritonitis, with pain, swelling, and effusion of 
fluid into the abdomen, or the symptoms of tubercular pericarditis. Death finally 
ensues with persistent hectic fever and increasing general emaciation and weakness. 
The whole affection usually runs a chronic course, lasts for months, and often 
shows marked remissions and temporary improvements. 

In very many cases the pleuritic effusion has throughout an apparently 
favorable course. After some weeks the fever ceases, the effusion is absorbed, the 
patient gets up, and is finally discharged as nearly well. Of course, some dullness 
and retarded motion often remain in the affected side, but even these may gradu- 
ally disappear. These cases, too, very often turn out in the end to be tubercular. 
After a longer or shorter period of apparent health, sometimes after the lapse of 
years, a " new " disease appears— that is, either a return of the pleurisy, a pleurisy 
on the other side, or some other acute or chronic tubercular affection. In such 
cases, too, we must look upon the former pleurisy, in an aetiological sense, as 
tubercular. It is not impossible, however, for even a tubercular pleurisy to 
be completely healed, and for the healing to be permanent, if no. other organ 
is at the same time affected by tuberculosis, especially if the lungs remain 
unaffected. 

Finally we must mention the cases where a pleuritic effusion develops second- 



PLEURISY. 



245 



arily to an already pronounced phthisis. Here too we almost always have to do 
with a tubercular pleurisy. 

The anatomical changes in tubercular pleurisy consist of the ordinary signs of 
inflammation, and also of the presence of the specific nodules of tubercle. The 
number of tubercles differs very much in different cases. The pleura is in some 
cases completely studded with miliary nodules, and in others we find the tuber- 
cles with the naked eye only in single spots. The effusion is usually of a sero-fibrin- 
ous character. Sometimes it is hsemorrhagic, as the majority of cases of appar- 
ently primary " hemorrhagic pleurisy " are generally of a tubercular nature. In 
rare cases the effusion may also be purulent. 

3. Purulent Pleurisy — Empyema. — We have already described the aetiology of 
empyema, and we have seen that it can be excited only by infection of the pleura 
with a specific virus which can set up suppuration. The clinical symptoms are 
usually severe. The fever is higher than in the other forms of pleurisy, but it is 
irregularly intermittent, and is often associated with chills. There are severe gen- 
eral symptoms beside the fever, such as great dullness, headache, and a dry tongue. 
We sometimes notice a slight oedema of the chest-wall on the affected side. Oth- 
erwise the local symptoms and disturbances are, of course, the same as in the other 
forms of pleurisy. If the pus is not evacuated artificially, the empyema may finally 
break externally or into the lungs {vide supra). In the latter case a very large 
expectoration of pus suddenly occurs, and is usually followed by pneumothorax. 

Diagnosis. — Our chief attention in regard to diagnosis is called to the distinc- 
tion between pleurisy and acute or chronic pneumonia, which is not very easy in 
all cases. We will therefore briefly contrast the distinctive features on physical 
examination. 

Inspection. — A. more marked distention of the affected side points to effusion ; 
it is absent in pneumonia. 

Percussion. — The dullness in pleurisy is complete, and the feeling of resistance 
on percussion is very marked ; in pneumonia, however, the dullness is rarely so 
marked, and there is often a tympanitic sound. The discovery by percussion of 
signs of displacement of the neighboring organs is of especial weight, as these 
signs are always absent in uncomplicated pneumonia. 

Auscultation. — Diminished or suppressed respiratory murmur points to pleu- 
risy, loud bronchial breathing and rales to pneumonia ; but we must not forget 
that in pneumonia auscultation may give the same signs as in pleurisy, if a 
bronchus is plugged. 

Vocal Fremitus. — Marked vocal fremitus over dullness is direct evidence of 
pneumonia, diminished or absent vocal fremitus of pleurisy ; but the vocal frem- 
itus may also be diminished in pneumonia if a bronchus is plugged. 

Beside the physical signs, we must of course consider the other symptoms — the 
manner of onset, the course of the disease, the fever, the sputum, the occurrence of 
herpes, etc. 

If we have diagnosticated a pleuritic effusion, the next question is always as to 
the character of the effusion, because the prognosis and treatment are to a large 
degree dependent upon this. Although certain well-known aetiological circum- 
stances, and the severity of the fever and the general symptoms, often permit us 
to suspect the nature of the effusion, whether serous or purulent, the only certain 
information comes from an exploratory puncture with a hypodermic syringe. 
There is not the least reason, if the syringe be carefully disinfected and the fluid 
be cautiously withdrawn, why we should not perform this perfectly safe experi- 
ment in all important cases, thus making the diagnosis certain. Beside a macro- 
scopic inspection, a careful microscopic examination of the fluid withdrawn is 
sometimes of importance. Beside the ordinary constituents — red and white blood- 



246 



DISEASES OF THE KESPIKATORY ORGANS. 



corpuscles, endothelial cells, and cholesterine crystals — we may sometimes find 
something of special diagnostic significance, like bacteria in septic pleurisy, car- 
cinoma-cells in cancerous pleurisy, etc. 

We can not always judge from the beginning whether a pleurisy is of tuber- 
cular character or not. We must observe in particular the general habit and the 
nutrition of the patient, and inquire into the hereditary predisposition and any 
previous illnesses. In the further course of the disease persistent hectic fever, 
slowly increasing emaciation and pallor, fresh relapses, and the onset of pulmo- 
nary symptoms, point to the tubercular character of the pleurisy. Every double 
pleurisy, and every pleurisy associated with pericardial or peritoneal symptoms, 
leads us most decidedly to suspect tuberculosis. A hemorrhagic character of the 
effusion, as we have said, points strongly to tuberculosis. Tubercle bacilli are 
usually not present in the fluid exuded in tubercular pleurisy, because the tuber- 
cular nodules on the serous membrane hardly ever ulcerate. 

Prognosis. — The prognosis, as regards the immediate danger of the disease, 
depends entirely upon the severity of the symptoms, and especially upon the 
dyspnoea. The prognosis, as regards the further course of the disease, depends 
chiefly upon the nature of the pleurisy; Many secondary and also many appar- 
ently primary extensive pleurisies recover completely and permanently after weeks 
or months. Unfortunately, we only too frequently have to give a doubtful or a 
directly unfavorable prognosis, especially if the tubercular nature of the pleurisy 
be probable or certain. The prognosis of empyema depends partly upon the 
underlying disease, but especially upon judicious and timely operative interfer- 
ence. The healing process in empyema may last for many months, but it may 
finally be complete. The different possibilities of a spontaneous rupture of 
empyema, internally or externally, have been mentioned above. With incom- 
plete healing, which leaves a pleural fistula, we must fear the appearance of gen- 
eral amyloid disease in various organs. 

In rare cases with large effusions sudden death occurs, an event which can not 
always be explained with certainty. Probably there are different factors possible, 
such as pulmonary embolism, cerebral embolism, sudden cerebral anemia, weak- 
ness of the heart, or the onset of pulmonary oedema. 

Treatment. — In the beginning of the disease the treatment is purely sympto- 
matic. We try to alleviate the patient's symptoms, the pain and dyspnoea, by 
local applications, especially by mustard plasters, warm poultices, which are 
usually more beneficial than cold, sometimes too by dry cups, also by embroca- 
tions with chloroform liniment, and, with severe symptoms, by morphine inter- 
nally or subcutaneously. Unfortunately, we can command but few remedies to 
check the inflammatory process in the pleura. If an ice-bag is well borne, it may 
be of service. The efficacy of the much-used painting with iodine is doubtful, but 
it may always be tried with a severe pleuritic pain. An iodoform ointment, one to 
fifteen, or iodoform collodion, perhaps deserves more confidence. If a large effu- 
sion has formed, we try to hasten its absorption by diuretics. Acetate of potas- 
sium, squills, or boro-tartrate of potassium and sodium* [tar tarns boraxatus, P. GL] 
may be prescribed. When there is weak action of the heart, infusion of digitalis 
may be given, alone or combined with diuretics. The attempt has also been made 
to draw off a large amount of water from the body, and thus to hasten the absorp- 
tion of the effusion, by prescribing drastic purgatives or diaphoretics, like pilocar- 
pine, salicylate of sodium, and hot packs. The so-called Schroth's treatment serves 
the same purpose — that is, withdrawing as much fluid as possible from the food — 
but the last-named methods of treatment generally have the result of exhausting 



[* "We would use the simpler bitartrate of potassium. — Tkans.] 



PLEURISY. 



and weakening the patient too much. We therefore make use of them only rarely. 
It is doubtful whether the internal exhibition of iodide of potassium can further 
the absorption of the effusion, as many physicians believe. Beside the treatment 
by drugs we must also take care to give the patient sufficient food, in order to pre- 
vent the loss of strength. 

In many cases the operative treatment of pleurisy — the evacuation of the effusion 
by puncture — is of the greatest importance. Many cases of pleurisy with effusion 
run a favorable course without it, and we consider it at least superfluous to punct- 
ure every effusion withoLit sufficient grounds, but puncture is often one of the 
most serviceable therapeutic influences at our command. The first . and most 
important indication for puncture is present when the effusion becomes directly 
dangerous to life from its size. As soon as the patient's dyspnoea reaches a dan- 
gerous degree, and the cyanosis becomes more marked and the pulse weaker, 
a puncture must be made as a direct vital indication. The benefit of such a punct- 
ure is often pronounced. The second indication is a too protracted absorption of 
the effusion. Puncture is indicated if the effusion does not disappear after an 
apparent remission of the inflammatory symptoms, especially after the fever has 
gone. We often see the further absorption start up and go on well as a result 
of this. As long as there is still high fever, we puncture only when the patient's 
symptoms demand it ; otherwise the pleura very soon fills up again and we gain 
nothing. 

[There is considerable danger in delaying interference with a large effusion, 
especially if it has come on pretty rapidly, however comfortable the patient may 
be. The liability to sudden and fatal dyspnoea under these circumstances is now 
well recognized. In private practice, when medical aid is not to be had at a 
moment's warning, no time should be lost in evacuating a moderate amount of 
the fluid if the effusion is very large.] 

As regards the performance of the puncture, we can not here go into all the 
numerous methods and forms of apparatus proposed. The distinctions are imma- 
terial. The simpler the method, the easier it is to perform, and hence the better 
it is. 

Every puncture must be preceded by an exploratory puncture in order to con- 
firm the diagnosis. A medium-sized trocar with a lateral opening, to which a 
rubber catheter can be fastened, serves to evacuate the fluid. Billroth's and 
Frantzel's trocars are useful. We can, of course, also puncture with a hollow 
needle, but the point of it is more irritating, and we can not so easily remove clots 
of fibrine as with a trocar. The instruments and the chest-wall at the point of 
puncture must be carefully disinfected. We usually choose rather a low point 
for puncture, somewhere in the seventh intercostal space, in the middle or poste- 
rior axillary line. The patient sits up in bed, but is held and supported by 
another person, where it is possible. Before and during the puncture he takes a 
little strong wine. A small cut of the skin beforehand aids the insertion of the 
trocar. In many cases, especially with a large effusion, we can evacuate a large 
part of the fluid by simple puncture and siphoning, since the prevailing pressure 
in pleuritic effusions is, with few exceptions, positive, from ten to twenty-five 
millimetres of mercury. The evacuating tube of the trocar must be previously 
filled with carbolized water and conducted under a layer of the same into the 
vessel prepared to receive the effusion. The evacuation of the effusion should 
always be slow and gradual. With large effusions we should not withdraw more 
than fifty ounces (1500 c. c.) at once. Since the pressure of many effusions is very 
slight, it . is usually advisable to promote the evacuation by means of aspiration. 
The forms of apparatus most used for this are those invented by Dieulafoy, and 
Potain. In puncture with aspiration we proceed more slowly and cautiously. 



248 



DISEASES OF THE RESPIRATORY ORGANS. 



[An ordinary Davidson's syringe makes a very satisfactory pump, and can 
always be obtained. The needle or trocar should be withdrawn immediately as 
soon as cough comes on, or the patient shows the slightest discomfort due to the 
removal of the fluid.] 

Unpleasant incidents which may cause a cessation of the process are rare. If 
the patient complains of dizziness and faintness, we must stop. Sometimes very 
severe cough occurs on puncturing, at which we must also stop. Sometimes we 
see, after the puncture, an abundant expectoration of frothy, serous sputum— 
" expectoration albumineuse " — a kind of pulmonary oedema, caused, perhaps, by 
a marked perviousness of the walls of the vessels, or by weakness of the left 
ventricle. 

When the process is over, we close the little opening with a bit of sticking- 
plaster. If we wish to be very careful, or if fluid still trickles through the point 
of puncture, we must do it up antiseptically. 

If the exploratory puncture has shown a purulent effusion, we can first evacuate 
the pus by puncture, if the vital indication exists. In some cases empyema 
recovers after a mere puncture, but in the great majority of cases puncture is not 
sufficient. Empyema is like an abscess, which can not heal until the pus is 
emptied. In empyema, therefore, the same indications are to be filled as in any 
large abscess — evacuation of the pus and attention to a free discharge of the secre- 
tion. If we puncture, and let the point of puncture close up, the pus usually col- 
lects again. We must therefore add drainage of the pleural cavity to puncture 
of the empyema. To this end, therefore, most physicians at present open the 
pleural cavity in empyema by an incision — " thoracotomy." We incise it by layers 
in the fifth or sixth intercostal space, outside of the mam miliary line. The length 
of the incision is some two or three centimetres. After the pus is evacuated, a 
large drainage-tube is inserted, fastened in place, and an antiseptic bandage 
applied. 

We can also recommend the following method of operation in empyema, often 
employed at the clinique here in Leipsic. We puncture, under the spray, with an 
ordinary large trocar. The pus is evacuated, and we have an artificial pneumo- 
thorax opening externally. Through the tube of the large trocar a long drainage- 
tube is pushed into the pleural cavity, and the trocar is drawn out over the tube. 
The drainage-tube now lies in the pleural cavity, and is prevented from slipping 
in by sticking a pin through it. Then an antiseptic bandage is applied, which at 
first must be changed frequently, as long as there is much secretion. If the pus 
has a sufficient exit, the fever will subside at once, in an uncomplicated empyema. 
Every fresh rise of temperature almost always depends upon the retention of pus. 
The point of puncture is soon changed to a good drainage-canal by granulations. 
We can then take out the tube, clean it, and easily reinsert it. If all goes well, 
we can gradually shorten the drainage-tube more and more, and finally remove it 
altogether. The cavity of the empyema has filled with granulations, and there 
follows a definite healing, almost always, of course, with marked contraction. 
Many cases do not run so undisturbed a course. If the exit is insufficient, we 
must sometimes dilate the opening with some blunt instrument, and insert a larger 
tube. In simple empyema, where the pus does not smell badly, it is unnecessary 
to wash out the pleural cavity with disinfecting fluids, like salicylic and boracic 
acid solution, permanganate of potassium, or dilute chlorine-water. Carbolic acid 
should not be used, on account of the danger of poisoning by it. If the' empyema 
is septic, or if there is from the first a stinking, sanious exudation, it is necessary 
to wash it out. We must then sometimes make a second counter-opening in the 
chest-wall in order to get a completely free discharge, and to wash out the pleural 
cavity well. The details upon this and upon many other special points in the 



PERIPLEURITIS AND ACTINOMYCOSIS. 



249 



treatment of empyema, and especially upon the resection of a rib, which is some- 
times necessary, are to be found in the text-books on surgery. 

In treating the chronic, contracted pleurisies with thickening, but without fluid 
effusion, methodical respiratory efforts, "lung-gymnastics," are of use. Beside 
these we should strengthen the general condition as much as possible. We should 
advise the patient to breathe deeply, and prescribe cold sponging of the chest daily. 
Inspiration of compressed air by means of a pneumatic apparatus is often accom- 
panied by good, results. Patients from the better classes, who have had a severe 
pleurisy, should be sent, if possible, to a suitable climatic health-resort. 



CHAPTER II. 
PERIPLEURITIS AND ACTINOMYCOSIS. 

Under the name of " peripleuritis " Wunderlich was the first to describe a rare 
form of disease, which consists of an inflammation of the connective tissue 
between the costal pleura and the ribs, and which terminates in the formation of 
an abscess. Similar cases have since been repeatedly observed, and all were char- 
acterized by the lack of any discoverable aetiology. There is neither a previous 
injury, nor a primary disease of the ribs or the pleura. 

The disease occurs chiefly in men. It usually begins suddenly with a chill, 
and runs its course with quite a high fever. In pronounced cases the local symp- 
toms have the greatest similarity to those of an empyema, but the greater protru- 
sion of the chest-wall is striking. The ribs are crowded apart by the abscess, and 
there is often spontaneous rupture externally, scarcely ever into the pleura. Per- 
cussion gives no symptoms of displace- 
ment of the neighboring organs, a distin- 
guishing point from empyema. It is of 
diagnostic significance that we can often 
discover normal lung-tissue containing air 
below the abscess. The mobility of the 
lower border of the lung is also usually 
retained, contrary to what is the case in 
empyema. Another important sign was 
first brought to notice by Bartels : the 
wall of the abscess relaxes on inspiration 
and becomes tense on expiration. We 
may also mention that acute nephritis has 
often been observed among the complica- 
tions. 

From these points we may be able to 
make the diagnosis during life, at least 
in many cases. The prognosis is quite 
unfavorable, but recovery does occur. 
The treatment can be only operative, and 
is quite analogous to that for empyema. 

As an appendix we will consider 
briefly here a disease to which probably many of the cases of peripleuritis belong 
— the so-called actinomycosis. This disease, which has lately become known 




250 



DISEASES OF THE EESPIEATOEY OEGANS. 



through Israel, Ponfick, Johne, and others, is a specific infectious disease, and 
depends upon the invasion of a fungus, the so-called radiating fungus— actino- 
myces bovis. In cattle, tumors which are caused by the actinomyces occur on the 
maxillary bones. In men the actinomycosis has so far been observed under the 
form of extensive phlegmonous suppuration, prevertebral purulent phlegmon, 
empyema, and peripleuritis. Here also the affection has repeatedly started from 
the vicinity of the lower jaw, whence the pus burrowed into the neck, ribs, ver- 
tebrae, etc. In each case the infection seemed to start from the cavity of the 
mouth. In some cases purulent foci have been observed in the lungs caused 
by actinomyces, and also metastatic foci in other internal organs. The forma- 
tion of widely branching fistulas burrowing through the tissue is characteristic. 

In the pus and the masses of granulations we find little yellow granules, con- 
sisting of a tangle of fibers of the fungus, on which alone the diagnosis depends. 
On the periphery the latter all run out into characteristic little clubs (see Fig. 26). 
It is still uncertain whether the actinomyces are to be reckoned among the schizo- 
mycetse or the hypomycetae. The prognosis of actinomycosis in men is usually 
unfavorable. The only possible treatment is surgical. 



CHAPTEE III. 

PNEUMOTHORAX. 

(Pyo-pneumothorax. Sero-pneumothorax.) 

iEtiology. — The formation of pneumothorax — that is, of a collection of air or 
gas in the pleural cavity — arises, in an overwhelming majority of cases, from the 
penetration of air into the pleural cavity through an opening in the pleura. The 
opening may be in the external chest-wall from a penetrating wound of the chest 
or an empyema operation, or it may be in the pulmonary pleura. Pneumothorax 
is by far most frequently associated with phthisis, when a cavity lying beneath the 
pulmonary pleura perforates into the pleural cavity. This is more apt to happen 
in comparatively acute phthisis than in very chronic forms, because the extensive 
adhesions and contractions in the latter hinder the development of pneumo- 
thorax. Pneumothorax usually appears in quite far advanced cases, but it may 
sometimes arise with but slight changes in the lung. 

Pulmonary gangrene or abscess, as well as phthisis, may cause pneumothorax 
by perforation into the pleural cavity. Pneumothorax may also arise from the 
rupture of an empyema into the lung. In some cases a perforation of the oesoph- 
agus or stomach into the pleura, as in gastric ulcer, has been observed, with 
the formation of pneumothorax. 

The development of pneumothorax from severe injuries, as from laceration 
of the lung, without injury to the chest-wall, is rare. Forced respiratory move- 
ments, associated with physical exertion, seem especially capable of exciting such 
a process. We have ourselves seen pneumothorax develop suddenly in a pre- 
viously healthy woman while hanging out her washing, and another time in a 
young man during very labored rowing. Both cases recovered rapidly and com- 
pletely. 

All the last-named causes, however, are far inferior to phthisis. We have yet 
to mention that in phthisis, too, there is sometimes a definite exciting cause — 
severe coughing, vomiting, or muscular exertion — which may favor the develop- 
ment of the pneumothorax. 

Many authors maintain that, by decomposition of a putrid pleuritic effusion, 



PNEUMOTHOEAX. 



251 



gas may be produced, and thus we may have pneumothorax, but such an event is 
extremely rare if it ever happens. 

Pathological Anatomy. — On opening the pleural cavity a part of the air usu- 
ally rushes out, sometimes with an audible noise. We then look into a large 
cavity filled with air, and find, in total pneumothorax, the lung completely 
retracted and lying compressed against the vertebral column. If, however, the air 
fills only a part of the pleural cavity, as a result of extensive adhesions of the 
pleurae, we speak of a circumscribed or sacculated pneumothorax. The amount of 
air contained in the pleural cavity may reach 2,000 cubic centimetres. The pressure 
which it is under is almost always positive — on an average five or ten centimetres 
of water. 

In the cases of pneumothorax arising from perforation of the pulmonary pleura 
we can usually make out the point of perforation in the lungs. This is more fre- 
quently situated in the upper lobe than in the lower. Sometimes it is already 
grown over or is covered by a layer of fibrine, and hence it can no longer be 
found. The opening is usually quite small, but it may reach the size of a ten- 
cent piece. Left-sided pneumothorax seems to be somewhat more frequent than 
right-sided. 

The pleura itself is only rarely normal. Usually agents of inflammation have 
entered it with the air, and hence it is found in a state of inflammation. A part 
of the cavity is then filled with effusion. This is usually wholly purulent — pyo- 
pneumothorax — or sero-purulent, but it may even be serous or sero-fibrinous — 
sero-pneumothorax, or hydro-pneumothorax. 

The neighboring organs, especially the heart and liver, are found pushed out 
of their normal position, as in large pleuritic effusions. 

Symptoms and Course. — The onset of pneumothorax (we speak in what 
follows especially of pneumothorax in phthisis) is quite often made known by a 
sudden pain, usually associated with an increase of the dyspnoea and of the general 
symptoms. There is sometimes a regular collapse. The temperature sinks 
below the normal, the pulse rises to 140 and over. The patient looks pale and 
cyanotic. He usually sits upright or is in a half -sitting position in bed, either 
more on the affected side, in order to use the other lung as much as possible for 
breathing, or more on the sound side on account of the pain. If the pneumothorax 
has come on as a result of the rupture of an empyema into the lungs, there is at 
the same time a very abundant expectoration of pus. 

Although in many cases the symptoms mentioned lead to a suspicion of pneu- 
mothorax, yet a certain diagnosis can be made only after a physical examination. 

Inspection gives a very marked distention of the affected side. The intercostal 
spaces are stretched out, or even protruded. In some cases, as we have ourselves 
noticed, there is a marked elastic " air-cushion feeling " on palpating the intercostal 
spaces. On respiration, the affected side is almost entirely motionless, while the 
excursions of the other side are the more marked. The displacement of the heart 
is often evident from the visible displacement of the apex-beat. 

Percussion gives over the pneumothorax a remarkably loud and deep note, but 
usually not tympanitic on account of the tension of the walls. It is especially 
important to note that this resonance extends beyond the normal limits of the 
lung on the right to the seventh or eighth rib, and on the left to the fifth or sixth, 
and sometimes even to the edge of the thorax. 

The displacement of the neighboring organs can also be made out by percus- 
sion. With right-sided pneumothorax we find the lower border of the liver dull- 
ness abnormally low, and the left border of the cardiac dullness pushed over to 
the anterior axillary line. In left-sided pneumothorax the cardiac dullness is 
usually entirely absent from its normal place, and is found instead to the right of 



252 



DISEASES OF THE RESPIRATORY ORGANS. 



the sternum. The left lobe of the liver is pushed downward, and we do not find 
tympanitic resonance in the semilunar space. 

In a large number of cases the absence of any respiratory murmur on auscul- 
tation is striking. This is in special contrast to the clear resonance on percussion. 
In other cases, however, we hear a number of metallic sounds, at least in many 
places and at many times, which are very characteristic of pneumothorax. First 
among these is amphoric, metallic respiration. This arises in open pneumothorax 
(vide infra) from the direct passage of the air in and out, but in all other cases it 
is the ordinary respiratory murmur of the larynx, trachea, and lungs, which has 
acquired a metallic timbre from resonance in the pneumothorax. In an analogous 
way arise the metallic sounding rales ["metallic tinkling "], and the metallic 
resonance of the cough and voice. Heubner has devised a particularly beautiful 
and practically important experiment for hearing the metallic noise in pneumo- 
thorax. If we strike lightly on a pleximeter with a little rod, usually the handle 
of a percussion-hammer, while we auscultnear it — the "rod percussion " — we very 
often hear quite a distinct high metallic sound. 

The vocal fremitus over a pneumothorax is usually diminished, but it may be 
felt in spite of quite a large collection of air. 

A number of special physical signs are found if a purulent or serous effusion 
be added to the pneumothorax. In the first place, the resonance is thereby rendered 
dull, to a greater or less extent, in the lower parts of the chest. The boundaries of 
the fluid by percussion show a very evident mobility, due to the patient's change 
of place, because the fluid in pneumothorax can move easily to all sides. Since 
the form of the air-space left must therefore change, the height of all the metallic 
sounds manifest anywhere must change too, when the patient sits up or lies down 
— Biermer's change of note. In many cases at every motion of the fluid, excited 
for example by slightly shaking the patient, there arises a metallic splashing 
sound, the so-called succussion of Hippocrates. 

Forms of Pneumothorax. — According to the condition of the perforation during 
life, we distinguish three kinds of pneumothorax (Weil). We speak of an " open 
pneumothorax," if the point of perforation remains open, so that the air on respi- 
ration constantly passes in and out of the pleural cavity. If the perforation is 
completely closed, we have a "closed pneumothorax." The third and most fre- 
quent form is the " valvular pneumothorax," in which air enters the pleural cavity 
at each inspiration, but on expiration there is a valve-like closure of the perfora- 
tion, and thus the air can not escape again ; but as soon as the pressure in the 
pleural cavity increases so that no more air can enter it on inspiration, the valvu- 
lar pneumothorax becomes closed. In open pneumothorax the pressure in the 
pleural cavity must be the same as the atmospheric pressure. A positive pressure 
in the pleural cavity can exist only in a closed or a valvular pneumothorax. 

The clinical diagnosis of the form of pneumothorax is not always possible, and 
has usually no great practical importance. The very loud, metallic, amphoric 
respiratory murmur, which may be heard in open pneumothorax, must be men- 
tioned, and Wintrich's change of pitch (see page 206) can sometimes be heard 
in this form. It is worthy of mention that symptoms of displacement of the 
neighboring organs must also arise in open pneumothorax. The predominant 
atmospheric pressure here is positive in contrast to the negative pressure in the 
other pleural cavity, and it is also in contrast to the normal negative pressure which 
previously acted on the upper surface of the diaphragm. A very marked protru- 
sion of the affected side, and very marked displacement of the heart and liver, 
however, speak most strongly against an open pneumothorax. Some authors have 
tried to find a point of distinction for the different forms of pneumothorax in the 
composition of the gas in the pleural cavity, but the results of chemical analy- 



HYDKOTHOE AX. HiEMATOTHORA X. 



253 



sis are still contradictory. According to Ewald, we find in open pneumothorax 
not over five per cent, of carbonic acid and about twelve to eighteen per cent, of 
oxygen ; in closed pneumothorax, however, fifteen to twenty per cent, of carbonic 
acid and ten per cent, at most of oxygen. If in an open pyo-pneumothorax or 
sero-pneumothorax the point of perforation lies below the level of the fluid, there 
sometimes arise on every inspiration metallic sounds, since the bubbles of air 
drawn in rise and come up through the fluid — the " water-pipe sound," " metallic 
tinkling." A peculiar sipping and short snapping sound on inspiration, heard 
by us in one case, seems to point directly to the existence of a valvular pneu- 
mothorax. 

Course of the Disease. — In many cases the occurrence of pneumothorax causes 
such a high degree of respiratory disturbance that death ensues in a few hours or 
days. In other cases the patient improves and may feel quite well for a long time 
in spite of his pneumothorax. Usually, of course, the disease which underlies the 
pneumothorax, commonly phthisis, leads to death after a longer or shorter period. 
Pneumothorax may sometimes heal. The healing usually takes place in this 
way, that the pneumothorax is first replaced by a fluid effusion, and then the lat- 
ter is gradually absorbed, but the air may also be wholly or partly absorbed. It 
depends upon the manner of origin of the pneumothorax, then, and upon the 
intensity of the underlying disease, whether the recovery is permanent or not. ' 

Diagnosis. — The diagnosis of pneumothorax is usually easy with careful exami- 
nation, but the symptoms may sometimes be of so little prominence as to excuse 
overlooking it. It is very difficult and often quite impossible to make a differen- 
tial diagnosis between very large cavities and a saccular pneumothorax, since both 
conditions must have in part precisely the same symptoms. We may mention as 
the chief points in distinction : A cavity is usually situated in the apex, pneumo- 
thorax in the lower part of the thorax ; over a cavity the chest-wall is often 
sunken in, over pneumothorax it is usually prominent ; the vocal fremitus is 
usually marked over a cavity, weak over pneumothorax ; symptoms of displace- 
ment, and also evident succussion, point to pneumothorax. 

Treatment. — The only remedy which can alleviate the often severe symptoms 
is morphine. In hopeless cases we may confine ourselves to prescribing this 
exclusively, both internally and subcutaneously ; but in cases where the patient's 
strength previously was fairly good, we may try to obtain, by operative inter- 
ference, an improvement of the symptoms, and finally a complete healing of the 
pneumothorax. If there is simple pneumothorax without a fluid effusion, we try 
to remove as much air as possible by aspiration. With a large serous effusion a 
puncture of the effusion is indicated, and with purulent effusion a simple puncture, 
or, better, puncture or incision with subsequent drainage. The method then is just 
the same as in the treatment of empyema. We must also state that the above- 
mentioned improvement or healing in pneumothorax has been repeatedly observed 
independently of any operative interference. 



CHAPTER IV. 

HYDROTHORAX. H2EMATOTHORAX. 

1. Hydrothorax. — We term the occurrence of a serous transudation into the 
pleural cavity, independent of an inflammation of the pleura, hydrothorax, or 
thoracic dropsy. The cause of hydrothorax is in rare cases a local hindrance to 
the outflow of venous blood or lymph from the thorax, as in compression of the 

\ 



254 DISEASES OF THE RESPIRATORY ORGANS. 



veins or of the thoracic duct by tumors ; but in the great majority of cases the 
hydrothorax is part of a general dropsy, occurring especially in pulmonary 
emphysema and in cardiac or renal disease. Hydrothorax is often first developed 
after marked cedema of the subcutaneous cellular tissue and ascites, but it may 
sometimes be one of the first symptoms of dropsy. It is usually bilateral, but it is 
often unilateral, or at least much larger on one side than on the other. The 
pleura itself is normal or else cedematous. We often find it traversed with a net- 
work of dilated lymphatics. The serous fluid in hydrothorax is distinguished 
from an inflammatory serous effusion by the smaller amount of albumen in it, by 
the scanty number of cell-elements, and by the absence of or the slight tendency 
to spontaneous coagulation. 

The clinical significance of hydrothorax lies in the hindrance to respiration 
which it causes. As a result of this the hydrothorax may be regarded in many 
cases, especially in renal disease, as the chief cause of death. The objective evi- 
dence of it comes from the physical examination, which of course must, in gen- 
eral, give the same signs as in pleuritic effusion. "We can note only the bronchial 
respiration from compression in hydrothorax, which is often very loud, and which 
may even give rise to a confusion with pneumonic infiltration in the lungs. 
This frequent and very loud respiratory murmur, contrasting with that of pleu- 
ritic effusion, is explained by the normal condition of the lungs and the absence of 
all adhesions. From the same reason, too, the change in the boundary of the 
dullness, as a result of the patient's change of position, is usually more marked in 
hydrothorax than in pleuritic effusion. We often hear crepitant rales over the 
hydrothorax, which arise in the retracted and partly atelectatic lung. The chief 
factor, however, in distinguishing hydrothorax from a pleuritic effusion is in 
the consideration of some existing primary disease. 

The treatment is directed especially to the underlying disease. If we succeed 
in regulating the heart's action, or in restoring the secretion of urine, the hydro- 
thorax often disappears with the other dropsical symptoms. If the dyspnoea 
caused by it reaches a dangerous degree, we often see great relief from aspirat- 
ing the fluid. The nature of the underlying disease, of course, renders the benefit 
in many cases only transitory. 

2. Hsematothorax. — Effusions of blood into the pleural cavity (hsematothorax) 
arise most frequently from traumatic lacerations of blood-vessels, rarely from the 
bursting of an aneurism of the aorta into the pleural cavity, from erosion of an 
intercostal artery in caries of the ribs, from the rupture of a cavity into the pleura 
in phthisis, if it simultaneously opens a blood-vessel, etc. In many such cases a 
typical exudative pleurisy follows the effusion of blood. The physical signs are 
the same as in other pleural effusions. Severe dyspnoea may demand the removal 
of the blood by puncture, or even eventually by an incision. 



CHAPTER V. 

NEW GROWTHS OF THE PLEURA. 

The majority of new growths occurring in the pleura are of a secondary nature. 
We sometimes find single metastatic nodules of cancer in the pleura after primary 
carcinoma of other organs, especially of the mammary gland and the lungs, but 
most carcinomata of the pleura arise from primary carcinomata of the lungs from 
a direct invasion of the pleura by the new growth. 



MEDIASTINAL TUMORS. 



255 



Of the primary new growths in the pleura, only one is of great importance — 
the endothelial carcinoma, first described by E. Wagner. This develops de novo, 
in a diffuse manner, from a proliferation of the endothelial cells of the lymphatics 
and the connective tissue. Metastases occur in the lungs, in the lymph-glands, in 
the liver, in the muscles, etc. 

Single secondary nodules of cancer in the pleura cause no special clinical symp- 
toms, but the cases of diffuse cancer of the pleura as a result of primary cancer of 
the lungs are important, inasmuch as the symptoms of disease of the pleura often 
quite predominate over the pulmonary disease. The dullness is more intense, the 
respiratory murmur and the vocal fremitus diminished. In one such case we saw 
a proliferation of the cancer upon the ribs in front so that there was externally a 
very marked circumscribed swelling. The condition of the sputum is the only 
thing that can give us definite information as to the point of origin of the new 
growth in the lungs (see the chapter on cancer of the lungs). 

Primary endothelial carcinoma of the pleura runs a course similar to chronic 
pleurisy. As we sometimes find a co-existing fluid effusion in the pleural cavity, 
displacement of the neighboring organs may occur. The affection goes on for a 
long time without fever, or with slight and irregular elevations of temperature. 
Most cancers of the pleura are associated with severe pain. 

The diagnosis of new growths in the pleura can usually be made only, if at all, 
in the more advanced stages of the disease. At first almost all the cases are 
regarded as simple or tubercular chronic pleurisy. The diagnosis is founded less 
upon the physical signs than upon the whole course of the disease, the habit of 
the patient, and the evidence of some metastases in the glands and other organs. 
In some cases characteristic elements of the new growth can be found by the 
microscope in the cloudy fluid obtained by an exploratory puncture. 

The prognosis is absolutely unfavorable, the treatment purely symptomatic. In 
endothelial carcinoma we might perhaps try arsenic internally. 



CHAPTER VI. 
MEDIASTINAL TUMORS. 

In the anterior mediastinum, in quite rare cases, extensive new growths occur, 
which are of importance on account of their severe clinical symptoms. The 
point of origin for the tumor is either the mediastinal lymph-glands, or the 
connective tissue, or sometimes the remains of the thymus gland. In their 
anatomical character the tumors are almost always sarcomata, usually lympho- 
sarcomata, rarely alveolar sarcomata. They usually occur in persons in youth or 
middle age, and are somewhat more frequent in men than in women. The special 
getiological factors are unknown. In some cases an injury is stated to be the 
cause of their origin. 

The clinical symptoms are usually of a very indefinite nature at first. The 
patient complains of general languor, headache, pain in the chest, and slight diffi- 
culty in breathing, and only gradually do severe subjective and objective symp- 
toms develop in the chest. 

The symptoms are in part directly due to the tumor, but in large part they are 
symptoms of compression, which arise from the gradually increasing pressure of 
the tumor on a number of neighboring organs. 

The pain in the chest, which is located chiefly in the sternal region, and is 
associated with a marked feeling of oppression, may be very severe. It sometimes 



256 



DISEASES OF THE EESPIEATOEY OEGANS. 



shoots into the lateral portions of the chest and into the arms, when it presses 
on the brachial plexus. 

The dyspnoea may finally increase to an extreme degree. A patient with 
lympho-sarcoma under our observation could, in the last days of her life, breathe 
only while standing. The dyspnoea is due to a compression of the heart and 
lungs, and sometimes to immediate compression of the trachea or a primary 
bronchus. In the latter case marked symptoms of tracheal or bronchial stenosis 
develop. Paralysis of the dilators of the glottis may also occur from a pressure 
paralysis of the recurrent nerves. Paralysis of one vocal cord has been repeatedly 
observed. In the case mentioned above a marked goitre developed, as a result of 
vascular stasis, which further increased the dyspnoea by pressure on the trachea. 
A hydrothorax from local venous stasis may also aid in increasing the dyspnoea. 

Pressure on the oesophagus, and disturbances of deglutition due to it, are rare. 
Pressure on the vagus nerve and the sympathetic sometimes causes anomalies in 
the frequency of the pulse, either marked acceleration or slowing of the pulse. 
If the sympathetic is involved there is inequality of the pupils. In some cases, 
by pressure on the tumor, an artificial dilatation of the pupil can be excited at 
will. By pressure on the vessels, especially on the superior vena cava, the sub- 
clavian vein, etc., oedema and cyanosis may arise in the corresponding parts of 
the body. 

Objective examination of the chest gives a marked diffuse prominence in the 
sternal region in a part of the advanced cases ; in other cases this swelling is 
absent. The discovery of an abnormal dullness in the anterior part of the chest 
is of diagnostic importance ; this usually joins the cardiac dullness on the left, 
and on the right it extends a varying distance beyond the right border of the 
sternum. The heart is often pushed somewhat to the left. We heard over the 
pulmonary artery in our case a marked systolic murmur, caused by compression 
of the vessel. A dissimilarity of the pulse on the two sides is not infrequent. 

The diagnosis of a mediastinal tumor is usually possible in cases with well- 
marked symptoms, but in other cases it is difficult and uncertain. The differential 
diagnosis between mediastinal tumors and aneurism of the aorta (q. v.) causes 
especially great difficulty. Tumors may also be confused with abscesses in the 
anterior mediastinum. 

The prognosis is in all cases absolutely unfavorable. The disease terminates 
fatally, sometimes after a duration of six months or a year. 

The treatment can be only purely symptomatic. Internally we may try iodide 
of potassium or arsenic, and externally iodoform ointment. In the last stages 
of the disease we must try to alleviate the patient's great distress somewhat, at 
least, by narcotics. 



DISEASES OF THE CIRCULATORY ORGANS. 



SECTION I. 
Diseases of the Heart. 
CHAPTER I. 

ACUTE ENDOCARDITIS. 

(Endocarditis verrucosa. Endocarditis ulcerosa.) 

iEtiology. — Excitants of inflammation of different sorts, which circulate in the 
blood, may settle on the endocardium, especially on the valves of the heart, and 
there give rise to an acute endocarditis. Endocarditis, therefore, in its etiological 
relations, is not to be regarded as a single disease ; infectious agents of inflam- 
mation especially, if not exclusively, seem to be its cause. 

The onset of acute endocarditis is a frequent and important symptom, especially 
in acute articular rheumatism. Endocarditis also occurs in certain diseases which 
are probably allied aetiologically to articular rheumatism, in certain forms of 
' hemorrhagic diseases,'' like peliosis rheumatica, and in chorea. The appearance 
of endocarditis as a result of gonorrhoea or of gonorrhceal rheumatism is rare, 
but it has certainly occurred. In the course of the acute exanthemata, too, like 
scarlet fever and measles, as well as in acute and chronic nephritis, we sometimes 
notice the appearance of an acute endocarditis. 

While endocarditis in the diseases previously named often takes a severe 
course, in many other infectious diseases — like typhoid, small-pox, and quite fre- 
quently chronic phthisis — slight inflammations of the endocardium are often 
found in the cadaver, which have an anatomical but not a clinical interest. 
These probably are not directly connected with the primary disease, but are a com- 
plication due to the absorption of septic material, the occurrence of this state of 
things being easily explained by the ulcerative processes of phthisis, the intestinal 
ulcers of typhoid, etc. We can probably explain in an analogous fashion the 
origin of the mild endocarditic aggregations which we sometimes find in people 
who have died of ulcerative carcinomata, and similar diseases. 

Acute endocarditis plays a very important role as a complication of severe 
septic and pysemic diseases. Beyond a doubt the same pathogenetic bacteria are 
here the cause both of the general sepsis and of the special acute endocarditis ; 
but the latter at times stands so prominently in the central point of the disease 
that we may very well call the whole disease from it, on the principle " a potiori 
fit denomination 

Finally, we have still to mention the important fact that acute endocarditis 
17 



258 



DISEASES OF THE CIRCULATORY ORGANS, 



quite frequently develops on the soil of an already existing old chronic endocar- 
ditis — the so-called acute recurring endocarditis. In women, pregnancy and the 
puerperal state sometimes seem to give the occasion for a recrudescence of the 
endocarditis ; but possibly the old endocarditis merely gives a favorable soil for 
a new infection. 

Pathological Anatomy. — We usually distinguish an endocarditis verrucosa, 
with the formation of large or small papillary nodules on the endocardium, and 
au endocarditis ulcerosa (endocarditis diphtheritica), with ulcerations as a result 
of the destruction and wasting away of the superficially necrosed tissue. The 
malignant, invariably fatal form of severe septic endocarditis is chiefly ulcerative 
endocarditis. Endocarditis verrucosa is the milder form, which is seen especially 
in acute rheumatism, but we can not draw either a sharp anatomical or a sharp 
clinical distinction between the two forms mentioned, since malignant cases of 
endocarditis verrucosa are also observed. It is at present still impossible to give a 
positive aetiological classification of the different forms of endocarditis. 

The endocardial growths are usually situated on the valves, especially on 
their edges of closure. More rarely we find them on the chordae tendineae and on 
the endocardium of the ventricle and auricle. In the mildest cases they are 
scarcely as large as the head of a pin, but in severe cases they may increase to 
quite large warty and glandular masses. Microscopically, the base of the nodule 
consists of a newly-formed vascular tissue, infiltrated with small cells, which on 
its surface changes to a granular, coagulated mass. This mass is formed partly of 
coagulated masses of albumen, destroyed cells, and fibrine deposited from the 
blood, and partly of micrococci. The micrococci are found without exception 
in all severe cases of ulcerative endocarditis — having been first discovered by. 
Eberth. In the milder forms of endocarditis verrucosa micrococci have also been 
found by Eberth, Klebs, and others, but their presence has not yet been confirmed 
in all cases. The endocardial ulcers arise from the destruction of the superficially 
necrosed nodule. If the thin valve in any place yields to the blood-pressure, we 
have the so-called acute valvular aneurism. Complete perforation of a valve, 
and tearing off of fragments of a valve and of the chordae tendineae, are also 
seen. 

The great majority of cases of acute endocarditis are situated on the valves of 
the left side of the heart — the mitral and aortic valves. Endocarditis on the tricus- 
pid valve is seldom seen except as a secondary affection in old cases of heart dis- 
ease. In a case of acute ulcerative endocarditis in a grown man seen by us, the 
process was confined exclusively to the tricuspid valve, and there were very many 
embolic abscesses in the lungs. This may be considered a great rarity. In con- 
trast to the ordinary localization of endocarditis we find fcetal endocarditis most 
frequently in the right side of the heart. 

Many other organs may be affected by the endocarditis, through embolism. In 
the benign endocarditis verrucosa the masses of fibrine deposited on the irregulari- 
ties of the valve furnish the embolic material. They cause large or small infarc- 
tions in the kidneys and spleen, embolic softening of the brain, etc. In the malig- 
nant, ulcerative forms, however, large numbers of bacteria get into the circula- 
tion at the same time with the necrotic masses of tissue which have been torn 
off. Here, then, we have to do, not merely with simple mechanical obstruction, 
but with infectious emboli. The emboli in ulcerative endocarditis, therefore, 
either give rise to embolic abscesses in the cardiac muscles, the kidneys, the 
spleen, the lungs, the retina, etc., or they result in haemorrhages, especially into 
the skin, but also into the kidneys, the brain, the retina, and the serous mem- 
branes. The origin of the haemorrhage is probably dependent upon the altera- 
tion of the wall of the blood-vessel from the bacteria. It is not yet known why 



ACUTE ENDOCAKDITIS. 



259 



in some cases abscesses are more frequent and in others haemorrhages. The two, 
however, may be combined. Embolic abscesses belong almost exclusively to the 
severe form of septic endocarditis. Haemorrhages are seen in this form, and also, 
without co-existing abscesses, in certain severe forms of endocarditis occurring in 
the course of acute rheumatism and allied diseases. 

We must also mention that the embolic origin of the haemorrhages can not 
always be made out, and that therefore in many cases they are to be regarded pro- 
visionally merely as due to the "action of the general infection." 

Clinical History. — Since acute endocarditis is not aetiologically a single disease, 
and since its clinical course is very different, in different cases, it seems advisable 
to us to describe, in what follows, the most important forms separately ; but it 
must be expressly noted that the individual forms can by no means be sharply 
defined, and that there are many intermediate forms. 

1. Slight endocarditis verrucosa is quite frequently found in the cadaver, with- 
out the slightest signs of any affection of the heart during life. The little papil- 
lary excrescences on the valves of the heart in phthisis, and carcinoma, whose 
aetiology has been described above, are to be classed under this head. 

2. The typical form of benign acute endocarditis is most frequent, clinically, in 
the course of acute articular rheumatism. It is much rarer in other infectious 
diseases {vide supra). In rare cases its appearance has been noticed as an appar- 
ently primary disease. 

It is only rarely associated from the outset with subjective symptoms, like pain 
in the cardiac region, palpitation, and dyspnoea. It is usually first discovered on 
physical examination of the heart. The impulse of the heart in many cases is 
abnormally strong and diffuse, the pulse is accelerated, but strong, often some- 
what jerky (pulsus celer), and usually regular, but sometimes a little irregular. 
Percussion at first shows no deviations from the limits of normal dullness. On 
auscultation, we hear at the apex, more rarely at the base, a loud blowing, systolic 
souffle. Diastolic murmurs are much rarer in acute endocarditis. The pulmonic 
second sound is often accentuated. Otherwise the physical signs in the heart are 
only slightly marked in many cases of acute endocarditis. This is explained if 
we remember that the occurrence of a heart-murmur is due wholly to the local- 
ization of the endocarditis, to the appearance of some valvular insufficiency, 
etc. 

Beside the direct symptoms pointing to the cardiac affection, the onset of an 
acute endocarditis is often, but not always, associated with fever, or, if fever were 
already present, with an increase of it, and of the general disturbance. Embolic 
processes may occur in the brain, the spleen, the kidneys, and the extremities, but 
they are comparatively rare. Sometimes a pericarditis develops as a result of the 
myocarditis (vide infra). 

It is hard to make any accurate statements as to the duration of this form of 
endocarditis. The physical signs may last for days or for several weeks. Com- 
plete recovery is possible, but in the majority of cases this form of acute endocar- 
ditis passes into chronic valvular disease of the heart. 

3. Malignant, non-septic form of acute endocarditis (" rheumatoid endocar- 
ditis" of Litten). In many cases this form is perhaps only a quantitative increase 
over the preceding form, but in other cases it is probably distinct from it aetiologic- 
ally. The severe general infection is usually quite prominent here, and the dis- 
ease resembles in many particulars the severe septic endocarditis. The objective 
signs in the heart are the same as in the preceding form, but more intense and 
extensive. The subjective symptoms in the heart, like palpitation and distress, 
may be quite pronounced, but they may also be almost wholly absent in this 
form. The general condition, however, is usually bad. There is sometimes high 



260 



DISEASES OF THE CIRCULATORY ORGANS. 



fever with an irregular or intermitting course, but in many cases the fever is 
remarkably low in spite of quite severe constitutional symptoms. 

The constitutional infection is very often manifested in these cases by the 
appearance of small or large haemorrhages in the skin, sometimes in the mucous 
membranes, as in the conjunctiva and the soft palate, and rarely in the retina. 
Secondary articular swellings often develop ; they are always of a serous charac- 
ter, and never purulent. Renal haemorrhages and acute hemorrhagic nephritis 
are quite frequent. Large emboli may also occur in the different organs in this 
form as in every other endocarditis. 

The duration of the disease extends over many weeks. In severe cases death 
ensues as a rule with an increased severity of the general condition, and often 
with severe cerebral symptoms, like stupor and dehrium. In milder cases, how- 
ever, the patient may finally get well. 

Regarding the occurrence of this form, we see it most frequently in acute 
articular rheumatism ; also, in rare cases, in gonorrhoea, where it comes on some 
three or f our weeks after the beginning of the urethral affection ; also in nephritis, 
chorea, peliosis rheumatica, etc. The apparently primary cases of this sort usu- 
ally belong to the recurrent form of acute endocarditis. 

4. The recurrent form of acute endocarditis consists of an acute increase of the 
endocardial process, brought on by some exciting cause, in an organ already suf- 
fering from chronic endocarditis. The acute disease may show all the gradations 
from the mildest grade to the severest forms. The mild cases often run their 
course without any special symptoms. To this form we must probably often 
refer the increase of fever which lasts a longer or a shorter time, and which we 
often see in patients with chronic valvular disease of the heart. In rarer cases 
the recurrent endocarditis comes on quite suddenly in the form of a severe acute 
disease. This sometimes seems to be clinically a primary, independent disease, 
especially if the previous chronic heart disease has up to that time caused no spe- 
cial symptoms. The patient is attacked with general malaise, headache, chills and 
fever. The latter may be quite high — 104° (40° C.) and over — or moderate, varying 
between 100° and 102° (38°-39° C), or it may be entirely absent. In many cases it 
is intermittent, when the increase is often associated with a chill. The symptoms 
in the heart may be quite pronounced, but in this form, too, they may be obscure 
and indefinite. In the further course of the disease we meet with cutaneous 
haemorrhages, retinal haemorrhages, articular swellings, large renal haemorrhages, 
or typical haemorrhagic nephritis — in short, just the same general type of disease 
as in the other malignant forms of acute endocarditis. The course is rarely rapid, 
and often lasts for weeks. Severe cases almost always end fatally. 

5. The severe septic ulcerative endocarditis has already been described as a 
complication of a general septic disease. We therefore refer to the appropriate 
chapter (see p. 98) for all particulars. Septic endocarditis is probably entirely 
distinct aetiologically from the forms so far described, and is manifested by quite 
a rapid fatal course, with severe typhoid or pyaemic symptoms. It is characterized 
anatomically, apart from the cardiac affection, by the appearance of metastatic 
abscesses in the various organs, but in many cases, as we have said, abscesses and 
haemorrhages are combined. 

Diagnosis. — The diagnosis of an endocarditis, coming on secondarily in the 
course of articular rheumatism and other diseases, can be made only by a physical 
examination of the heart. We must therefore give constant attention to the con- 
dition of the heart in diseases which we know may give rise to the development 
of endocarditis. 

The diagnosis of the malignant form of endocarditis often causes great diffi- 
culty, especially if the patient is not seen until the later stages. It is often con- 



VALVULAR DISEASE OF THE HEART. 



261 



fused with typhoid, meningitis, or acute miliary tuberculosis. Examination of the 
heart may furnish direct 'signs, but, as we have said, these are often absent or doubt- 
ful. Of the other symptoms the cutaneous and retinal haemorrhages are of special 
diagnostic importance, since they are very much rarer in the other diseases which 
may give rise to the confusion. The acute hsemorrhagic nephritis, too, in connec- 
tion with the other symptoms, is, at least to a certain degree, characteristic of 
malignant endocarditis. The course of the fever is of diagnostic value only when 
it is decidedly intermittent. A careful search for some setiological factor is very 
important for diagnosis in all cases. 

Prognosis. — In the description of the course of the disease we have already 
mentioned the prognosis of the different forms. The severe cases of acute endo- 
carditis, which are m part complicated by the presence of an underlying affection, 
usually, and the cases of severe septic endocarditis always end fatally. In mild 
cases recovery is possible, but the process of repair is often so incomplete that 
chronic valvular disease of the heart develops from the acute endocarditis. 

Treatment. — The chief requisite in the treatment of every endocarditis is as 
complete rest as possible for the patient. If ice is well borne, the continuous 
application of an ice-bag to the cardiac region is of service. Digitalis may be 
indicated under some circumstances with a weak and irregular action of the heart, 
but on the whole this remedy is not often used in acute endocarditis. With severe 
local symptoms, like oppression and dyspnoea, we prescribe mustard plasters and 
small doses of morphine, and in some cases local blood-letting. Weakness of the 
heart is to be combated by stimulants — wine, camphor, and ether. 

The treatment is also to be directed against the primary disease, although we 
can rarely succeed in influencing the endocarditis in this way. In articular rheu- 
matism especially, which is the most frequent cause of acute endocarditis, salicylic 
acid is unfortunately almost wholly powerless against the endocarditis. 

In the severe forms of endocarditis the treatment can be only purely sympto- 
matic, and we try to keep up the patient's strength as much as possible. The exhi- 
bition of large doses of salicylic acid or quinine has usually no result, or only a 
temporary one. In many cases the use of Fowler's solution, kept up for a long 
time, seems to us to be of service. 

[For remarks upon the alkaline treatment of rheumatism, see page 856.] 



CHAPTER II. 

VALVULAR DISEASE OF THE HEART. 

{Chronic Endocarditis.) 

iEtiology. — A large number of cases of chronic valvular disease of the heart 
proceed from acute endocarditis. Hence the frequent statement in the history 
of heart disease that the patient has formerly had articular rheumatism, once or 
many times. As a result of the endocarditis, which has its chief seat on the cardiac 
valves, there is considerable thickening of the valvular connective tissue. Pro- 
cesses of contraction also take place, and also adhesions, and finally in many 
cases quite marked calcification. All these processes must have the necessary 
result, that such deformed valves can no longer fulfill their well-known physio- 
logical functions in regulating the circulation. There arises considerable disturb- 
ance in the circulation of the heart itself, and, as an immediate result of it, a dis- 
turbance of the general circulation, the pernicious effects of which must finally 
be detected in the system. 



262 DISEASES OF THE CIRCULATORY ORGANS. 

In quite a large number of cases of heart disease, however, we can not obtain 
a history of acute endocarditis. We have to do here with an endocarditis which 
is chronic from the start, which also leads gradually to thickening, contraction, 
adhesion, and calcification of the valves. The aetiology of this chronic sclerotic 
endocarditis is still obscure in many of its relations. The same injurious influ- 
ences which cause acute articular rheumatism, probably, act on the patient in a 
chronic manner from the beginning ; at least, we not infrequently learn from 
patients with chronic heart disease, without previous acute articular rheumatism, 
that in former years they have suffered repeatedly from slight rheumatic symp- 
toms, to which they have paid but little attention. In typical chronic arthritis 
deformans, too, heart disease occurs, though not very often. In other cases, how- 
ever, we must consider the possibility of other injurious influences, partly infec- 
tious, and partly, perhaps, of a chemical or mechanical nature. Chronic alcohol- 
ism, perhaps also chronic nicotine poisoning, and also constitutional syphilis, true 
gout, and immoderate muscular exertion, are the exciting causes which chiefly 
come to our notice. The chronic heart disease in such cases often develops at the 
same time with, and from the same causes as general endarteritis, or atheroma of 
the vessels. To this we may ascribe the origin of many cases of heart disease in 
advanced age. The influence of chronic . nephritis is not to be disputed in the 
development of chronic valvular disease. A hereditary predisposition to heart 
disease is not very frequent, but yet it can be made out with certainty in many 
cases. We have ourselves seen five members of the same family who have suf- 
fered from chronic heart disease, some from pure valvular disease and some from 
severe so-called idiopathic hypertrophy. Perhaps the very frequent occurrence of 
heart disease in many families is also connected with a special family predisposi- 
tion to rheumatic affections, the occurrence of which predisposition can not, in 
our opinion, be denied. Finally, a small number of cases of heart disease, espe- 
cially in the right side of the heart, depend upon anomalies of development of the 
heart — congenital heart disease. 

Of 163 cases of undoubted chronic valvular disease which we have seen in the 
last few years, 86 cases might with great probability be ascribed to articular rheu- 
matism, while in 77 cases the patients have never suffered from rheumatic symp- 
toms. In part of the last-named cases no definite cause could be ascertained, and 
in the rest perhaps some one of the factors mentioned above was to be found. A 
number of women referred their symptoms to previous pregnancies and parturi- 
tions. As has also been noted by others, the cases without previous articular 
rheumatism were more often aortic disease than mitral. 

Valvular disease of the heart occurs at every age of life. The time of origin 
of most cases, corresponding in part to the occurrence of acute articular rheuma- 
tism, falls in youth and middle age, somewhere between eighteen and forty. In 
the female sex heart disease is somewhat more frequent than in the male. 

General Pathology of Valvular Disease of the Heart.— Every valve of the heart 
in order to fulfill its physiological task must, on the one hand, open perfectly at 
the right time in order to furnish a free passage to the blood-current through 
the appropriate orifice, and must, on the other hand, close firmly and perfectly at 
the right time, in order to make any abnormal backward flow of blood impossible. 
In both relations the function of the valves may be disturbed by chronic endo- 
carditis, the disturbance being the result of their anatomical changes. If the tips 
of the valves are shortened on their free edges by contraction, or if the complete 
unfolding of the auriculo-ventricular valves is hindered by a shortening of then 
chordae tendineae, the closure of the valve can not be complete. At the moment 
when the closure of the valve is necessary a fissure remains open between its 
apices. We call this condition an insufficiency of the valve. On the other hand, 



VALVULAR DISEASE OF THE HEART. 



263 



the valves may lose their capability of free and sufficient separation from one 
another, as a result of thickening and calcification of the connective tissue, and 
also as a result of adhesions of the points of the valves with one another. At 
the moment when the blood-current should pass freely through the open orifice, 
the valve remains a stiff, narrow ring, through which the blood must force its 
way — stenosis of the orifice. The changes in the valves are often of such a sort 
that they cause at the same time both an insufficiency of the valve and a stenosis 
of the orifice. The thickening and calcification of the valves in stenosis cause, 
as a rule, a valvular insufficiency at the same time, but an insufficiency, set up by 
a contraction of the edges of the valves, may occur without a coincident stenosis 
of the orifice. 

The action of every valvular disease affects the blood-current first in th^ way : 
that a stasis of the blood ensues, beginning at the diseased valve and extending 
backward against the current. The flow of blood through the pulmonary veins, 
and also through the veins of the body, is impeded, and the filling of the arte- 
rial system is thus diminished. To avoid repetition, we will describe more par- 
ticularly, in the pathology of the disease of individual valves, the precise circum- 
stances under which this disturbance of the circulation occurs. Every such 
abnormal distribution of the blood, and the necessary slowing of the circulation, 
from the increased tension in the venous system on the one hand, and the dimin- 
ished tension in the aortic system on the other, would soon exert a most per- 
nicious influence on the whole body, if a number of compensatory processes did 
not develop in the heart itself. We shall see how the disturbance of circulation 
in disease of each individual valve can be overcome by the increased work of cer- 
tain definite portions of the heart, and how the heart does in fact respond to 
these increased demands put upon its working strength. It is one of the wisest 
contrivances in our organism, that the heart has control of a reserve fund of 
strength, which comes into action, if need be, in a way to compensate as far as 
possible for any disturbance of the circulation. This explains why a man with 
valvular disease of the heart may be almost perfectly well for a long time, while 
the increased work of certain portions of his heart is able to keep up an approxi- 
mately normal circulation in spite of the existing valvular disease. We call a 
heart disease, in which there is at least no marked disturbance of circulation, a 
compensated heart disease. 

The abnormally increased work, which single portions of the heart must per- 
form in every case of disease in order to keep up the normal circulation, leads to 
hypertrophy of that portion, just as in any other muscle. This hypertrophy does 
not consist of an increase in thickness of the individual muscular fibers, but 
chiefly in an increase in number. The whole diameter of the cardiac muscle 
increases, and thus its capacity for work naturally becomes greater. It goes with- 
out saying that increased nutritive processes and a large supply of nourishment 
for the heart are necessary to bring about such a hypertrophy, by which alone a 
compensation of the heart disease is possible for a long time. Hence we find the 
secondary hypertrophy of the heart absent, or at least only imperfectly developed, 
in weak people, especially in such as have suffered from some other chronic wast- 
ing disease beside the heart disease, like phthisis or carcinoma. 

Although the compensatory processes in the heart can prevent for a long 
time any marked disturbance of the circulation, the already overburdened heart 
can no longer completely satisfy any additional demands upon it, even in a com- 
pensated heart disease. Hence patients with a compensated heart disease are free 
from subjective disturbance from their trouble only when they take complete 
bodily rest, while the signs of a disturbed circulation usually become quite appar- 
ent on a comparatively slight physical exertion. 



264 



DISEASES OF THE CIRCULATOEY ORGANS. 



The hypertrophied cardiac muscle can seldom fulfill permanently the abnor- 
mally great demands made upon its strength. There finally comes a condition of 
"fatigue," of "cardiac insufficiency." The cause lies either in the increase of the 
valvular disease, so that the hindrance to the blood-current caused by it can no 
longer be completely overcome, or in the fact that the nervous and muscular ele- 
ments in the heart have their function gradually impaired by a disturbance of 
circulation in the heart itself. In short, in every heart disease the moment may 
finally come when the capacity of the heart has reached its limit, and hence the 
compensation of the heart disease ceases. The results of stasis now appear with 
increasing severity in the different organs, as we shall learn to recognize them 
later on, and the patient finally succumbs to them, unless some intercurrent event 
puts an end to life sooner. 

After these general remarks, which will be understood better from what fol- 
lows, we will pass on to the special description of the different forms of heart 
disease and their physical signs. 

1. Insufficiency of the Mitral Valve. 

Mitral insufficiency is one of the most frequent forms of heart disease. It 
develops in acute or chronic endocarditis of the mitral valve, from contraction of 
the free edges of the valve or from shortening of the chordae tendinese. In rare 
cases it comes on from partial adhesion of the valves with the walls of the 
ventricle. 

The closure of the mitral valve occurs normally at each systole of the left ven- 
tricle. It prevents the return of blood from the left ventricle to the left auricle. 
If the mitral valve is insufficient and its closure is incomplete, at every systole of 
the left ventricle a part of the blood is accordingly thrown back from it intp the 
left auricle through the open space of the ostium venosum. This abnormal back- 
ward wave encounters the blood-current coming in an opposite direction into the 
left auricle from the pulmonary veins. Since these two opposing currents rebound 
on each other, and since the backward wave of blood presses through the open 
space in the mitral orifice, decided vertiginous movements arise in the blood, 
which are the cause of a loud blowing, systolic murmur in the heart. We hear 
this murmur loudest at the apex of the heart, corresponding to the laws of con- 
duction in the thorax ; yet it usually is propagated so far that it may often be 
heard at the other cardiac orifices, although weaker. A loud systolic mitral mur- 
mur can also be heard sometimes in the back, on the left and occasionally on the 
right. Only in a few cases do we find the murmur louder nearer the base of the 
heart than at the apex, corresponding more to the anatomical position of the mitral 
valve. We often hear the first sound of the heart at the apex beside the murmur, 
but sometimes we do not. The second sound is often not to be heard at the apex, 
probably because it is obscured by the relatively protracted murmur. 

Since the left auricle, at each systole of the ventricle, receives blood from two 
sides — its normal quantity from the pulmonary veins, and beside that the abnor- 
mal blood-wave from the left ventricle — it becomes much dilated. At the next 
diastole of the left ventricle the whole amount of blood collected in the auricle 
under increased pressure pours into the left ventricle through the mitral valve, 
which is now wide open (supposing a pure insufficiency of the valve without any 
stenosis). We see, then, that in pure mitral insufficiency the left ventricle must 
be overfilled during the diastole. The left ventricle must also expel in the follow- 
ing systole an abnormally large amount of blood. As by this contraction only a 
part of the blood reaches the aorta in the direction of the normal blood-current 
and a part pours back into the auricle, the work of the left ventricle proper is 
not made easier. This is the explanation, then, why, in pure mitral insufficiency, 



VALVULAR DISEASE OF THE HEART. 



265 



the left ventricle is dilated as a result of its increased filling in diastole, and is 
kypertrophied as a result of its increased labor. The general arterial tension thus 
remains approximately normal. It is not increased, since a part of the abnormal 
amount of blood, which pours out of the left ventricle at every systole, flows back- 
ward into the auricle. About the normal amount of blood reaches the aorta, and 
hence the radial pulse, in pure mitral insufficiency, remains of about normal 
strength and tension. 

The anomalies in the movements of the blood in mitral insufficiency are still 
further noticeable. We have already seen that the left auricle is dilated from 
its overfilling. It also becomes hypertrophied, as far as its weak muscular 
structure permits, but it is not in itself capable of compensating for the disturb- 
ance which the pulmonary circulation suffers from the mitral insufficiency, for 
the back current from the left ventricle, and the consequent high pressure in the 
left auricle, must plainly offer an abnormal hindrance to the flow of blood from 
the pulmonary veins. This stasis sets back through the pulmonary capillaries 
and arteries into the right ventricle. This may be recognized, on the physical 
examination, by the change in the pulmonic second sound, which is louder, more 
valvular, and "accentuated," since the closure of the semilunar valves in the 
pulmonary artery now takes place under the abnormally high pressure which 
prevails in the arteries of the lungs. The right ventricle has the task of over- 
coming this abnormal stasis in the pulmonary circulation. It can overcome the 
abnormal resistance in the pulmonary circulation by increased work, and as a 
result it becomes hypertrophied. As long as the hypertrophy of the right ven- 
tricle suffices to maintain the normal pulmonary circulation, the stasis extends 
no farther backward, but in the later stages of heart disease we see the right ven- 
tricle becoming paralyzed, and more and more dilated as a result of stasis. The 
flow of venous blood from the body into the right auricle and ventricle is also 
rendered more difficult. The signs of venous stasis become manifest ; the patient 
has a cyanotic hue, congestive oedema appears in the face and the extremities, 
symptoms of passive congestion of the liver, spleen, and kidneys appear, and, in 
short, there is developed the picture of an uncompensated heart disease. 

If we now sum up the physical signs of mitral insufficiency, the different 
methods of investigation give the following results : 

Inspection. — The cardiac region often seems rather prominent, as a result of 
the hypertrophy of the heart. This protrusion is most marked in young people, 
with a yielding thorax. The apex-beat is somewhat displaced toward the left as a 
result of the hypertrophy and dilatation of the left ventricle, and it is quite marked. 
Beside that, we often see and feel a diffuse pulsation in the whole cardiac region. 
In the epigastrium we sometimes see or feel an epigastric pulsation proceeding 
from the hypertrophied right ventricle. In cases which are no longer perfectly 
compensated the stasis in the veins of the body is rendered apparent by the general 
cyanotic appearance of the patient and the marked filling of the jugular veins in 
the neck. Undulatory or pulsating movements often occur in the latter (see tri- 
cuspid insufficiency, below). 

Palpation. — This confirms the abnormal strength of the apex-beat, and its dis- 
placement to the left. We often feel a systolic thrill at the apex of the heart — a 
" cat's purr " — by laying the hand flat on the chest. This whirl of blood, which 
is audible as a murmur, may be perceived as a fine tremor of the chest- wall. 

The radial pulse is quite strong, and usually regular. The sphygmographic 
tracing of it gives nothing characteristic in mitral insufficiency. 

Percussion. — This usually gives at first only a moderate increase of the heart's 
dullness to the left, and a little upward, but in the later stages there is at the same 
time an increase of the heart's dullness to the right, caused by hypertrophy and 



266 DISEASES OF THE CIRCULATORY ORGANS. 



dilatation of the right ventricle. The whole area of cardiac dullness may finally 
extend two fingers' breadth beyond the right edge of the sternum, and to the left 
it may reach the mammillary line, or even pass beyond it. 

Auscultation. — At the apex of the heart we hear a loud, quite long, pure sys- 
tolic blowing murmur, limited to the systole, either replacing the first sound or in 
addition to it. The second sound is often obscure or inaudible at the apex, but 
the pulmonic second sound is increased and accentuated. Auscultation of the 
vessels gives nothing characteristic. 

2. Stenosis of the Mitral Orifice (Mitral Stenosis). 

Mitral stenosis often develops in chronic endocarditis of the mitral valve, as a 
sequel to a previous insufficiency. The valve constantly becomes stiffer and more 
rigid, and the signs of stenosis gradually predominate over those of insufficiency. 
Hence we very often find stenosis and insufficiency of the mitral valve combined, 
but often the signs of stenosis are so much more prominent that we can properly 
speak of a pure mitral stenosis. 

The disturbance which the circulation suffers in mitral stenosis is much greater 
than in mitral insufficiency. In mitral stenosis the orifice may finally become so 
narrow that it scarcely admits an ordinary lead-pencil. The influx of blood into 
the left ventricle is accordingly much impeded. During the diastole of the left 
ventricle the blood must force its way through the stiff and narrow ring of the 
mitral valve. Thus irregular vertiginous movements develop in the blood, which, 
in the majority of cases, give rise to an audible diastolic murmur. In mitral 
stenosis the left ventricle receives a very small amount of blood. Hence, in 
mitral stenosis, the left ventricle is usually small, its cavity contracted, and the 
amount of blood thrown into the arteries with the systole is less than normal. 
In high degrees of mitral stenosis the radial pulse is weak and small, and, beside 
that, we often find it irregular (see Fig. 27). If we find a hypertrophy of the left 




Fig. 27.— Pulse-curve in marked mitral stenosis. 



ventricle in marked mitral stenosis, as sometimes happens, for which there is no 
special cause at hand, it is probably always to be referred to a previous insufii- 
ciency of the mitral valve. 

The hindrance to the flow into the left ventricle in mitral stenosis soon leads 
to a marked stasis, which extends to the right side of the heart through the left 
auricle, and the pulmonary veins, capillaries, and arteries. The left auricle is 
dilated first, and its walls are hypertrophied, but it can overcome only a very small 
part of the resistance at the mitral orifice. The right ventricle can, by more work, 
so increase the pressure in the pulmonary vessels that, in spite of the narrowed 
orifice, an approximately sufficient quantity of blood may pour into the left ven- 
tricle. Hence we find in mitral stenosis a very marked hypertrophy and dilata- 
tion of the right ventricle. The stasis in the pulmonary circulation, manifest 
objectively by the accentuation of the pulmonic second sound, has as a result a 
gradually developing ectasis of the pulmonary capillaries. Thickening of the 
intima of the pulmonary arteries and veins also usually develops. (See the chap- 
ter on brown induration of the lungs.) 

The results of physical examination are as follows : 

Inspection.— The whole cardiac region may seem slightly prominent, as a result 



VALVULAR DISEASE OF THE HEART. 



267 



of the hypertrophy of the heart. The heart's action is usually extended over a 
larger area, but in pure mitral stenosis the apex-beat is no stronger than usual. 
We have often noticed a marked pulsation in the epigastrium, produced by the 
right side of the heart. The jugular veins are often prominent, and show the dif- 
ferent forms of undulatory and pulsating movement. 

Palpation. — This also gives signs corresponding to the more extended action 
of the heart. We sometimes feel the pulsation of the dilated right ventricle even 
to the right of the sternum. In a number of cases we feel a diastolic thrill at the 
apex of the heart, which alone may almost establish the diagnosis of mitral 
stenosis. This thrill arises from the same vertiginous currents in the blood which 
form the basis of the diastolic murmur {vide infra). The radial pulse is small in 
every severe mitral stenosis, and is very often irregular. 

Percussion. — Percussion gives especially an increase of the heart's dullness to 
the right, reaching to the right border of the sternum or beyond it. The dull- 
ness also often extends farther to the left than normal. This may have its 
origin in a co-existing hypertrophy of the left ventricle {vide supra), or it depends 
on a dilatation of the right side of the heart so great that the left ventricle is 
pushed farther to the left and backward by it. 

Auscultation. — The characteristic auscultatory sign of mitral stenosis is the 
diastolic murmur at the apex. This is never so loud and blowing as the systolic 
murmur of insufficiency, but it usually sounds more rolling or rippling. It is 
loudest at the apex, and it is transmitted only slightly toward the base. Since, as 
has been said, the left ventricle in mitral stenosis is sometimes pushed to the left 
and backward by the very much enlarged right ventricle, in looking for the mur- 
mur we must often go far to the left, in order not to auscult the right ventricle 
only. 

The origin of the murmur is easily explained. In the diastole of the left 
ventricle the blood-current must force its way through the narrow mitral orifice, 
whence vertiginous movements arise in the blood, and produce the murmur. 
Since the blood flowing through the narrow orifice has a current of relatively 
slight intensity, the murmur produced by it can not be very loud. Even in the 
highest degrees of mitral stenosis the murmur is often quite low. The murmur 
often comes on in the second half of the diastole — namely, when, by the contrac- 
tion of the left auricle, the blood-current is at last hurried through the narrow 
orifice. We call such a murmur, audible at the end of the diastole only, a presys- 
tolic murmur, since it usually passes immediately into the first sound. 

It is by no means very rare that the murmur is absent in marked mitral 
stenosis. If such cases do not come under observation until the last stages of the 
disease, the mitral stenosis can readily escape recognition. We have ourselves 
often seen the previously distinct diastolic or presystolic murmur in mitral stenosis 
gradually disappear completely with the increase of the heart disease. In these 
cases the intensity of the blood-current through the narrow orifice becomes so 
slight that an audible murmur is no longer produced. The sounds that are heard 
arise probably from the right ventricle. 

The first sound at the apex is retained in pure mitral stenosis, and often it is 
even remarkably loud and valvular, a condition which we usually try to explain 
by the theory that the difference (the "difference in tension") between the 
abnormally slight tension of the valve in diastole, in mitral stenosis, and its 
high tension in systole is relatively great. If insufficiency of the valve co-exists, 
we may hear a systolic murmur with the first sound or instead of it. 

The very marked accentuation of the pulmonic second sound, the result of 
the abnormally high tension in the pulmonary artery, is almost constant. It 
fails only in very anaemic, weak people, or in co-existing insufficiency of the 



268 



DISEASES OF THE CIRCULATOEY OEGANS. 



tricuspid valve {vide infra). The second sound at the base is very often 
" divided " or reduplicated. The closure of the semilunar valves in diastole 
does not happen at the same time in the pulmonary artery and in the aorta, on 
account of the unequal tension in the two vessels, so that consequently the two 
sounds are heard, one shortly after the other. Although this division of the 
second sound is particularly frequent in mitral stenosis, it is by no means a 
pathognomonic sign of it, as must be borne in mind. 

Mitral stenosis is one of the severest forms of heart disease. It almost always 
causes severer subjective symptoms than mitral insufficiency. Hypertrophy of 
the right ventricle can also maintain for a long time an approximately complete 
compensation in stenosis, but the signs of marked stasis in the pulmonary circula- 
tion, and further in the veins of the body, are apt to appear quite early. The 
dyspnoea becomes more marked, and dropsical symptoms gradually arise and 
cause a fatal termination. 

3. Insufficiency of the Semilunar Valves of the Aorta. 

Insufficiency of the aortic valves is most frequently due to contraction of the 
free edges of the valves. Tears, perforations, or adhesions of the valve to the 
wall of the vessel more rarely lead to insufficiency. The cause of all these 
changes is either an endocarditis affecting the valves, or a general atheroma of 
the arteries, which gradually invades the valves from the intima of the aorta. 

The function of the aortic valves is to close tightly at the period of diastole of 
the left ventricle, in order to prevent any return of blood from the aorta into the 
ventricle. If these valves are insufficient — that is, if they do not close perfectly at 
each diastole — there is a return current of blood from the aorta into the left ven- 
tricle. The left ventricle then receives blood during its diastole from two sides : 
the normal flow from the left auricle, and the blood which comes back from the 
aorta. These two currents of blood, directed against each other, meet in the left 
ventricle during its diastole, give rise to a marked vertiginous movement of the 
blood there, and thus cause a characteristic diastolic murmur. 

As a result of the excessive expansion of the left ventricle at every diastole, it 
finally becomes permanently dilated. Dilatation of the left ventricle therefore 
forms a constant anatomical lesion in every aortic insufficiency, and is shown not 
only in the dilatation of the whole ventricular cavity, but also in the very char- 
acteristic flattening of the trabecular and of the papillary muscles. The abnor- 
mally great filling of the ventricle during diastole, moreover, gives rise to increased 
labor ; for the left ventricle must expel an abnormally large amount of blood at 
each systole, which is of course a sort of task of Sisyphus, since a part of the blood 
thrown out constantly rolls back into it. The increased labor must always lead 
at last to a hypertrophy of the left ventricle, which may attain the highest degree 
of any form of valvular disease. 

From the facts enumerated we can easily understand the physical signs of 
insufficiency of the aortic valves. 

Inspection. — Great hypertrophy of the left ventricle often causes a marked 
protrusion of the whole cardiac region. The very strong apex-beat, displaced 
downward and to the left, is especially striking. It may usually be seen in the 
sixth intercostal space, outside the left mammillary line, and sometimes even at 
the anterior axillary line. Beside that, we often see a marked diffuse tremor of 
the whole cardiac region. 

Palpation. — We can appreciate the heart's action to a still greater extent by 
palpation than by inspection. The apex -beat is very resistant, massive, and 
plainly heaving — that is, the finger or stethoscope applied to the apex is lifted by 



VALVULAR DISEASE OF THE HEART. 



269 



the beat at every systole. In rare cases a diastolic thrill, corresponding to the 
diastolic murmur, can be felt over the base of the heart. In two such cases, 
observed by us, the murmur had a marked musical character {vide infra). The 
appearances in the arteries are given below. 

Percussion. — Percussion gives an extension of the cardiac dullness to the left, 
beyond the left mammillary line and even to the anterior axillary line, caused by 
the hypertrophy and dilatation of the left ventricle. The upper boundary of the 
cardiac dullness is normal, or it begins farther up at the third rib. The right 
boundary is in its normal place at the left border of the sternum, but it may also 
be pushed farther to the right, either because the large left ventricle itself causes 
an extension of the whole heart to the right, or because the right ventricle is also 
hypertrophied. The latter change occurs in pure aortic insufficiency when the 
compensation is no longer complete, and the stasis extends backward from the 
left ventricle, through the pulmonary circulation, into the right side of the heart. 

It may also be remarked here that, in insufficiency of the aortic valves, the 
ascending aorta is often considerably dilated by the marked impulse from the 
amount of blood pouring into it. A moderate degree of dullness is found over 
the dilated aorta, which in aortic insufficiency may sometimes be made out at 
the sternal end of the second right intercostal space. 

Auscultation. — Insufficiency of the aortic valves is characterized by a long- 
drawn, loud, blowing diastolic murmur, the origin of which has been explained 
above. The place in which the murmur is heard loudest is not the sternal end 
of the second right intercostal space, the ordinary point for auscultation of the 
aorta, but it almost always lies farther to the left and above it. Corresponding to 
the backward current of blood toward the left ventricle, which begets the mur- 
mur, we hear the latter loudest at the upper part of the sternum or even at its left 
border. In some cases the murmur assumes a marked " musical character " — that 
is, there is' a definite high musical tone, which is due to a tendinous fiber, arising 
from a wearing away of the valve, and set in vibration by the diastole, or to some 
similar cause. The diastolic murmur is often audible at the apex, but it is low 
there. On systole we hear, over the aorta, the first sound normal, or else a short, 
rougher murmur, if the changes in the aortic valves cause at the same time a 
slight stenosis of the orifice. It is very remarkable that, as Traube first pointed 
out, we often hear the first sound at the apex very obscure and dull, or else a short 
systolic murmur instead of it. This obscurity of the first sound at the apex is of 
theoretical interest, because it contradicts the hypothesis that the first mitral 
sound is a muscular sound. It would be especially incomprehensible, on this 
theory, why the first sound is so obscure in insufficiency of the aortic valves, in 
spite of the hypertrophied and toiling left ventricle ; but if we regard the first ven- 
tricular sound as originating in the mitral valve, then, according to Traube, 
its absence in aortic insufficiency may be explained by the fact that the mitral 
valve during the ventricular diastole is thus put in a certain degree of tension by 
the backward current of blood. The greater tension, which now exists during 
the ventricular systole, does not suffice to produce a sound in the valves, since the 
origin of a valvular sound does not depend upon the absolute intensity of the ten- 
sion, but upon the amount of the sudden increase of tension. The systolic mur- 
mur, often heard at the apex in aortic insufficiency, may depend upon a co-exist- 
ing true mitral insufficiency, but it is probably often due to a relative insufficiency 
of the mitral, since the valves, which are normal in themselves, can no longer cause 
a perfect closure of the left mitral orifice as dilatation of the left ventricle comes on. 

Symptoms in the Peripheral Arteries. — Such remarkable symptoms are 
found in the peripheral arteries in aortic insufficiency that they demand a brief 
special description. The first striking symptom is the strong pulsation, not only 



270 



DISEASES OF THE CIRCULATORY ORGANS. 



of the larger, but also of the smaller arteries, even those of which the pulsation is 
not generally visible. We see and feel not only a strong pulsation in the carotids, 
but also a strong pulsation in the tortuous brachial artery, in the radial, ulnar, 
temporal, dorsalis pedis, etc. We sometimes feel an arterial pulse in the liver 
through the abdominal walls. 

The rapid decline of the pulse— the pulsus celer [Corrigan pulse]— is most charac- 
teristic of aortic insufficiency, and is to be felt especially in the radial artery. An 
abnormally large quantity of blood is thrown into the arteries from the hyper- 
trophied and dilated left ventricle ; hence the high ascent of the pulse ; but since 
at the next diastole of the ventricle the blood escapes again in two directions, into 
the capillaries and back into the ventricle, an abnormally rapid and deep decline 
of the pulse follows the high ascent of its wave — a condition which explains the 
" jumping," " springing " pulse (pulsus celer) in aortic insufficiency. The quality 
of the pulse may be plainly recognized also in the sphygmographic tracing (see 
Fig. 28). The abnormal backward wave may even be detected in the capillaries. 
We often see a marked pallor of the finger-nails at every diastole of the heart in 
patients with aortic insufficiency — Quincke's capillary pulse. 

The auscultatory phenomena over the arteries are partly connected with the 
changing conditions of tension of the arterial walls. We very often hear a short, 
rough, systolic murmur in the carotid. The second sound, which is recognized as 



ulnar, the palmar arch, and the dorsalis pedis, a marked valvular sound, which is 
changed by pressure on the artery, especially in the larger arteries, to a loud ste- 
notic murmur. The double sound in the femoral (Traube's double sound) is quite a 
frequent phenomenon, about the origin and significance of which there has been 
much discussion of late years. The double sounds either follow each other shortly, 
so that the first seems something like a preparatory blow for the second, or they are 
separated from each other by a longer interval, like the two sounds of the heart. 
Traube explained the origin of the first sound by the sudden tension of the vessel- 
wall, as in the simple femoral sound, and the second sound by the sudden relaxation 
of it. Friedreich has pointed out in regard to this that, in co-existing tricuspid 
insufficiency, a sound may also be produced in the femoral vein by tension of the 
venous valves. The double sound in the femoral may probably have, as a rule, 
different causes of origin. It is, of course, by far the most frequent in aortic insuffi- 
ciency, but it has also been repeatedly observed in other forms of heart disease, as 
in mitral stenosis. The so-called Duroziez's double murmur in the femoral is more 
rare, and it is noticed almost exclusively in aortic insufficiency. This is when we 
hear, by pressing the stethoscope on the femoral, two murmurs plainly distinct from 
each other, of which the first comes from the passage of the systolic blood- wave, 




Fig. 28.— Pulse -curve in aortic insufficiency. 



the transmitted aortic 
second sound, is ab- 
sent. Instead of it we 
sometimes hear trans- 
mitted the weak aor- 
tic diastolic murmur. 
The sound of the me- 
dium-sized and small- 
er arteries is very char- 
acteristic. By apply- 
ing the stethoscope 
lightly we hear over 
the femoral, over the 
brachial, and often 
over the radial, the 



VALVULAR DISEASE OF THE HEART. 



271 



and the second from the passage of the abnormal backward wave coming from the 
periphery of the vascular system through the artificially contracted vessel. 

Aortic insufficiency is in so far a comparatively favorable form of heart disease 
for the patient, that it may be almost perfectly compensated for years by hyper- 
trophy of the left ventricle. Many patients with moderate aortic insufficiency 
feel quite well, and are even capable of quite hard w T ork. They have not the 
slightly cyanotic hue which almost all patients with mitral disease have, but they 
have a normal or even a pale color. If, however, the signs of disturbed compen- 
sation once arise, the severest sequelae may develop quite rapidly in aortic insuffi- 
ciency. The left side of the heart can no longer satisfy the abnormally great 
demands upon it. Hence the stasis of the blood sets backward through the pul- 
monary circulation and into the veins of the body. The difficulty in breathing 
becomes more marked, dyspnoea appears, and the patient dies with the symptoms 
of general dropsy. We will speak more fully below of certain intercurrent events 
in aortic insufficiency, such as cerebral haemorrhage and pericarditis. 

4. Stenosis of the Aortic Orifice. 

Except for the mild forms of aortic stenosis, which often come on with aortic 
insufficiency, aortic stenosis is a rare disease. It arises from marked thick- 
enings and calcifications, and especially from adhesions of the aortic valves with 
one another. The stenosis may become so considerable that the orifice is finally 
reduced to nothing but a small fissure, through which the left ventricle must force 
the blood at its systole. The vertiginous movements thus arising in the blood 
produce a loud systolic murmur. The left ventricle is compelled to do greater 
work in consequence of the increased resistance of the aortic orifice, and hence 
becomes hypertrophied. Since it demands more time to drive its contents through 
the narrow orifice than it does under normal conditions, we often find in aortic 
stenosis a marked slowing of the pulse, but the pulse, as we can conceive, is also 
small, and the artery feels contracted and hard. 

On physical examination of the heart we find the apex-beat displaced outward, 
corresponding to the hypertrophy of the left ventricle ; but nevertheless it is by 
no means very strong ; it is even sometimes remarkably weak, which condition is 
explained in part by the slower contraction of the ventricle, and in part from the 
absence of the backward impulse (compare the Gutbrod-Scoda theory of the heart- 
beat). 

Percussion gives an extension of the heart's dullness to the left. The right 
ventricle is also dilated and hypertrophied to a moderate degree in the later stages, 
if the stasis extends backward through the pulmonary circulation. 

On auscultation, we hear over the aorta a very loud " sawing," long-drawn, 
systolic murmur, which is usually transmitted to the right, corresponding to the 
course of the aorta, in distinction from the diastolic murmur of aortic insufficiency. 
It is usually to be heard loudest at the sternal end of the second right intercostal 
space, but it is audible to a lesser extent over almost the whole heart. It is usually 
detected as quite loud over the carotids. The aortic second sound is low or not to 
be heard at all. With co-existing insufficiency of the valve it is replaced by a 
diastolic murmur. 

The character of the pulse has already been mentioned. The pulse is small, 
and is sometimes even in contrast with the strength of the apex-beat ; in compen- 
sated cases it is regular and often slow, to a slight, or sometimes to a great degree. 
The sphygmographic tracing (see Fig. 29) gives a low wave, and the compara- 
tively slow rise and fall of the limbs of the curve. 

An aortic stenosis of a mild degree may be quite well borne by the patient for 
a long time. In stenosis of a higher degree we sometimes notice peculiar symp- 



/ 



272 



DISEASES OF THE CIRCULATORY ORGANS. 



toms, which probably must be referred to anaemia of the brain, especially attacks 
of dizziness and faintness. Epileptic attacks have even been observed. In other 
respects the same disturbances of compensation finally appear, as in all other 



Fig. 29. — Pulse-curve in stenosis of the aortic orifice. 

forms of valvular disease. The whole course of the disease is more unfavorable 
than that of aortic insufficiency, but, on the other hand, it is more favorable than 
that of mitral stenosis. 

5. Insufficiency of the Tricuspid Valve. 

Insufficiency of the tricuspid valve is extremely rare as an independent 
disease of the heart, but a secondary insufficiency of the tricuspid is quite fre- 
quent, and is therefore of practical interest, and it accompanies other already- 
existing' valvular diseases in the left side of the heart. This arises either from a 
secondary endocarditis on the tricuspid, in quite an analogous manner with mitral 
insufficiency, or it is a so-called relative tricuspid insufficiency. This name we 
give to that form of insufficiency which develops when the edges of the tricuspid 
valve, normal in themselves, can at last no longer meet one another, from the 
increasing dilatation of the right ventricle. 

The necessary result of tricuspid insufficiency is, that in every systole of the 
right ventricle a backward current passes through the open tricuspid orifice into 
the right auricle, and thence into the veins of the body. The tricuspid insuffi- 
ciency ensuing in other forms of heart disease must, therefore, increase the stasis 
in the veins of the body, and is thus far an unfavorable complication. It has a 
compensatory significance only so far as it affords relief to the pulmonary circu- 
lation. Since a part of the blood passes back from the right ventricle into the 
veins, less blood than usual must reach the pulmonary arteries. The decrease in 
tension thus produced in these arteries makes itself apparent on auscultation, since 
the accentuation of the pulmonic second sound in valvular disease of the mitral 
orifice diminishes when tricuspid insufficiency takes place. 

That tricuspid insufficiency must result in a hypertrophy of the right ven- 
tricle is explained in just the same way as the hypertrophy of the left ventricle 
in mitral insufficiency, from the increased influx of blood into the right ventricle 
during its diastole and at a higher pressure ; but this effect of tricuspid insufficiency 
can only rarely be made out accurately in any individual case, since the right ven- 
tricle is usually already hypertrophied as a result of the disease in the left side of 
the heart. 

The most important symptom from which we can especially diagnosticate tri- 
cuspid insufficiency is the venous pulse. The cause of this is the backward wave 
of blood prodiiced at each systole of the right ventricle. As long as the venous 
valve above the bulbus jugularis is closed, we usually see only a "bulbar pulse," 
but very soon the venous valve also becomes insufficient from the continued 
impulse of the blood, and then a strong, purely venous pulse is visible along the 
whole course of the jugular vein up to the vicinity of the mastoid process. The 
contraction of the right auricle very often causes a decidedly weaker elevation of 
the vein, which just precedes the marked pulsation caused by the ventricular 
systole (anadicrotic venous pulse). On account of the straighter course of the 
right innominate vein, the jugular venous pulse is often stronger on the right side 
than on the left. We must state, however, that the jugular venous pulse is not an 



VALVULAR DISEASE OF THE HEART. 



2T3 



absolutely certain sign of tricuspid insufficiency, since it may arise in hypertrophy 
of the right side of the heart without any insufficiency of the tricuspid, from the 
closure of the valves. 

If there is pulsation in the bulb of the jugular vein and the jugular valve is 
still capable of closing, a low, audible, venous, valvular sound may be produced by 
its closure. A sound may also arise in tricuspid insufficiency, as has been already 
said, by the tension of the valves in the femoral vein. A visible pulsation in the 
larger veins of the extremities is very rare, but in tricuspid insufficiency we quite 
frequently feel a hepatic venous pulse. This may be quite apparent even in many 
cases where the jugular venous pulse is absent, because the veins in the liver are 
without valves. 

Auscultation over the right side of the heart gives a systolic murmur in insuffi- 
ciency of the tricuspid, arising from the regurgitating blood-current. This may 
be heard loudest over the lower part of the sternum, or at the sternal end of the 
right fifth rib. The significance of this murmur in diastole, however, is impaired 
by the fact that it can not always be separated from the systolic mitral murmur 
that often co-exists. 

6. Stenosis of the Tricuspid Orifice. 

Stenosis of the tricuspid orifice is an uncommonly rare disease, and hence it is 
without practical significance. It has usually been observed, up to the present 
time, as a congenital form of heart disease, almost always combined with other 
anomalies of development in the heart. 

The physical signs of tricuspid stenosis can easily be constructed theoretically. 
The first result must be a marked dilatation of the right auricle, and the occur- 
rence of a diastolic or presystolic murmur over the right side of the heart. From 
the rarity and complex character of the cases, however, we have, so far, rarely had 
an opportunity to confirm these theories at the bedside. 

The prognosis of this form of heart disease is very unfavorable, since a long- 
continued compensation by increased labor on the part of the right auricle is 
scarcely conceivable. 

[Seventy cases of tricuspid stenosis have been collected by Bedford Fen wick, 
whose analysis affords good grounds for thinking that the lesion is often acquired. 
In fifty per cent, of the cases there was a clear history of rheumatism, and nearly 
all of the patients were more than twenty years of age at the time of death. 

This lesion is never found alone, but invariably combined with mitral stenosis ; 
all but eight of the cases were in women. Fen wick thinks that the influence of 
sex lies in the less onerous nature of the work of women than of men, the granu- 
lating edges of the valves being kept more in apposition, thus healing with 
adhesion and causing obstructions at the orifice.] 

7. Insufficiency of the Pulmonary Valve. 

Insufficiency of the pulmonary valve is also a very rare form of heart disease. 
It occurs as a congenital anomaly, often combined with other failures of develop- 
ment, or as a disease acquired after birth. The anatomical changes in the valve, 
which lead to insufficiency, are precisely analogous to those which cause insuffi- 
ciency of the aortic valve. 

The physical signs of this form of valvular disease consist chiefly of a marked 
dilatation and hypertrophy of the right ventricle, to be made out by percussion, 
and of a loud diastolic murmur over the pulmonary valve. These signs are 
explained in just the same way as the precisely analogous signs in the left ven- 
tricle in aortic insufficiency. 

In general, pulmonary insufficiency, like aortic insufficiency, seems to be able 
18 



274 



DISEASES OF THE CIECULATOEY ORGANS. 



to be compensated quite well for a long time by hypertrophy of the right ventricle. 
In many cases a co-existing patency of the foramen ovale also seems to be of favor- 
able influence, so far as it thus lessens the stasis in the right auricle and the veins 
of the body, while it renders easier the filling of the left ventricle. 

8. Stenosis of the Pulmonary Orifice (Pulmonary Stenosis). 

While the stenosis of the pulmonary orifice acquired in later life is also so rare 
that it has only a slight practical significance, the congenital pulmonary stenosis 
is of far greater importance. It is, on the whole, the most frequent of the con- 
genital forms of heart disease.* Its origin is to be referred either to an endocar- 
ditis of the pulmonary valves during foetal life, or to anomalies in the development 
of the heart. The stenosis is often situated not merely at the pulmonary orifice 
itself, but farther back in the conus arteriosus, which seems to be narrowed by the 
formation of myocardial cicatrices. The pulmonary artery itself is often also nar- 
rowed as a whole. In the majority of cases we find, in addition, other anomalies of 
development in the heart, especially patency of the foramen ovale, great defects in 
the ventricular septum, and, in about half the cases, patency of the ductus Botalli, etc. 

The symptoms of congenital pulmonary stenosis sometimes appear soon after 
the birth of the child. The first thing that strikes us is the appearance of marked 
cyanosis, which is constant or else comes on with crying, or with movements of 
the body. Many children, however, reach a fair age, five or ten years, but rarely 
more. In some cases the heart disease may be so perfectly compensated that the 
child may be comparatively well for a long time, and severe disturbances may 
appear only after several years. 

As a rule, children with congenital pulmonary stenosis present outwardly a 
very striking picture. The cyanosis is especially noticeable in the face, the lips, 
the nose, and the hands and nails. The parts mentioned feel cool. The eyes are 
often somewhat prominent, as there is a slight cedematous swelling about them. 
The peculiar club-like thickening of the terminal phalanges of the fingers and 
toes, a result of stasis, as in many cases of bronchiectasis, is very characteristic. 
The nails also present a characteristic claw-like curvature. 

The whole development of the child is remarkably backward. The muscular 
development and fatty layer are slight. The gums are sometimes very spongy and 
disposed to bleed. In severe cases the child suffers from faintness, vertigo, etc. 

On physical examination of the heart, we usually find the cardiac region rather 
prominent. Percussion gives an increase of the heart's dullness, especially toward 
the right. This extension of the dullness is due to the hypertrophy of the right 
ventricle, which must arise in the same way as hypertrophy of the left ventricle 
in aortic stenosis. On auscultation, we hear a loud systolic murmur, which is per- 
ceptible over the whole heart, but which has its greatest intensity at the sternal 
end of the second left intercostal space. The eddies of blood, which produce the 
murmur, may also often be felt by the hand as a systolic thrill. In some cases, how- 
ever, we miss the murmur in pulmonary stenosis, just as in mitral stenosis. The 
pulmonic second sound is weak or inaudible, or it is replaced by a murmur if there 
is also insufficiency of the valve. 

The course of congenital pulmonary stenosis is always unfavorable. As has 
been stated above, only a few children get beyond the age of fifteen years. Death 
ensues, either with general disturbances of compensation like dyspnoea and dropsy, 

* We must omit a fuller description of all the other congenital anomalies in the heart, as they have 
far more pathological than clinical interest. We will refer to the text -books on pathological anatomy, 
and especially to the detailed work of Kauchfuss on the subject in Gerhardt's %i Handbuch der Kiuder- 
krankheiten," Bd. iv. 



VALVULAR DISEASE OF THE HEART. 



275 



as in every other form of heart disease, or from complications. Among the latter, 
we may mention especially the very frequent development of phthisis. 

9. Combined Valvular Diseases of the Heart. 

Although in what has preceded we have dealt with the several forms of valvu- 
lar disease of the heart separately, in order to present them in a general way, yet 
in reality combinations of them often occur in the most manifold forms. We find 
especially, as has already been mentioned, stenosis of an orifice co-existing with 
insufficiency of the accompanying valve ; but diseases of two or more different 
valves are not infrequent, combined in the most diverse manners. The physical 
signs of these " combined forms of heart disease " may, of course, be inferred from 
the signs of anomalies of single valves, but the phenomena are often so compli- 
cated that the diagnosis of combined heart disease is generally much harder than 
that of the simple forms. Sometimes the single forms neutralize one another in 
their action. For example, the left ventricle is usually small in pure mitral ste- 
nosis, but, if aortic insufficiency be also present, it is nevertheless found dilated, at 
least to a certain degree. The influence of an absolute or relative tricuspid insuf- 
ficiency on the action of mitral disease, especially the decrease in tension in the 
pulmonary vessels caused by it, and also the diminished accentuation of the pul- 
monic second sound, have been mentioned above. 

In reference to the clinical symptoms of combined heart disease we may say, 
on the whole, that, in a large number of cases, the disease of one valve stands out 
as predominant in the whole picture of the disease. The other anomalies are only 
slightly noticeable, and have often arisen later. Hence, we may find at the 
autopsies of patients, who, during life, have shown the symptoms of disease of 
only one particular valve, unimportant changes, like fresh endocarditis, on the other 
valves, which have been without clinical significance. 

General Comparison of the most Important Physical Signs in Valvular 

Disease of the Heart. 



Form of 
Heart Disease. 



1. Mitral in- 
sufficiency. 

2. Mitral 
stenosis. 



3. Aortic in- 
sufficiency, 



4. Aortic 
stenosis. 



Inspection. 



Strong apex-beat, 
often somewhat 
displaced out- 
ward. 

Area of cardiac im- 
pulse enlarged, 
epigastric pulsa- 
tion. 



Apex - beat very- 
strong, displaced 
downward and to 
the left. Visible 
pulsation of the 
medium - sized 
and smaller ar- 
teries. 



Apex - beat dis- 
placed to the left. 



Palpation. 



Systolic thrill at 
the apex. Quite 
strong radial 
pulse. 

Diastolic thrill at 
the apex. Small 
and often irregu- 
lar pulse. 



Very strong, heav- 
ing apex - beat. 
Pulsus celer. 



Heart's action not 
very strong. 
Pulse small, 
sometimes slow. 



Percussion. 



Hypertrophy of 
the left, later of 
the right ven- 
tricle. 

Hypertrophy of 
the right ven- 
tricle. 



Marked hyper- 
trophy of the 
left ventricle. 



Hypertrophy 
the left ■ 
tricle. 



of 



Auscultation. 



Loud systolic murmur 
at the apex. Pul- 
monic second sound 
accentuated. 

Diastolic or presys- 
tolic murmur at the 
apex. First sound 
sometimes loud 
Pulmonic second 
sound accentuated, 
and sometimes 
double. 

Loud diastolic aortic 
murmur, especially 
overthe upperp'rt of 
the sternum. Sounds 
in the arteries (fe- 
moral and brachial 
sounds, etc.). Some- 
times a double sound 
or double murmur 
in the femoral. 

Loud systolic aortic 
murmur, transmit- 
ted to the right. 



276 



DISEASES OF THE CIRCULATORY ORGANS. 



[Bramwell reports that of 131 cases with macroscopic valvular lesion, the tri- 
cuspid was implicated in 33*58 per cent. ; in all but 12 per cent, of these the 
changes were recent. Hence he thinks that tricuspid endocarditis is generally 
recovered from, and this he attributes to the relatively small strain to which that 
valve is subjected. The obvious therapeutic deduction is the importance of rest 
in mitral endocarditis.] 

General Sequels atcd Complications of Valvular Disease of the Heart. 

After having discussed in what precedes the mechanism of the single forms of 
valvular disease, and the physical signs derived from it, we must now describe a 
number of symptoms and sequelae which may be present to a greater or less 
degree in all forms of valvular disease. With them we must also mention cer- 
tain peculiarities of the individual forms. 

1. Subjective Symptoms. — Fully compensated heart disease may exist, at least 
for a long time, without any subjective symptoms. This is especially the case in 
aortic insufficiency, more rarely in mitral insufficiency. Stenoses of the mitral 
and of the aortic valves almost always cause subjective symptoms. These symp- 
toms often do not exist as long as the patient keeps perfectly quiet physically and 
mentally, but they come on from definite causes. 

The existing subjective symptoms in heart disease are by no means always 
referred, in the first place, to the heart itself. It sometimes happens that the 
patient comes to the physician complaining of various digestive disturbances, or 
in other cases of headache, vertigo, etc. The physical examination alone permits 
us to recognize the heart disease. As a rule, the patient's first and chief complaint 
is directed toward his difficulty in breathing. The shortness of breath, which 
increases on any physical exertion, comes on quite early in many cases. In the 
later stages it is almost always the most distressing symptom. It arises as a result 
of the overfilling of the pulmonary vessels with blood, and the consequent delay 
in the pulmonary circulation, and impairment of the transfer of gases in the 
lung. In the later stages the anatomical changes in the lung tend to increase the 
dyspnoea. The expanded pulmonary capillaries diminish the lumina of the alveoli 
(compare the chapter on brown induration of the lungs). A chronic bronchitis 
often develops as a result of the stasis. A high degree of cardiac hypertrophy 
may also increase the dyspnoea in a purely mechanical fashion by compression of 
the left lower lobe of the lung. The highest degrees of dyspnoea appear if hydro- 
thorax and pulmonary oedema finally develop. From what has been previously 
said, it is to be understood that mitral disease, which directly impairs the pulmo- 
nary circulation, leads to dyspnoea sooner than aortic disease. In heart disease the 
dyspnoea sometimes occurs paroxysm ally (cardiac asthma, stenocardiac attacks), 
a symptom which probably depends upon a suddenly developing weakness of the 
heart, especially of the left ventricle. 

Palpitation is the first subjective symptom to be mentioned which is referred 
directly to the heart. It is not yet accurately determined under what circum- 
stances the action of the heart is perceived by the patient himself. We sometimes 
see an uncommonly strong action of the heart, as in aortic insufficiency, which is 
not perceived at all subjectively by the patient himself. In other cases, where 
objectively the heart is not especially active, palpitation forms the patient's chief 
complaint. It usually first appears when the heart disease is no longer fully 
compensated. It is increased or first excited by physical exertion or mental 
excitement. In many patients attacks of palpitation occur without any discover- 
able external cause, due apparently to nervous disturbance. They are sometimes 
associated with a striking acceleration of the pulse, the so-called tachycardia. 



VALVULAR DISEASE OF THE HEART. 



277 



Pain in the cardiac region is only rarely present in heart disease. The patients 
more frequently complain of an indefinite feeling of pressure and oppression in 
the chest, but attacks of severe pain in the cardiac region do occur, especially in 
patients with aortic insufficiency — pain shooting into the shoulders and arms, the 
exact cause of which is unknown. Pains in the epigastrium and abdomen, which 
sometimes form the chief annoyance of the patient, usually depend upon passive 
congestion of the liver {vide infra), or upon the tension of the abdominal walls 
from ascites, oedema, etc. 

We must finally mention here the rheumatoid pains in the joints and muscles, 
from which many patients with heart disease suffer. 

The greatest subjective distress occurs in the latest stages of heart disease, 
if general dropsy develops. The patient's helplessness usually reaches a high 
degree. All motions of the body are difficult, the dyspnoea and oppression in the 
chest constantly increase, until death finally releases the patient from his mourn- 
ful condition. 

2. Sequelae in the Heart Itself. — We have already discussed the most impor- 
tant sequelae of valvular disease in the heart itself, its hypertrophies and dilata- 
tions. It remains for us to describe the influence of the cardiac disease on the 
frequency and regularity of the heart's action, and also to discuss some secondary 
diseases of the cardiac muscle and of the pericardium. 

In every well-compensated heart disease the heart's action may for a long time 
be of approximately normal frequency and regularity. We often find a constant 
and moderate acceleration of the pulse, which is easily increased from temporary 
causes. Permanent slowing of the pulse is rare in valvular disease of the heart. 
It is most frequent in aortic stenosis, where it is in part of compensatory signifi- 
cance. Marked changes in the frequency of the pulse depend upon severe dis- 
turbances of the nervous apparatus in the heart. Hence they are associated with 
irregular action of the heart as a rule. The frequency of the pulse may then 
reach 120 or 140 a minute. Diminutions of the frequency to 50 or 30 are much 
rarer. We may mention as a rare but interesting symptom the sudden attacks of 
enormous acceleration of the pulse to 200 or more — tachycardia — which seem to 
be especially frequent in mitral disease. In the interval there is usually a quiet 
action of the heart and a complete compensation of the heart disease. The 
increase in the pulse comes on quite suddenly, and is frequently associated with 
subjective feelings of palpitation and distress. It may last for several hours and 
then disappear again, also quite suddenly. The precise cause of these attacks is 
unknown. We may probably regard it as a temporary paralysis of the inhibitory 
apparatus in the heart. 

Arhythmia of the heart is of still greater importance than anomalies of the 
pulse-frequency. It always points to a severe disturbance of the nervous appa- 
ratus of the heart. The general circulatory disturbance which follows every valv- 
ular disease must of course make itself felt in the heart itself, and the nerves and 
ganglia of the heart can not remain undisturbed by it. Hence we generally see 
marked variations in the frequency and rhythm of the heart's action along with 
the other signs of beginning disturbance of compensation ; but daily clinical 
experience teaches us that there is not a perfect parallelism between the two symp- 
toms. We find often enough in heart disease quite a considerable irregularity of 
the pulse without any of the other signs of marked disturbance of compensation, 
and, on the other hand, we see in many patients an almost perfect regularity of 
the pulse up to death. In mitral disease, especially in mitral stenosis, arhythmia 
of the heart is much more frequent than in aortic disease. 

We can not here discuss in detail the different forms and symptoms of cardiac 
irregularity. An inequality in the intensity of the single beats is very often asso- 



278 



DISEASES OF THE CIRCULATORY ORGANS. 



ciated with the irregularity ; the irregular pulse is also an unequal pulse. The 
weaker heart-beats sometimes cause a pulse which is no longer perceptible in the 
radial artery, so that we can determine the true frequency of the heart-beat, not 
by counting the radial pulse, but only by auscultation of the heart. The occur- 
rence of the so-called pulsus bigeminus is of interest (see Fig. 30). A second 
weaker contraction follows the first strong systole, even before the ventricular 

diastole has fully ended, and then comes a longer 
pause. We feel alternately a strong and quite 
weak pulse. The latter may be imperceptible, so 
that it can be made out only by the sphygmograph. 
In such cases, with co-existing tricuspid insuffi- 
ciency, we sometimes find the number of the 
venous pulsations twice as great as the number 
Fig. 30.— Pulsus bigeminus. of the radial pulsations, because the second weaker 

contraction of the heart produces a visible venous 
pulse, but not an appreciable radial pulse. On the whole, the pulsus bigeminus 
is a bad sign, since it always points to a marked disturbance of the cardiac inner- 
vation ; but it may also pass away again and give place to a regular action of the 
heart. 

Chronic valvular disease of the heart is often combined with anatomical 
changes in the cardiac muscle, and sometimes in the pericardium. 

Among the changes in the cardiac muscle, cloudy swelling, and especially fatty 
degeneration of the muscular fibers, are the most frequent. The fatty degenera- 
tion of the muscle occurs either in a diffuse form, or in the form of little yellow- 
ish spots, which are plainly visible on the papillary muscles and trabecular. The 
opinion has often been expressed that fatty degeneration of the muscles is the 
cause of the disturbance of compensation ; that the cardiac muscle performs its 
increased work until fatty degeneration ensues and reduces its strength. This 
theory does not entirely correspond to the facts. We have often seen the great- 
est disturbance of compensation in valvular disease when section of the cardiac 
muscle showed no fatty degeneration, and, on the other hand, we have seen great 
fatty degeneration of the heart, as in pernicious anaemia, when there were no 
signs of cardiac weakness during life. Anatomically, with our present aids to 
research, we can hardly ever decide with certainty whether the cardiac muscle 
was still capable of performing its normal functions or not. The usual state of 
the case is probably this, that fatty degeneration of the cardiac muscle is a result 
of the disturbance of compensation, and especially of the deficient supply of arte- 
rial blood containing oxygen to the muscle (see the chapter on anaamia). 

A further affection of the cardiac muscle in valvular disease is the frequent 
presence of cicatricial changes and so-called myocarditic nodules in the sub- 
stance of the heart. Chronic endocarditis may directly invade the subjacent 
parts of the cardiac muscles and set up a chronic inflammation there, but the 
cardiac cicatrices usually have another origin. The connective-tissue thickening 
beneath the endocardium is the result of a simple atrophy of the superficial mus- 
cular fibers from the increased internal pressure of the blood, as in mitral or 
aortic insufficiency. The connective-tissue nodules within the cardiac muscle, 
however, depend upon a deficiency in the local supply of arterial blood. Simple 
sclerotic thickening of the coronary arteries, or complete embolism, or thrombosis 
of a small branch of one of them, is the evident cause of these circumscribed cica- 
trices. It is certain that the latter may reduce the capacity of the cardiac muscle 
for work, but, on the other hand, we often find cicatrices of myocarditis without 
any signs of a previous disturbance in the compensation of the heart. A fuller 
discussion of this will be found in the next chapter. 




VALVULAR DISEASE OF THE HEART. 



279 



Pericarditis is not very rare as a result of chronic valvular disease. It is 
always a dangerous complication, and may cause death. Regarding its origin, 
we have found that almost all the cases of heart disease complicated with peri- 
carditis show changes in the aortic valves. Hence it does not seem improbable to 
us that the origin of the secondary pericarditis in such cases is due to a direct 
invasion of the pericardium by the excitants of inflammation from the aortic 
valves through the walls of the blood-vessels. 

3. Symptoms of Stasis in the Different Organs of the Body.— As has frequently 
been mentioned in what precedes, the results of stasis of the blood make them- 
selves manifest in heart disease in various organs. We have already spoken of 
the important results of blood stasis in the lungs. It remains for us to discuss 
the symptoms of stasis in the veins of the body. 

As soon as the flow of venous blood into the right side of the heart is no 
longer unhindered, the venous stasis is shown by the cyanotic appearance of the 
patient. This cyanosis may exhibit any degree. In heart disease which is, on 
the whole, still well compensated, it is recognized only by the practiced eye of 
the physician as a slight bluish tinge to the lips, the alse of the nose, the cheeks, 
or the nails. With the increase of the disturbance of compensation the cyano- 
sis increases, if it be not diminished by the co-existence of general anaemia. In 
mitral disease, especially in mitral stenosis, the cyanosis is usually more marked 
than in aortic disease. The large veins also become plainly visible as a result of 
their complete filling, especially the large external jugulars. 

A further important symptom which follows the venous stasis is the oedema, 
the dropsy of heart disease. As we know from general pathology, every venous 
stasis, if it reaches a certain grade, leads to a transudation of the fluid of the blood 
from the capillaries. If the lymphatics can no longer carry this transudation 
away, it collects in the meshes of the tissues and leads to oedema. The oedema of 
heart disease, therefore, does not appear until the venous stasis has reached a certain 
degree, and the compensation of the heart disease has become imperfect. It first 
appears in those parts where there is a particularly loose tissue, as in the eyelids 
and the scrotum, or where mechanical conditions favor its origin. The legs usu- 
ally swell first, especially about the ankles, because here the stasis of the venous 
blood is increased by gravity. At first, slight oedema appears only temporarily 
and by day, and disappears again as the body is in bed at night ; but, as the dis- 
turbance of compensation increases, the oedema also constantly grows worse, espe- 
cially in the dependent parts of the body, until finally it may reach the highest 
degree of dropsy. Beside the oedema of the skin, transudations into the internal 
cavities develop, especially into the abdomen and the pleural cavity. 

The patient's distress is decidedly increased by marked oedema, as has already 
been said. All the motions of the swollen extremities are considerably impaired. 
Hydrothorax and ascites increase the dyspnoea, the former by compression of the 
lungs, the latter by upward pressure on the diaphragm. The passage of urine 
may be rendered very difficult by oedema of the prepuce. Beside that, we must 
mention that the very oedematous skin is quite apt to become the seat of f uruncu- 
lar and erysipelatous inflammations. 

The results of stasis in the internal organs may be best seen in the liver, spleen, 
and kidneys. 

Passive congestion of the liver is manifested by quite a considerable increase 
in the size of the organ. The lower boundary of the liver dullness extends 
several fingers' breadth beyond the edge of the ribs, and the lower border of the 
liver may often be plainly felt. Quite severe pain in the hepatic region some- 
times arises from the tension of the capsule of the liver. In the later stages the 
liver may grow smaller again from the partial atrophy of its cells. 



280 DISEASES OF THE CIKCULATOEY OEGANS. 



A jaundiced coloring of the skin often develops in heart disease, as a result of 
passive congestion of the liver, or perhaps sometimes from a secondary duodenal 
catarrh. The peculiar mixture of a cyanotic and slightly jaundiced hue of the 
skin is very characteristic in many cases, especially in mitral disease. 

Passive congestion of the spleen arises if the stasis of the blood extends to the 
splenic vein. The spleen increases in size and becomes firm and dense. It is 
often hard to make out the congestion from the increase of the splenic dullness, 
because percussion of the spleen is uncertain if there be also ascites, hydrothorax, 
etc. We can often, however, plainly feel the enlarged spleen under the edge of 
the ribs on the left. 

We recognize passive congestion of the kidneys by the changes in the urine. 
The amount diminishes ; the urine becomes darker, more concentrated, of a 
higher specific gravity, and of greater acidity. A sediment of uric acid or of 
sodic urate very commonly forms in it. In marked degrees of stasis there is 
albumen in the urine. The amount of albumen is usually slight, but it may 
amount to one third or one fourth of its volume. Under the microscope we find, 
in the urine of simple passive congestion, only an occasional hyaline cast, and a 
few red and white blood-corpuscles. Genuine acute or chronic nephritis, however, 
may also develop as a complication in heart disease. 

We may refer the numerous gastric and digestive disturbances, like loss of 
appetite, vomiting, constipation, and diarrhoea, from which such patients often 
suffer, to the stasis in the blood-vessels of the stomach and intestines. 

4. Embolic Processes. — The slowing of the circulation, and the disturbances in 
the nutrition of the walls of the vessels, which readily result from it, often give 
rise in heart disease to the formation of thrombi. These are either situated in the 
heart itself, on the diseased valves, in the recesses between the trabecule, in the 
auricles, etc., or they form in the veins, especially in those of the lower extremity. 
From these thrombi fibrinous plugs may easily be set loose, and enter the circu- 
lation, and thus give rise to embolic processes in distant organs. Some of the 
embolisms, whose clinical relations are especially important, have been more fully 
described elsewhere, and will be mentioned only briefly here. 

Embolism of the pulmonary arteries, proceeding from venous thrombi or from 
thrombi in the right side of the heart, gives rise to the development of the hsemor- 
rhagic infarction of the lungs. Its pathogenesis and symptoms have already 
been discussed in a previous section (see page 229). 

Embolism of the cerebral arteries is a common cause of apoplectic attacks, 
which are not infrequent in heart disease, and which usually lead to hemiplegia. 
The anatomical cause of the hemiplegia in these cases is the embolic softening of 
the brain, which develops. The details of this are given in the section on cerebral 
diseases (see page 698). 

Embolism of the larger arteries of the extremities, like the femoral and the 
brachial, is much rarer than the forms mentioned. It leads to embolic gangrene 
of the extremities, unless an adequate collateral circulation can be established. 
The skin of the peripheral parts, the fingers or toes, first becomes cool, bluish, 
and at last, if the circulation be wholly checked, almost black. The gangrene 
advances slowly, usually in the course of weeks. Ulcerations develop as the 
necrotic portions are thrown off. The affection is extremely painful. The patient 
soon becomes very miserable from the pain and the septic fever that usually 
attend the ulcerations, and extensive gangrene almost always ends fatally. 

Embolism of the renal artery, and the formation of an ensuing hemorrhagic 
infarction, may run its course clinically without symptoms, but sometimes it 
may be recognized by the sudden appearance of blood in the urine. 

Embolic infarctions of the spleen are often marked by swelling of the 



VALVULAR, DISEASE OF THE HEART. 



281 



spleen and by severe perisplenitic pains. In other cases it is wholly without 
symptoms. 

Embolism of a mesenteric artery is a very rare event. Its symptoms consist 
of a sudden intestinal haemorrhage, of severe colicky pains, general collapse, and 
symptoms of peritonitis. 

5. Complications on the part of the Nervous System— The most important 
complication on the part of the nervous system — embolic softening of the brain — 
has already been mentioned. We must also state that cerebral haemorrhage may 
occur in heart disease. It is especially frequent in aortic insufficiency, either 
as a result of co-existing atheroma of the cerebral arteries, or perhaps it is partly 
due to the abnormally high tension of the walls of the vessels during systole. 

Mental disturbances have been repeatedly observed in chronic valvular disease. 
They are the result of the disturbance of the circulation, and the consequent im- 
pairment of nutrition in the brain. Hence they usually make their first appear- 
ance in the last stages of heart disease, at the same time with the other disturbances 
of compensation. The psychoses in heart disease most frequently have the char- 
acter of melancholia, but conditions of excitement also occur. 

6. Secondary affections of the joints are not rare in heart disease. As acute 
endocarditis develops in the course of acute articular rheumatism, so, on the other 
hand, rheumatic pains in the muscles and joints, and even acute swelling of the 
joints, associated with fever, appear in the course of chronic heart disease. Both 
affections — that of the heart and that of the joints — arise from the same specific 
cause of disease, and hence they may occur in varying succession. 

7. General Symptoms — Fever. — In congenital heart disease, as we have said, 
the child's general nutrition is very backward. In heart disease in adults, how- 
ever, we by no means always see an injurious influence on the general condition 
of nutrition. In many patients we even see a remarkably good development of 
fat. A marked general disturbance of nutrition, such as great anaemia and gen- 
eral emaciation, often develops in the later stages, especially in aortic insuffi- 
ciency. The latter is of course often hidden by the oedema. 

In general, chronic heart disease runs its course without fever, but periods often 
occur in the course of the disease when there is a moderate and usually irregular 
fever. Marked disturbances of the general condition may or may not be associated 
with it. The basis of the fever is probably due to an acute exacerbation of the 
endocarditis, except, of course, in accidental complications. All variations occur, 
from a mild febrile movement without further symptoms to a severe acute recur- 
ring endocarditis (q. v.). In other cases the fever is connected with secondary 
swelling of the joints, or with embolic processes. 

General Course and Prognosis of Valvular Disease of the Heart. 

The course of valvular disease of the heart is in most cases very chronic, and 
may last for years. As long as there is a complete compensation, the patient 'feels 
almost perfectly well ; sometimes he even has no misgivings as to his trouble. 
The slight difficulty in respiration and the incapacity for physical exertion are 
noticed, but little attention is paid to them, because the patient is used to them. 
In other cases there is a moderate disturbance for a long time, but it may be borne 
quite easily if the patient is rational and prudent in his conduct. 

We can not make any general statement as to the length of the stage of com- 
pensation, because cases differ very greatly in this respect. It depends in part 
upon the intensity of the heart disease, in part upon the external conditions 
under which the patient lives, and in part, certainly, upon the different indi- 
vidual capacity for work and power of resistance in the heart. Thus it happens 



282 DISEASES OF THE CIRCULATORY ORGANS. 



that many cases last for decades, while in others severe sequelae appear within a 
few months. Extei'nal injurious agencies, acting on the patient, are of great 
influence on the course of heart disease. Severe physical exertion, injudicious 
manner of living, intercurrent febrile diseases, mental disturbances, care, and 
anxiety are often accompanied by noticeable injurious results. 

If the first signs of disturbed compensation appear, if severe dyspnoea, slight 
oedema of the ankles, etc. , develop for the first time, these symptoms may disap- 
pear again completely under proper treatment. Severe disturbances of compen- 
sation even, great general dropsy, associated with very weak and irregular action 
of the heart, may disappear, after a few weeks' duration, and the patient may 
feel quite well again. Exacerbations of the disease may come on several times 
and as often improve. Finally, of course, the improvement is incomplete. Per- 
sistent oedema and the other results of venous stasis ensue, the symptoms con- 
stantly increase in severity, especially the dyspnoea, until the patient dies after a 
long and distressing illness. Sometimes in heart disease Cheyne-Stokes's respira- 
tion occurs in the last stages before death. 

In regard to the single forms of valvular disease, aortic insufficiency generally 
gives the best prognosis, inasmuch as it may be very perfectly compensated for 
many years, but, if severe disturbance of compensation once occurs in this form of 
heart disease, it gives a very unfavorable prognosis, since, as a rule, we can not 
make it disappear again. Mitral insufficiency is also quite a favorable form of 
heart disease, which may be compensated for a long time. Mitral stenosis is 
decidedly more unfavorable in its prognosis, and is associated with more disturb- 
ance ; but in all mitral diseases very severe conditions may improve once or even 
repeatedly. Aortic stenosis is also capable of quite good compensation, and in this 
respect it is even more favorable for the patient than mitral stenosis, but it often 
causes persistent cerebral symptoms, depending on anaemia of the brain, such as 
headache and vertigo. 

Whether established valvular disease of the heart is curable is a question which 
can not be answered unconditionally in the negative. Of course in the great 
majority of cases it is in itself incurable ; its sequelae only can be prevented or 
removed to a certain degree. In children and young people, however, cases some- 
times do occur, as we ourselves have seen, in which there are all the signs of a 
pronounced heart disease, but after a long time they disappear again completely. 
Of course it is very hard to decide whether we really have to do with a valvular 
disease that has been cured, because simple dilatation of the heart, relative insuf- 
ficiency of the valves, anaemic cardiac murmurs, etc., may easily give rise to con- 
fusion with pure valvular disease of the heart. 

Among the dangerous intercurrent accidents in valvular disease we must make 
especial mention of embolic processes, which may occur suddenly and without 
warning. The different forms of embolism have been mentioned above, and also 
the occurrence of cerebral haemorrhage in heart disease. Intercurrent acute dis- 
eases, like typhoid and pneumonia, often take a very severe and dangerous course 
in patients with heart disease, because they make increased demands upon the 
heart's capacity for work. 

Treatment gf Valvular Heart Disease. 

1. Prophylaxis. — Our remedies to prevent the development of heart disease 
are very limited. To prevent the development of endocarditis in articular rheu- 
matism is in no way possible by the present method of treating acute rheumatism 
with salicylic acid. The probability of the onset of endocarditis may be lessened 
only so far as the whole duration of the disease is often considerably shortened by 
salicylic acid. 



VALVULAE DISEASE OF THE HEART. 



283 



We can also do little in the way of prophylaxis against the development of heart 
disease that is chronic from the start, since the cause of the disease is in many 
cases wholly unknown to us. Those injurious influences deserve the most atten- 
tion which may favor the development of arterial atheroma and its consequent 
chronic valvular disease. Undue indulgence in alcohol, too much smoking, and 
injudicious and luxurious ways of living, are especially to be looked after in this 
regard. The part which these factors play, however, in the development of a pure 
valvular disease, is certainly much less than their influence upon the develop- 
ment of certain functional and nervous disturbances of the heart (see a later 
chapter). 

[There is evidence that the alkaline treatment of acute rheumatism lessens the 
danger of cardiac cominications (see page 856).] 

2. Treatment of Compensated Heart Disease. — If we have to treat a heart 
disease that already exists, but which is at the same time fully compensated, our 
treatment must be chiefly hygienic. The patient must be made aware of his heart 
disease without making him needlessly anxious. He must be told that his further 
good health depends in great part upon his own conduct, his discretion, and his 
perseverance. The patient must avoid everything which makes great demands 
upon the heart, or which may have a directly injurious influence on it. All 
violent bodily exertion, too intense mental work, and also all excesses in eating, 
drinking, smoking, etc., must be avoided. That the physician's directions will 
often thus collide with the demands of the patient's occupation, as well as with 
his favorite amusements and his habits, should not deter the physician from 
demanding the accomplishment of his prescriptions, at least as far as possible. 

We may often send patients with well-compensated heart disease, or with 
only slight disturbances of compensation, to the country or to a bath with advan- 
tage. The choice of a place is directed by individual indications. We may send 
corpulent patients to Marienbad, Kissingen, or Homburg, and weaker patients to 
an iron bath or to a climatic health-resort. It is often advisable for patients who 
have a tendency to bronchial catarrh or to rheumatic affections to pass the winter 
in the South. We may mention Nauheim as a bath which has obtained a special 
reputation of late in heart disease. 

Treatment by drugs is usually unnecessary in compensated heart disease. We 
do not know a remedy which has a directly favorable action on heart disease. 
The protracted use of iodide of potassium, Fowler's solution, arsenite of antimony 
("granules of antimony"), nitrate of silver, etc., has been recommended. The 
efficacy of these remedies is not proven. We can always try them if a mild dis- 
turbance makes a prescription desirable and other remedies are not especially 
indicated. Preparations of iron, like tinctura ferri acetatis,* or a solution of the 
pyrophosphate, may sometimes be prescribed judiciously in compensated valvular 
disease. 

3. Treatment of Disturbances of Compensation. — As soon as the compensa- 
tory activity of the heart begins to be impaired in valvular disease, and as soon 
as severe dyspnoea and oedema ensue, we must, in the first place, almost always 
seek a remedy which can certainly have a favorable influence upon the action of 
the heart. This remedy is digitalis. Digitalis, in small doses, has the property 
of reducing the frequency of the pulse, and also of strengthening the individual 
heart-beats, and thus increasing the blood-pressure. Digitalis is indicated in every 
case of heart disease if disturbances of compensation appear, and if the pulse also 
is abnormally small, of abnormally low tension, of increased frequency, and 
irregular. The desired action of digitalis, then, is to make the pulse slower, 



The Germans have no good tincture of the chloride of iron. — Trans. 



284 DISEASES OF THE CIRCULATORY ORGANS. 



more regular, and of higher tension. Under the influence of an increase of the 
arterial pressure so produced, the disturbances of compensation disappear in a 
way that is often surprising ; the urine especially becomes more abundant, the 
scanty, dark, concentrated urine of passive congestion disappears, the amount 
excreted daily increases, and the urine therefore becomes clear and of a low spe- 
cific gravity. The oedema also disappears, the dyspnoea ceases, the head is clear, 
the general condition is better — in short, a complete compensation of the heart 
disease may be re-established. This change is sometimes accomplished in a com- 
paratively short time — in a few days or weeks. 

The dose in which digitalis is to be prescribed can not be given quite accu- 
rately, because the amount of the active principle which the plant contains does 
not seem to be quite alike in different places. This is the explanation of the 
somewhat different theories as to the amount of the dose to be employed. In gen- 
eral, we should begin with small doses. We usually prescribe an infusion of the 
leaves of a strength of 1 or 1*5 parts of digitalis to 150 parts of distilled water — a 
teaspoonful every one or two hours. The addition of syrup causes the medicine to 
decompose more easily, and is quite useless. The favorite addition of diuretics, 
liquor potassii acetatis, 30 parts, or boro-tartrate of potassium and sodium, four 
to eight parts added to the infusion, diminishes the strength of the remedy. It is 
advisable to give digitalis in powder, because we can thus define the dose more 
accurately. We prescribe powders of one or two grains of digitalis leaves (grm. 
0 •05-0*1) with seven or eight grains of sugar (grm. 0*4), and give that amount 
every two or three hours. It is often a good plan to inclose the powder in cap- 
sules. The other preparations of digitalis, the vinegar and the tincture, are less 
active. We usually prescribe the latter when a patient with a moderately per- 
sistent disturbance of compensation is to use digitalis in small doses for a long 
time. We have not yet succeeded in isolating the active principle of digitalis in 
a durable form. The " chgitaline " preparations, brought into the market up to 
the present time, are uncertain in their action, and hence are properly but little 
prescribed. 

Digitalis is a remedy which is not free from danger, because there is a stage in 
its action, which readily appears, when it is injurious. The pulse then sinks below 
the normal, becomes weaker and also irregular and intermittent, if it was previously 
regular. The patient's general condition becomes bad, nausea and vomiting set 
in, and a state resembling collapse may arise. Therefore this is the first rule, never 
to prescribe digitalis in large doses unless the patient can be observed constantly 
and carefully. As soon as the first signs of the unfavorable action of digitalis 
occur, the remedy must be at once omitted. Then we give some strong wine, 
or strong cafe noir, to prevent the patient's further collapse. Since digitalis 
is one of the remedies which have a so-called cumulative action, the occurrence 
of symptoms of poisoning may be quite rapid and unexpected. We do well, 
therefore, if the desired favorable action follows the exhibition of digitalis, if the 
pulse has become quieter and more regular, and diuresis has been established, to 
omit the digitalis. We usually let the patient take the remedy for four or five 
days and then omit it. The action of the digitalis thus continues for several days 
afterward. After leaving off the digitalis we usually prescribe a diuretic, like 
acetate of potassium, squills, boro-tartrate of potassium and sodium, or diuretic 
herbs. If the pulse again becomes rapid and irregular, we at once resume the 
digitalis. In such cases, where the patient has used digitalis repeatedly, we must 
gradually increase the dose. The patient gets accustomed to the remedy, as hap- 
pens with so many other drugs. There is no maximum dose, and in individual 
cases we must find out the requisite amount by trial. Many patients finally 
become genuine " digitalis eaters," and can not exist without large doses — severity- 



VALVULAK DISEASE OF THE HEART. 



285 



five grains (grm. 5) or more of the powder a day. In very many cases, unfortu- 
nately, the favorable action of the digitalis finally ceases entirely with large doses. 
The remedy is then no longer " borne," and we must omit it entirely. By that 
time the last stage of the disease has also usually occurred. 

If we have to treat a patient with symptoms of stasis, in whom the pulse seems 
neither especially small nor frequent, nor irregular, digitalis is not indicated, or 
at least it must be used very cautiously and in small doses. The question is often 
hard to decide whether to give a patient with aortic insufficiency digitalis or not. 
In this form of heart disease there is often a very strong, regular, and of course 
abnormally frequent pulse, in spite of the most pronounced disturbance of com- 
pensation. With this we must not forget that, in spite of the high pulse, the 
pressure in the medium-sized arteries is low, and hence in most patients with 
aortic insufficiency we can very well at first make a trial with digitalis, which is 
often crowned with success ; but we must begin with cautious doses and test the 
action of the remedy in every instance. 

In many cases, but fortunately not often, the digitalis is not borne from the 
start, because it excites severe nausea and vomiting. In general the incidental 
action of digitalis on the stomach is one of its troublesome properties. If the 
digitalis is not borne in one form, we try to see if it be not better borne in another. 
We give the powder instead of the infusion, or vice versa, or we try another 
preparation, like the tincture. In such cases we sometimes succeed in getting a 
sufficient action from digitalis if we give it as an enema, using a one-per-cent. 
infusion. 

Caffeine deserves the first mention among the substances having a similar 
action, which have of late been recommended as substitutes for digitalis by Lepine, 
Riegel, and others. Given in repeated small doses, a total of fifteen to twenty 
grains a day (grm. 1*0 to l - 5), it often slows, regulates, and strengthens the activ- 
ity of the heart, and also increases the arterial pressure. The salicylate of caffeine 
and sodium are chiefly used, three to five grains (grm. 0*2 to 0"3) of the powder, 
and also the benzo-citrate of caffeine in the same or smaller doses. It is also given 
subcutaneously. Beside caffeine, we may also mention here adonis vernalis and 
convallaria majalis ; but both substances are very uncertain in their action, so 
that at best we should try them when digitalis and caffeine are not borne or have 
no effect. 

[Digitalis is used more commonly in this country in the form of the tincture. 
The urine affords a good guide as to the safety of the continuance of the drug ; as 
long as the renal secretion is free in quantity, and increasing rather than dimin- 
ishing, there is no danger of the toxic effects. It is, consequently, a good plan to 
follow carefully the twenty-four-hour quantity of urine when this can be done. 

There are cases in which digitalis must be taken for long periods, but it should 
then be given only twice a day, with twelve hours' interval between the doses, 
unless the patient has ready access to his physician. There is then less risk of 
toxic symptoms. To the list of drugs the action of which is similar to those of 
digitalis and for which they may be substituted, if it disagrees or is without effect, 
may be added helleborein and spartein sulphate (gr. j-ij). Fraser reports well of 
strophanthein ; but a more extended use is desirable. 

In mitral cases, with or without secondary tricuspid regurgitation, where the 
cyanosis and other symptoms show that the right heart is engorged with blood 
which it can not propel onward, the relief afforded by venesection, or by a dozen 
leeches in the hepatic region, may be very great. Until the veins are relieved 
either in this way or by free purgation, digitalis and stimulants are useless, and 
a resort to them results merely in a loss of time, and perhaps in a loss of life 
which might be saved.] 



286 



DISEASES OF THE CIRCULATORY ORGANS. 



4. Symptomatic Treatment. — Some symptoms which often occur in heart dis- 
ease demand a special description. 

Dropsy is a symptom of venous stasis, and disappears if compensation be 
restored, spontaneously or by the use of digitalis. Complete rest in bed and eleva- 
tion of the swollen parts serve as the chief aid in removing the dropsy. Dropsical 
patients ought also to change their position in bed frequently, if possible, that 
there may not be too much oedema collected in the dependent portions of the 
body. It is a good plan to wrap up the swollen arms and legs with flannel band- 
ages under gentle pressure. Mild massage of the cedematous parts may sometimes 
be of advantage. Of internal remedies we may consider, beside digitalis, the dif- 
ferent diuretics, especially if digitalis be not indicated or be not well borne. 

In the last stages of heart disease the patient's condition may be particularly 
distressing from the severe general oedema. It is then justifiable to remove the 
ascites or hydrothorax by puncture and to let the oedema drain out by scarifica- 
tion of the skin — little pricks with the point of a knife — in order to procure relief 
for the patient. The scarification of the skin, however, is dangerous and is not to 
be employed without urgent indications, because erysipelatous inflammations, etc., 
may very easily ensue at the point of incision. We can recommend little silver 
capillary trocars (the so-called Southey's trocars), to which a thin rubber tube is 
attached. By the aid of these trocars we can drain off large amounts of serum. 
We must always use great cleanliness, however, and the utmost disinfection of the 
skin, by carbolized jute or salicylated cotton. In patients with heart disease it is not, 
as a rule, advisable to attack the dropsy by sweating, by hot packs, or pilocarpine. 

The dyspnoea of heart disease is usually the most distressing symptom which 
demands relief. Here, too, our chief task is of course to regulate the compensation ; 
but if this no longer succeeds, we must try to relieve the dyspnoea symptomatic- 
ally. Morphine is the most efficient in this respect. In general, morphine is, next 
to digitalis, the most indispensable remedy in the treatment of severe heart disease. 
It is usually well borne and procures great relief, especially if given subcutane- 
ously. If we have to do with the last stage of the disease, we need not spare large 
doses. Otherwise, of course, caution is necessary. In practice we must often pre- 
scribe external applications to the chest, mustard-plasters, hot poultices, and also 
hot foot-baths with mustard, ashes, etc. In severe cases their action is slight. 
Acetate of lead in large doses sometimes seems to have a favorable influence in 
severe dyspnoea, especially with threatening pulmonary oedema. We give the 
powder, up to a grain and a half (grm. 0"1), every two or three hours, and it is 
often a good plan to add half a grain or a grain (grm. 0*03 to 0*05) of opium. 
We can also frequently obtain distinct relief for the patient by a vigorous drastic 
purge, with compound infusion of senna or gamboge. Inhalations of nitrite of 
amyl have rarely a favorable action. 

Palpitation, constant or paroxysmal, is met by applying ice to the cardiac 
region ; sometimes the " heart-flasks,'' made of tin, act very well. In patients 
with aortic insufficiency, and very excited action of the heart, we may recommend 
the protracted use of ice. The narcotics are the most efficient internal remedies, 
especially morphine, which of course we should use only in severe cases. If the 
palpitation is of a lesser degree, we may try bromide of potassium, or cherry-laurel 
water, eventually with equal parts of tincture of digitalis, twenty to thirty drops 
two or three times a day. 

The subcutaneous use of morphine is again by far the most potent remedy in 
the stenocardiac attacks, associated with pain and a feeling of distress. We may 
also use cutaneous irritation, mustard-plasters, etc., and ice. 

We may prescribe bitter remedies— tinctura amara (P. G.), or compound tinct- 
ure of cinchona— and muriatic acid, for the loss of appetite, in case this is not 



MYOCARDITIS. 



287 



improved by regulating the activity of the heart. Beside that, we must always 
take care to get a regular evacuation of the bowels, if possible. 

For the attacks of faintness and vertigo, occurring especially in aortic stenosis, 
as a result of cerebral anaemia, we may prescribe a horizontal position, and stimu- 
lants, wine, ether, and Hoffmann's anodyne. If the cerebral symptoms depend 
upon venous stasis, we try to remove it by ice, mustard-plasters to the neck, and 
thorough derivation to the intestines. 

Especial accidents and complications, like pulmonary cedema, infarctions, or 
apoplexy, are to be treated according to the usual rules. 



CHAPTER HI. 
MYOCARDITIS. 

{Indurated Degeneration, Myodegeneration of the Heart. Infarction of the Heart. Sclerosis of the 

Coronary Arteries.) 

JEtiology and Pathological Anatomy— We have of late learned to know inti- 
mately a number of affections of the heart in which all the results of disturb- 
ance of the circulation may finally appear, without any evidence of anatomical 
disease of the values, either during the patient's life or at the autopsy. We have 
to do here with a lesion of the cardiac muscle itself, or of its nervous apparatus, 
which can reduce the functional capacity of the heart for work, and thus excite 
precisely the same disturbances of the circulation as are produced in valvular dis- 
ease of the heart by purely mechanical conditions. 

In a number of cases — but by no means in all, as we shall see in the next chap- 
ter — we succeed in detecting striking anatomical changes in the cardiac muscle. 
The heart is on the whole enlarged, chiefly dilated, though its walls are usually 
hypertrophied (vide infra). In pure, uncomplicated cases the valves prove entirely 
normal. If, however, we examine the cardiac muscle closely, we find it studded 
with whitish, lustrous, indurated spots, often very abundant and arranged irregu- 
larly. They consist microscopically of cicatricial connective tissue, while the 
muscular fibers have wholly or in large part been destroyed. The seat of this 
induration is chiefly in the left ventricle, especially at the apex and in its anterior 
wall, but we may also find indurations in other portions of the heart. We often 
see them appearing through the endocardial or pericardial surface of the heart 
as dull, slightly sunken places. The papillary muscles may also undergo marked 
cicatricial degeneration. 

The changes in the heart just depicted were formerly considered to be of an 
inflammatory nature, and hence were given the name of myocarditis ; but their 
development is connected, in the great majority of cases, as Weigert, Ziegler, 
Huber, and others have shown, with changes in the coronary arteries and their 
branches. In most of the uncomplicated cases of so-called myocarditis we find 
marked atheromatous changes in the coronary arteries, usually coincident with a 
more or less extensive, general arterio-sclerosis (vide infra). These changes may 
lead in circumscribed places to a complete closure of a branch of the coronary 
artery by thrombosis, and thus give rise to the formation of a true infarction of 
the heart by cutting off the further blood-supply. These infarctions show, in 
fresh cases, a decided brownish -yellow, haemorrhagic color. The finer histological 
changes consist in a loss of their nuclei by the muscular fibers, and their degenera- 
tion into a crumbling, cheesy detritus. By the new formation of connective tissue 



288 



DISEASES OF THE CIECULATOEY OKGANS. 



the peculiar cardiac indurations finally arise, which are therefore to be regarded 
as true infarction cicatrices. 

In many cases of indurated degeneration we can not discover any complete 
closure of the branches of the coronary artery by thrombosis. Here we have to 
do only with changes in the caliber of the vessel by the arteriosclerotic process, 
and a consequent diminution of the arterial blood-supply to the cardiac muscle. 
In all places where this diminution of the blood-supply reaches a high degree, we 
also find a gradual deterioration of the muscular fibers, and their replacement by 
connective tissue. Where the arterial blood-supply is adequate, either directly or 
from the collateral circulation, the muscles remain intact. This is the reason why 
we often find sclerosis of the coronary arteries unaccompanied by indurated 
myocarditis. 

Beside the cases of uncomplicated myocarditis just described, we often see the 
same cicatricial changes in the cardiac muscle combined with valvular affections. 
The cardiac indurations, then, are either due to a co-existing sclerosis of the coro- 
nary arteries, or they stand in a closer relation to the endocardial process. The 
endocarditis may invade the cardiac muscle immediately. This method of origin 
of the myocarditis may be easily recognized by the localization and extent of the 
diseased parts. In other cases the endocarditis may give rise to embolic processes 
in the cardiac muscle. Thus the embolic infarctions of the heart arise in just the 
same way as do the thrombotic infarctions above described. 

It remains for us to describe a number of sequelae and combinations of indu- 
rated myocarditis. As a result of the extensive cicatricial formation, it may hap- 
pen that a circumscribed portion of the wall of the heart, usually of the left ven- 
tricle, becomes thin and yields to the blood-pressure acting upon it from within. 
Thus arises a partial protrusion of the wall of the heart, a so-called cardiac aneu- 
rism. Such an aneurism, and also an extensive, fresh infarction in the heart, may 
in very rare cases lead to a rupture of the heart, with effusion of blood into the 
pericardium, and sudden death. The fact is more important clinically, because it 
is much commoner, that, in places where the cardiac cicatrices reach the endocar- 
dium, parietal thromboses may form in the heart, and may give rise to embolic 
processes in distant organs. 

Dilatation of single portions of the heart, especially of the ventricles, depends 
upon an increased general yielding of the walls of the heart. If at the same time 
there is a hypertrophy of the cardiac muscle, we must look for special causes for 
it. Hypertrophy of the left ventricle usually depends upon co-existing general 
arterio-sclerosis, upon co-existing contracted kidneys, and the like. Hypertrophy 
of the right ventricle may have its origin in co-existing chronic pulmonary affec- 
tions, like emphysema. In some cases the hypertrophy of the right ventricle is 
due to the inadequate action of the left ventricle. If the left ventricle begins to 
grow weak, the stasis backward from it must extend through the pulmonary ves- 
sels into the right side of the heart. In consequence of the increased demands 
upon the right ventricle this becomes hypertrophied. In cases of indurated 
myocarditis combined with valvular disease, the hypertrophy of single portions 
of the heart depends of course in part upon the valvular disease. 

Regarding the special serological factors, which lead to sclerosis of the coro- 
nary arteries, and thus to indurated myocarditis, they are in many cases as much 
unknown as the causes of arterio-sclerosis in general (vide infra). Chronic alco- 
holism and luxurious habits of life are very often the predisposing causes which 
are to be put in the first rank ; but often, too, they are not. Perhaps constitu- 
tional syphilis plays a not unimportant part, since it may lead to like changes in 
the coronary arteries, as it has long been known to do in the cerebral vessels. 
Constant mental excitement is also regarded as a causal factor ; but this must be 



MYOCAEDITIS. 



289 



regarded as mueli more a cause of the conditions to be described in a following 
chapter. Heredity, however, is of greater influence, as it seems to play a certain 
part in the development of arterio-sclerosis. Finally, we must remember that the 
atheromatous process occurs much more frequently in advanced life than in young 
people ; hence indurated myocarditis is a disease chiefly to be observed in old peo- 
ple. Men are more frequently attacked by it than women. 

Although we have so far spoken exclusively of chronic indurated degeneration 
of the cardiac muscle, which, as we have said, is not of a peculiarly inflammatory 
nature, we must also add that there are true purulent inflammations in the car- 
diac muscle. These are part of the symptoms of a general, infectious, and espe- 
cially a pyaemic process, or of malignant acute endocarditis, so that we may refer 
to the description of these diseases in regard to abscess of the heart. 

Clinical History. — We must first mention that sometimes quite extensive cica- 
tricial formation may be found in the cardiac muscle in the cadaver, without the 
occurrence of any manifest symptoms referable to the heart daring life. We see, 
then, that the heart may, under some circumstances, undergo quite a considerable 
loss in its contractile substance without injury. 

In many cases, however, the heart's capacity for work suffers so much that 
the same symptoms arise as in valvular disease. The course of such cases may be 
very chronic. The symptoms begin quite gradually. The patient first has a 
slight dyspnoea or palpitation, and a feeling of distress in the chest, but only from 
external causes, like slight physical exertion. He sometimes suffers from a strik- 
ing general weakness. He gets tired easily, and feels heavy, and in part incapa- 
ble of any mental activity. The symptoms gradually increase, and just the same 
results of disturbance of the circulation appear as in all the other forms of heart 
disease. The difficulty in breathing becomes more marked, oedema occurs, signs 
of stasis in the liver, intestines, and kidneys appear — in short, the well-known 
type of every uncompensated heart disease develops. 

Physical examination of the heart shows marked anomalies of the heart's 
action in all severe cases. The pulse is often irregular in regard to its rhythm 
and the intensity of its single beats, but the arhythmia may also be wholly absent 
in spite of the degeneration of the myocardium, as we have often convinced our- 
selves. The pulse is at first quite strong and full, later it becomes weaker, of 
lower tension, and at last sometimes very small and scarcely perceptible. It is 
often increased in frequency, but we quite often notice in chronic myocarditis, 
especially in the early stages, a persistent slowing of the pulse to 60, 50, or even 
less, in a minute. With this slowness of the pulse there is also frequently irregu- 
larity of the heart's action, especially the appearance of occasional double beats 
(bigeminus). Percussion usually shows an increase of the heart's dullness, due 
to dilatation or hypertrophy of the heart, the increase being either general or 
chiefly to one side. Auscultation shows the absence of any murmur, and hence 
the absence of valvular disease. The heart-sounds are distinctly audible, and 
sometimes quite loud and valvular, but in the later stages often low and obscure. 
The pulmonic second sound is accentuated, when there is stasis of the pulmonary 
circulation. In several cases we found the second sound for a long time very 
plainly divided — reduplicated. We must also mention that sometimes in pure 
myocarditis a systolic murmur is heard at the apex which is due either to a rela- 
tive insufficiency of the mitral valve, or to its incomplete closure, as a result of 
defective muscular action of the left ventricle. 

The whole course of chronic myocarditis is in most of its relations precisely 
analogous to that of chronic valvular disease, so that we need not describe its 
peculiarities in detail. The patient is alternately better and worse again. Severe 
symptoms of general stasis and manifest weakness of the heart may appear, and, 
19 



290 DISEASES OF THE CIECULATOEY OKGANS. 



under favorable circumstances, may disappear again. The picture of the disease 
may be complicated by embolic processes in the brain, the lungs, etc., which usu- 
ally arise from thrombi in the heart {vide supra). Finally, sometimes after the 
disease has lasted for years, the patient dies from general dropsy or from some 
intercurrent disease. 

We must make especial mention of one symptom which has often been brought 
into special relation with sclerosis of the coronary arteries and with chronic myo- 
carditis. We mean the attacks of so-called angina pectoris, the stenocardiac 
paroxysms. These attacks consist of a sudden, intense pain in the cardiac region, 
which shoots into the back, the left shoulder, and the left arm. This pain is asso- 
ciated with a marked feeling of constraint and distress. There is no particular 
dyspnoea in pure angina pectoris. The attacks last from a few minutes to half an 
hour, and may be interrupted by entirely free intervals. 

We can not deny that such attacks occur in indurated myocarditis, due to 
sclerosis of the coronary arteries, but, on the other hand, many cases run their 
course without angina pectoris, and angina pectoris may also occur both in other 
forms of heart disease and as a pure neurosis. Hence we must not overestimate 
the significance of angina pectoris in the diagnosis of sclerosis of the coronary 
arteries. Beside angina pectoris, attacks of dyspnoea (cardiac asthma) and of 
faintness also occur in chronic myocarditis, the faintness being especially fre- 
quent in cases associated with a slow pulse. The dyspnoea is usually due to a 
sudden weakness of the left ventricle, while the origin of the faintness is not yet 
fully explained (cerebral anaemia ?). 

It is a very important clinical fact that, in not very rare cases, indurated myo- 
carditis is the sole apparent cause of sudden, apoplectiform death. It usually 
happens in elderly people, in comfortable circumstances and good livers, who up 
to that time have not regarded themselves as really ill ; but they have repeatedly 
had slight attacks of vertigo, of constraint, etc. Suddenly a sort of apoplectic 
attack comes on, often after some definite cause, after dinner, or after some physical 
exertion or mental excitement. Death follows in a few moments, or after a deep 
coma that lasts for several hours or even days. The diagnosis often remains 
in doubt in such cases, especially if we have not known the patient previously. 
The autopsy shows, as the sole pathological lesion, a sclerosis of the coronary arter- 
ies, with a more or less extensive cicatricial formation in the heart. Apparently 
in these cases the moment must suddenly arise when the supply of blood to the 
heart is insufficient, and thus death is caused. Experiments upon artificial closure 
of the coronary arteries, by Cohnheim and others, agree perfectly with the clini- 
cal facts above mentioned. Artificial narrowing of the coronary arteries may 
also be well borne for a long time, until suddenly both halves of the heart stand 
still in a condition of diastole. In rare cases sudden death may also be due to 
embolism of the main trunk of the coronary artery, or, as we have seen our- 
selves in one case, to the bursting of a focus of myocarditis with haemorrhage into 
the pericardial cavity. 

Diagnosis. — The diagnosis of chronic myocarditis is by no means always easy 
and certain. We must first make out the presence of heart disease in general. 
This is usually easy to do from the secondary symptoms of stasis, the condition 
of the pulse, the heart's dullness, etc. Then the question arises whether we have 
to do with a valvular disease or with a myopathic disease of the heart. Here aus- 
cultation must chiefly decide. The absence of a heart murmur, in spite of other 
definite signs of heart disease, speaks against valvular disease, but not with com- 
plete certainty. All murmurs may be absent in the last stages, especially with 
a high degree of mitral stenosis, and hence we may easily confuse mitral stenosis 
with myocarditis, especially when there is marked arhythmia of the heart. On 



IDIOPATHIC HYPERTROPHY AND DILATATION OF THE HEART. 291 



the other hand, we have already stated that, in pure myocarditis too, with the 
valves intact, functional murmurs may be present, which may lead to an erro- 
neous opinion as to valvular disease. If by long observation we have excluded 
a valvular disease, we always have left the distinction between myocarditis and 
pure idiopathic hypertrophy of the heart, or fatty heart (see the following chap- 
ters). We hold it impossible to make this distinction with certainty. The condi- 
tions of disease mentioned all furnish the same clinical picture of cardiac insuffi- 
ciency, but during life we can only suspect what finer anatomical relations, are 
the ones which cause this insufficiency, and we can never diagnosticate it with 
certainty. Irregularity of the pulse occurs both in indurated myocarditis and in 
pure hypertrophy and dilatation, without discoverable cicatricial nodules in the 
substance of the heart. Attacks of angina pectoris or cardiac asthma, the evi- 
dence of co-existing sclerosis of the arteries of the body, like the radial, temporal, 
or femoral, in connection with other symptoms, make the diagnosis of indurated 
myocarditis probable, but never completely certain. In cases, too, with a sudden 
apoplectic attack — " heart apoplexy " — it is often impossible to make a certain dis- 
tinction between it and cerebral embolism, or cerebral haemorrhage. 

Prognosis. — The prognosis is as serious as in every valvular disease. Recovery 
is impossible, but even extensive cicatricial formation in the heart may probably 
last for years without causing much disturbance. We must always be prepared 
for the occurrence of disturbances of compensation, and the manifold sudden 
accidents to which patients with myocarditis are exposed, but we can not foretell 
the time of their occurrence. 

Treatment. — The treatment is just the same as in valvular disease of the heart. 
We should observe especially the same prophylactic and general hygienic rules : 
the utmost physical and mental rest, a simple manner of life, a cautious reduc- 
tion of flesh for the corpulent, avoidance of large amounts of alcoholic beverages, 
restriction in smoking, , a quiet country residence in summer or the use of some 
bath (Carlsbad, Marienbad, or Kissingen), and in winter, under certain circum- 
stances, residence in a milder climate. With disturbance of compensation, and 
with abnormally frequent, weak, and irregular action of the heart, digitalis is 
indicated, just as in valvular disease. In cases with an abnormally slow pulse, 
however, we can not use it, but we must proceed according to the other prevailing 
symptoms. In attacks of angina pectoris the subcutaneous injection of morphine 
is by far the most efficient and often an indispensable remedy. We may also try 
nitrite of sodium, 1 or 2 parts to 120 of water, two or three teaspoonf uls daily. In 
cardiac asthma, stimulants like ether and camphor, and often narcotics, are indi- 
cated. Mustard-plasters, cold and warm poultices, hot foot-baths, etc., are also 
employed. Iodide of potassium and arsenic are especially recommended for con- 
tinued use in myocarditis. The first remedy sometimes seems to be of service, and 
is especially to be recommended where there is a suspicion of former syphilis. 
With regard to all further details we must refer to the preceding chapter. 



CHAPTER IV. 

IDIOPATHIC HYPERTROPHY AND DILATATION OF THE HEART. 

(Over -exertion of the Heart. Weakened Heart.) 

-Etiology and General Pathology. — Beside the forms of heart disease already 
described, cases not infrequently occur which furnish all the signs of an uncom- 
pensated heart disease during life, and which show at the autopsy a hypertrophy 



292 DISEASES OF THE CIRCULATORY ORGANS. 



of tlie heart or a dilatation of its cavities, but no other abnormality, either in the 
valves, in the coronary arteries, or in the cardiac muscle. The cardiac hypertro- 
phy, which involves the left ventricle chiefly, but often both ventricles, can not be 
regarded as secondary in the ordinary sense of the word, for in the heart itself and 
in the other organs we find nothing which can call forth a secondary hypertrophy 
of the cardiac muscle, no valvular disease, no chronic nephritis, no general arterio- 
sclerosis, and no pulmonary emphysema. Hence we term these cases " primary 
idiopathic " cardiac hypertrophy, in the sense that we can not discover any other 
primary disease in them. Nevertheless, we must also look for factors in such 
cases which during life result in increased work for the heart, because only thus 
can we understand the development of this form of cardiac hypertrophy. 

Such factors may in fact often be discovered. In a few rare cases a congenital 
narrowness of the aortic system plays a part, since by this the heart's work is 
manifestly increased in a way that is easily comprehended. The observations 
upon this point, however, are very scanty, so that we can not yet estimate with 
certainty the practical significance of this arterial anomaly. 

Excessive physical exertion is of much greater ^etiological importance. We 
not infrequently see idiopathic cardiac hypertrophy develop in the hard-working 
classes — in blacksmiths, locksmiths, pack-carriers, and vine-dressers ("Tubinger 
heart "). The increased work of the heart upon every physical exertion is here 
repeated almost every day in the year, and must finally lead to a marked degree 
of hypertrophy from labor. This is the chief form which has been termed "over- 
exertion of the heart." 

We can probably bring many cases of idiopathic cardiac hypertrophy into 
relation with long-continued excess in taking food and pleasure. Although 
it is hard to explain the intimate physiological connection, we can not deny 
the clinical fact of the frequent occurrence of cardiac hypertrophy in bon- 
vivants. Perhaps the injurious influence of alcohol plays a not unimportant 
part here. 

Finally, however, there are always a number of cases left in which none of 
the causes so far mentioned can be discovered. In these cases we are inclined to 
conjecture that there is an abnormal nervous irritation of the heart, which excites 
it to increased activity, and hence finally causes its hypertrophy. The cases 
which seem to be connected with continued mental excitement in business men, 
etc., probably belong to this group. We may also recall the cardiac hypertrophy 
in exophthalmic goitre {vide infra). 

Since the exciting causes above mentioned for the origin of the so-called idio- 
pathic cardiac hypertrophy do not by any means constantly result in this condi- 
tion, we must also assume a special individual, and sometimes apparently a 
hereditary predisposition, a congenital or acquired weakness of the cardiac muscle. 
A healthy, strong heart can respond to the increased demands made upon its 
activity up to a certain degree. We are even justified in considering a certain 
degree of hypertrophy in such cases as by no means pathological, just as there is 
nothing pathological in the hypertrophied muscles of a gymnast ; but experience 
shows that the relations of the cardiac muscle are different from those of the 
muscles of the body, for the hypertrophied heart does not permanently fulfill the 
increased demands put upon it, but it gradually begins to be paralyzed, and 
becomes insufficient. Hence the English physicians, since Stokes's time, term 
the cases of cardiac insufficiency, without any apparent coarse anatomical lesions 
of the valves or muscle, "weakened heart." This term does very well for those 
cases where the symptoms of cardiac insufficiency have appeared before much 
hypertrophy has developed. There are pure cases of weakened heart in which 
the heart seems merely dilated and its walls flabby, and not at all or only slightly 



IDIOPATHIC HYPERTROPHY AND DILATATION OF THE HEART. 293 



hypertrophied. Such a condition shows all the clinical symptoms of a chronic 
heart disease with disturbed compensation. 

It may be mentioned here that dilatation of , the heart may be very acute in 
its development under certain circumstances, if great demands are temporarily 
made upon a heart which is not capable of very much exertion. Acute dilata- 
tion of the heart has been seen in soldiers after a few forced marches. We once 
saw a case in a previously healthy man who fell into the water and could only 
with difficulty be saved from drowning. Acute dilatation also occurs in the 
course of severe febrile diseases, like typhoid, intermittent, or pneumonia, which 
are sometimes associated with manifest weakness of the heart. In previously 
diseased hearts, too, acute dilatation may develop after some special cause. These 
acute dilatations may in many cases be restored, but they always point to a cer- 
tain degree of existing weakness of the heart. 

Clinical History. — Idiopathic dilatations and hypertrophies of the heart may 
certainly exist for a long time without causing the patient any subjective dis- 
turbance. The symptoms begin when the heart can no longer respond to the 
demands made upon it, and when it begins to be paralyzed. Then all the symp- 
toms of cardiac insufficiency arise, in just the same way as in valvular disease 
and in the severe muscular diseases of the heart. Hence we need not go into the 
details of the peculiarities of disturbances of compensation again. The whole 
list of symptoms of stasis, as well as the attacks of angina pectoris and cardiac 
asthma, described in the preceding chapter, also occur in idiopathic hypertrophies 
and dilatations of the heart. 

The whole course of the disease differs considerably in individual cases. Some- 
times there is moderate difficulty in breathing for a long time, especially on any 
physical exertion. The patient often complains of great general languor, of 
nervous irritability, and sometimes of attacks of vertigo, of attacks of faintness, 
and a tendency to perspiration. The appetite is poor, and there is very often con- 
stipation. The condition often becomes quite suddenly worse after any marked 
injurious influence which acts on the patient, especially after great physical exer- 
tion or mental excitement. The pulse is small, weak, and irregular, the dyspnoea 
and oppression in the chest increase, the amount of urine diminishes, and oedema 
appears in the legs. We now have the complete type of an uncompensated 
heart disease. With proper treatment the symptoms may disappear again ; but, 
sooner or later, they return. Death finally ensues from general dropsy or from 
some complications or intercurrent attacks, among which we may mention em- 
bolic processes. 

If the patient keeps away from all injurious influences by a discreet and pru- 
dent way of living, the course of the disease may be quite favorable for years. It 
is not improbable that a number of mild cases may be restored to health, or at 
least remain stationary. 

Diagnosis. — The diagnosis is based on the presence of the serological factors, 
and on the same symptoms as generally point to a disturbance in the heart — 
namely, palpitation, shortness of breath, acceleration and arhythmia of the pulse, 
etc. Physical examination in the later stages of the disease gives an increase of 
the heart's dullness in both directions, usually chiefly to the right. Auscultation 
permits us to exclude valvular disease by finding the heart-sounds everywhere 
distinct. We have left then only the hypothesis of an idiopathic hypertrophy of 
the heart or a chronic myocarditis. As we have already said, we consider it 
impossible to make a clinical distinction between these two diseases, although 
they are serologically and anatomically distinct. We can diagnosticate the 
enlargement of the heart, its functional disturbances, and the intactness of its 
valves, but whether the substance of the heart is simply hypertrophied or is 



294 DISEASES OF THE CIRCULATORY ORGANS. 



studded with the indurations of myocarditis, can only be suspected ; it never can 
be decided with certainty. Arhythmia of the pulse may exist, in spite of the lack 
of all indurations, and it may be absent in spite of extensive cicatricial formation. 
We may often enough find that the autopsy confirms our hypothesis of myocar- 
ditis, made from the setiological factors, from the evidence of atheroma in the 
external arteries, from the existing cardiac insufficiency, and from certain charac- 
teristic symptoms like stenocardiac attacks and sudden death ; but just as often, 
even with extensive clinical and pathological experience, we shall have to admit 
diagnostic errors and confusion between chronic myocarditis and simple cardiac 
hypertrophy. 

Treatment. — Prophylaxis is of the greatest importance. It is directed against 
all those injurious influences whose serological relation to the origin of so-called 
idiopathic cardiac hypertrophy has been mentioned above. As soon as the first 
signs of a functional disturbance of the heart arise, the patient should be made 
aware of the very serious importance of a prudent manner of life. Moderation 
in eating and drinking, the utmost avoidance of all physical exertion, mental 
excitement, and of all toxic substances, like alcohol and nicotine, are to be most 
urgently advised. A bath resort at Marienbad, or Kissingen, may in the early 
stages of the disease be accompanied by the best results. (Compare also page 940.) 

The other hygienic and medicinal treatment is just the same as in valvular 
disease. Digitalis acts most favorably if it be prescribed in accordance with the 
proper indications, which we have mentioned in the treatment of valvular disease. 



CHAPTER V. 

FATTY HEART= 

{Cor adiposum. Fatty Deyeneration of the Heart.) 

iEtiology and Pathological Anatomy.— By the name of " fatty heart " we often 
mean, at present, two quite distinct conditions of the heart — the one an abnormal 
deposit of fat in the heart, and the other a fatty degeneration of the muscular 
fibers of the heart. The first is usually one symptom of great general corpulency. 
At the autopsy of very fat people we sometimes find the heart entirely inclosed in 
a thick capsule of fat. The fat is situated chiefly in the external pericardium and 
beneath the visceral pericardium. It is usually very marked along the course of 
the larger vessels within the grooves of the heart, but in marked cases the fat also 
involves the muscular substance, The heart itself is otherwise quite normal or 
somewhat hypertrophied or dilated. There are sometimes also present sclerosis 
of the coronary arteries and indurations of myocarditis. 

We have already mentioned fatty degeneration of the muscular substance of the 
heart, however, as a frequent result of valvular disease. In myocarditis and idio- 
pathic cardiac hypertrophy, and in the secondary hypertrophy after chronic nephritis 
and pulmonary emphysema, we also meet with fatty degeneration. We often find 
it, as well as fatty degeneration of other organs, in severe acute infectious diseases, 
in phosphorus poisoning, and in all marked primary and secondary anaemias. 
Under the microscope we find the muscular fibrillse studded with little drops 
of fat, which may be so numerous that the nuclei and the transverse striation of 
the fibers are quite concealed by them. We often find albuminous granules, 
beside the fatty granules, which disappear on the addition of acetic acid (" cloudy 
swelling of the cardiac muscle "). If the fatty degeneration is of high degree, we 



FATTY HEAET. 



295 



can easily recognize it with the naked eye. Beneath the endocardium, especially 
on the trabeculae and papillary muscles, we see very fine and delicate yellow points 
and striae. With great fatty degeneration, as in phosphorus poisoning and per- 
nicious anaemia, the whole cardiac muscle is manifestly yellow, and also soft and 
flabby. It is claimed that rupture of the heart may occur with marked fatty 
degeneration. 

In fatty degeneration of the cardiac muscle the fat comes from the decomposi- 
tion of albumen in the muscular cells. The cause of it is probably a defective 
supply of oxygen, which has either a general cause, as in anaemia and phosphorus 
poisoning, or a local cause, as disturbed circulation in the heart in heart disease. 
The details of this are given in the chapter on anaemia (page 874). 

Clinical Symptoms. — Fatty degeneration of the heart has no special clinical 
symptoms. In the conditions under which we know it often occurs we can 
usually suspect it during the life-time of the patient, but we can not diagnosticate 
it. We must also mention that the frequently-expressed opinion, that fatty degen- 
eration of the heart is the cause of general cardiac weakness, is not very often the 
case. In pernicious anaemia there is often quite a strong and a perfectly regular 
pulse up to death in spite of the most marked fatty degeneration. 

We can not say much that is certain in regard to the clinical symptoms of a 
deposit of fat in the heart. " Fatty degeneration of the heart " always plays a far 
larger part in popular speech than it does in reality. It is certainly a fact that diffi- 
culty with the heart and respiration is very often observed in fat people. Exam- 
ination of the heart, which, however, is made decidedly difficult by the thick pan- 
niculus adiposus, often shows in such cases an increase of the cardiac dullness, a 
small and sometimes irregular pulse, and low but clear heart-sounds. The 
difficulty may be very considerable, attacks of angina pectoris and cardiac 
asthma may come on, and death may follow with increasing dyspnoea and general 
oedema. In many cases, indeed, the autopsy shows nothing but a large deposit of 
fat in the heart, and fatty infiltration of its muscular substance. Hence both 
cavities of the heart are usually dilated, and the heart is hypertrophied. Cases of 
genuine hypertrophy and dilatation of the heart develop, however, in very fat 
people, in whom the deposit of fat in the heart is relatively slight — cases which 
apparently belong to the idiopathic cardiac hypertrophy described in the previous 
chapter. It must remain uncertain whether the two conditions, the obesity and 
the cardiac hypertrophy, depend upon the same cause — excessive supply of nutri- 
ment — or whether the great collection of fat in the body is a factor which checks 
the circulation, and in this way leads to the development of cardiac hypertrophy 
(see the chapter on obesity, page 936). Finally, we find the fatty heart often com- 
bined with sclerosis of the coronary arteries and cicatrices in the heart, where 
again the two conditions — the arterial sclerosis and the obesity — may depend upon 
the same cause. 

We see, then, that it is impossible to make an absolute clinical definition and 
diagnosis of the fatty heart, although we would not wholly deny its importance 
in many cases, especially in marked fatty infiltration of the muscular substance 
of the heart. Yet we must mention the fact that, in many cases, there may 
be a very great fatty deposit in the heart, which all through life causes no 
symptoms. 

Treatment. — A great part of the disturbance in respiration in fat people 
depends not upon the cardiac weakness, but on the corpulency itself. The great 
bulk of the body, and the hindrance to the activity of the respiratory muscles, are 
very important factors. Treatment directed against the respiratory disturbance 
must hence chiefly attack the corpulency itself, and thus in many cases we also 
relieve the action in the heart. The detailed description of the hygienic methods 



296 



DISEASES OF THE CIRCULATORY ORGANS. 



of cure to be employed here is to be found in the chapter" on obesity (page 
936). 

In regard to the special treatment of the cardiac symptoms, this does not differ 
from the rules and indications that obtain in other forms of heart disease. 



CHAPTER VI. 
NEUROSES OF THE HEART. 

1. Angina Pectoris (Stenocardia).— Angina pectoris is a group of symptoms 
which we have already had to mention repeatedly as a frequent complication in 
different cardiac affections, like indurated myocarditis, aortic insufficiency, etc. 
The same symptoms are also seen as a pure neurosis, especially in anaemic persons, 
or in connection with other nervous diseases, like hysteria, epilepsy, and the psy- 
choses. We know almost nothing as to the exact aetiology of the disease. In 
quite a large number of published cases excessive smoking has been advanced as 
an aetiological factor. 

The most essential symptom of the paroxysm consists of a severe pain in the 
cardiac region, shooting up into the left, or, more rarely, into the right shoulder. 
There is also a general feeling of constraint and anxiety — the "precordial 
anxiety." The action of the heart is usually somewhat accelerated, either weak 
or intermittent, or strong. The skin during the paroxysm is often pale and cool, 
but at the end of it there may be profuse sweating. The individual attack lasts 
sometimes only a few minutes, and sometimes half an hour or more. In many 
cases the paroxysms return very frequently, almost daily, but in others there may 
be intervals of weeks or months. 

Many theories have been advanced as to the nature of angina pectoris, but 
none of them have any certain foundation. Since the sensory fibers of the heart 
rise from the vagus (but partly, perhaps, from the sympathetic also), we usually 
term angina pectoris a neurosis of the vagus. 

The prognosis of the disease is not very favorable. Although life itself is very 
rarely endangered by the paroxysms, we only occasionally succeed in permanently 
preventing their return. 

The treatment of the paroxysm is purely symptomatic. Cutaneous irritants, 
like mustard plasters to the chest, and foot-baths, are almost always used, but 
they have but little effect. A subcutaneous injection of one sixth to one third of 
a grain of morphine (grm. 0*01-0 *02) is the best palliative. All the other reme- 
dies, like nitrite of amyl, inhalations of chloroform, atropine, coniine, etc., are 
uncertain. Nitrite of sodium has been especially recommended lately (see p. 158). 

Many remedies have also been used to prevent the return of the paroxysms : 
arsenic, sulphate of zinc, nitrate of silver, bromide of potassium, quinine, etc. 
We usually try one of these remedies, but without promising any certain benefit 
from them. Favorable results are often obtained from electrical treatment — either 
the application of the faradic brush to the cardiac region, or cautious galvaniza- 
tion of the vagus and sympathetic in the neck, or in the cardiac region. Methodi- 
cal cold-water cures have also resulted m improvement in some cases of angina 
pectoris. 

Finally, of course, we must pay attention to any underlying diseases, like 
anaemia, and epilepsy, and to the removal of injurious influences which may 
affect the disease (smoking!). 



NEUEOSES OF THE HEAET. 



297 



[In well-marked angina sudden death during a paroxysm is not very rare. In 
Dr. Arnold, of Eugby, the first attack proved fatal. The patient may, however, 
live for years — cases of survival for upward of twenty, and one even of thirty, 
years being recorded. Flint has known recovery to occur. The prognosis depends 
somewhat on the condition of the cardiac valves and walls ; but changes, espe- 
cially in the latter, may escape detection by any save a very skillful observer. 
Walshe states that in every one of twenty-four cases he examined during life he 
found physical signs of changes either in the heart, the aorta, or both. The 
experience of Balfour and Latham is similar. 

With regard to treatment, it is true that morphia, subcutaneously, brings relief ; 
but the duration of the attack is short, the physician is not always at hand, and 
there are scarcely any circumstances under which it is right to arm a patient with 
a hypodermic syringe in this any more than in other diseases. 

Nitro-glycerine is not only a palliative in most, but also a prophylactic in 
many cases. To cut short an attack, it can be carried in the pocket ; to prevent 
recurrence, it can be taken twice or thrice daily. The nitrite of sodium seems to 
act equally well, but has not been so long in use. The nitrite of amyl is service- 
able chiefly at the moment of attack. It is put up in glass capsules, one of which 
can be crushed in a handkerchief and the contents inhaled ; it is so volatile that 
it can be preserved ready for use in scarcely any other way. 

The value of the nitrites is greater than the author would seem to allow.] 

2. Nervous Palpitation. — By " palpitation " we understand the subjective sensa- 
tion of the movements of the heart. It is usually excited by increased action of 
the heart, but there is no constant relation between the intensity of the cardiac 
pulsations and the subjective feeling of them. "We sometimes observe that 
patients with aortic insufficiency do not perceive the very strong action of their 
hypertrophied hearts, while in other cases the patient complains of a troublesome 
feeling of palpitation, although the action of the heart does not appear objectively 
to be especially increased. 

We term cases " nervous palpitation " where the patient complains of palpita- 
tion when a physical examination of the heart shows no anatomical change 
in it. As a rule, in these cases we really have to do with a heart whose action is 
increased by abnormal nervous influences. In many cases the palpitation arises 
from slight external causes, which may give rise to little or no palpitation in a 
healthy person, as, for example, after the slightest mental excitement, after any 
slight physical exertion, after taking food, after indulging in certain drinks, 
like tea, coffee, wine, or beer, or in certain positions of the body, as in lying on 
the left side. Here, then, we have to do with an abnormal sensitiveness of the 
heart to external irritation, but in other cases there is probably a kind of hyper- 
esthesia of the patient to the movements of the heart, so that the movements that 
are normal in strength are felt in a troublesome manner. 

The patient rarely complains of continuous palpitation ; it usually occurs in 
more or less sharply defined paroxysms. Very commonly in pure nervous palpi- 
tation we have to do with people who, in general, suffer from other nervous, hys- 
terical, and neurasthenic symptoms, or they are anaemic persons, chlorotic girls, 
etc. ; but, on the other hand, nervous palpitation may occur in very full-blooded, 
" plethoric " people. 

The diagnosis of nervous palpitation can be made only when repeated careful 
examination shows no objective abnormality in the heart. In many cases, as 
when there are anaemic murmurs, the decision may be quite difficult. We must 
always pay particular attention to the whole constitution and the general impres- 
sion which the patient makes. 

The prognosis is so far favorable in that the disease is not dangerous. In many 



298 DISEASES OF THE CIRCULATORY ORGANS. 



cases improvement and final recovery may be effected, but other cases, of course, 
oppose all therapeutic efforts very obstinately. 

The treatment must first be directed to improve the patient's general constitu- 
tion. Anaemic persons are to be treated with iron, quinine, and strengthening diet. 
We put full-blooded people, however, on scanty fare, and prescribe for them bitter 
waters, or a bath cure at Marienbad or Kissingen. Where there is hysteria or 
neurasthenia, it requires special treatment. We should avoid all the aetiological 
influences which seem to excite palpitation. As a symptomatic indication we 
should recommended the patient especially to keep in a quiet position. The use 
of cold to the cardiac region — cold compresses and ice-bags — often acts beneficially. 
Among internal remedies we must employ nervines, and in severer cases even 
narcotics. Among the former we must mention especially ethereal tincture of 
valerian and bromide of potassium, which have repeatedly done us good service. 
Digitalis is usually of little service in pure neuroses of the heart, but we may give 
it as an experiment, giving fifteen to twenty drops of the tincture with the same 
amount of cherry-laurel water. 

3. Tachycardia. — A peculiar and quite rare neurosis of the heart, tachycardia, 
consists of an enormous frequency of the pulse, coming on in paroxysms, up to 200 
beats and more a minute. We have already mentioned these paroxysms as a rare 
symptom in heart disease, in mitral and also in aortic disease, but precisely similar 
attacks may occur as a pure neurosis without any discoverable lesion of the heart. 
They have been observed in anaemic and nervous, and also in corpulent persons. 
In young people the same condition sometimes occurs after the course of diph- 
theria {vide supra). In men we must consider the possibility of the action of 
injurious dietetic influences, like drinking and smoking. The individual attack 
usually begins quite suddenly, by day or by night, sometimes without any cause, 
but often it is apparently produced by certain exciting causes, especially at times 
by overdistension of the stomach. The patient feels that the attack is coming, he 
becomes anxious and restless, and looks pale ; but there are not as a rule, at least 
according to our experience, any symptoms like a state of praecordial anxiety, 
dyspnoea, or attacks of faintness. We notice in the heart itself, during the attack, 
chiefly a great acceleration of the heart-sounds. We sometimes hear indefinite, 
adventitious murmurs. The action of the heart is often quite regular, but there is 
not infrequently manifest arhythmia during the attack. Increase of the heart's 
dullness has been repeatedly observed. In a case of paroxysmal tachycardia, in a 
patient who had cirrhosis of the liver, we could certainly detect a considerable 
acute dilatation of the heart in every attack, which disappeared again soon after. 

We know little that is definite as to the nature of the attacks. The affection is 
usually regarded as a temporary paralysis of the vagus. 

We may also state here that paroxysmal and constant tachycardia have also 
been repeatedly observed in anatomical lesions of the cardiac nerves and their 
centers, in tumors and other affections in the vicinity of the medulla oblongata, 
and in compression of the vagus in the neck from tumors, and aneurisms. 

The prognosis of tachycardia depends first upon the nature of the underlying 
disease. We do not know whether a permanent recovery is possible in idiopathic 
cases, but we can always succeed in improving the condition. The treatment dur- 
ing the attack consists in enjoining complete bodily rest, and in applying ice to the 
heart. With marked subjective disturbance we should give bromide of potassium, 
or even, under some circumstances, a small injection of morphine. The best 
way to guard against the return of the attacks is to give precise hygienic direc- 
tions, suited to the patient's constitution and manner of life. The continued use 
of iodide of potassium has sometimes seemed to us to be of service. 



PERICARDITIS. 



299 



SECTION II. 
Diseases of the Pericardium. 

CHAPTER I. 

PERICARDITIS. 

{Inflammation of the Pericardium^) 

iEtiology. — In rare cases pericarditis is an apparently primary, idiopathic dis- 
ease. Such cases may either recover or end fatally, the autopsy showing no 
cause for the origin of the pericarditis. It is stated, in some cases, that an injury 
is to be regarded as the cause of pericarditis, but, in the great majority of cases, it 
is a secondary affection coming on in the course of other diseases. Pericarditis 
quite frequently develops in acute articular rheumatism, much more rarely in 
other infectious diseases, in scarlet fever, measles, pyaemic processes (when it 
is purulent), scurvy, and purpura haemorrhagica (when it is haemorrhagic). 
Among the chronic diseases in the course of which pericarditis sometimes appears 
we must mention especially chronic nephritis. Pericarditis has also been observed 
in a few cases in patients with carcinoma. 

A large number of cases arise from an extension of the inflammation from the 
vicinity. Thus we not infrequently see pericarditis as a result of pleurisy, espe- 
cially on the left side, and in pneumonia complicated with pleurisy. New growths 
and ulcerative processes in the oesophagus, in the vertebrae, in the bronchial 
glands, or in the lungs, also lead at times to perforation into the pericardium 
and a consequent inflammation. The pericarditis, too, which not very rarely 
comes on in the course of chronic valvular disease, is probably usually to be 
regarded as an extension of the inflammation. As has already been mentioned, it 
is most frequent, according to our experience, in aortic disease, so that we may 
suspect a direct conduction of the agents of inflammation through the aortic walls 
into the pericardium. Pericarditis may also develop as a result of myocarditis, 
abscess of the heart, etc. 

Tuberculosis plays a very important part in the aetiology of pericarditis. No 
small number of apparently primary cases of pericarditis turn out at the autopsy 
to be tubercular. This apparently comes on in quite an isolated way, or as one 
symptom of a special localized form of tuberculosis, which we term tuberculosis of 
the serous membranes. In many cases we can discover the origin of a tubercular 
pericarditis from the direct extension of a tubercular pleurisy. In apparently 
primary cases the occurrence of the infection may sometimes be explained by the 
discovery of a tubercular lymph -gland, which has broken through into the peri- 
cardium. 

Pericarditis is usually a disease of youth and middle life, but it may also occur 
in advanced age. 

Pathological Anatomy.— Ordinary* pericarditis involves the two surfaces of the 
internal pericardium in a circumscribed or diffuse manner. Inflammations of the 
outer surface of the pericardial sac are termed external pericarditis (vide infra). 
The anatomical processes in pericarditis are precisely analogous to those in inflam- 
mations of the serous membranes in general, especially of the pleura. 

We usually divide pericarditis into fibrinous, sero-fibrinous, haemorrhagic, and 
purulent (or ichorous) forms, according to the character of the exudation. The 
fibrinous and sero-fibrinous forms, with an abundant fluid effusion into the peri- 
cardial cavity, are the most frequent, occurring in articular rheumatism, in valvu- 



300 DISEASES OF THE CIECULATOEY OEGANS. 



lar disease of the heart, etc. Both layers of the pericardium are covered with 
masses of fibrine, which often show a reticular or villous arrangement (cor 
villosum). Beside that, we find more or less of a fluid effusion which distends 
the pericardium. The fluid is of a serous nature, and contains more or less numer- 
ous flakes of fibrine, and is turbid from the admixture of cells — pus-corpuscles, and, 
in part, desquamated endothelium. Pure purulent pericarditis is always the 
expression of a specific infection of the pericardium. It is seen in pyaemic dis- 
eases, as a result of empyema, and in perforation of abscesses, cancers of the oesoph- 
agus, etc., into the pericardium. A hsemorrhagic effusion is seen chiefly in tuber- 
cular pericarditis. In this we find miliary tubercles, and little cheesy nodules in 
the inflammatory new growths, beside all the signs of inflammation. The specific 
tubercular changes are sometimes recognizable with the naked eye, but at other 
times we have to use the microscope to find them. Hsemorrhagic pericarditis also 
occurs in general hsemorrhagic diseases, like scurvy, and in weak and debilitated 
people, like drunkards. 

In long-continued pericarditis the cardiac muscle almost invariably undergoes 
changes. The heart is usually flabby and dilated, and the muscle often shows 
fatty degeneration. After the pericarditis has lasted a long time there is often 
quite a considerable atrophy of the cardiac muscle, in which it is partly replaced 
by fat tissue. We have already mentioned the occurrence of pericarditis in con- 
nection with valvular disease and degenerations of the myocardium. 

In favorable cases of pericarditis we may have a perfect recovery. The so- 
called maculce tendineaz sometimes remain in the pericardium as residua of a 
past circumscribed pericarditis. In some cases the pericarditis leads to an adhe- 
sion of the two layers of the pericardium to each other, and obliteration of the 
pericardial cavity (vide infra). In many cases a chronic pericarditis finally 
develops from the acute form, or the whole affection takes a more chronic course 
from the outset. In this way chronic adhesions of connective tissue arise, and 
great thickening of the pericardium, but the amount of fluid is usually small. 
Sometimes the chronic pericarditis is interrupted by an acute exacerbation of the 
disease. 

Clinical Symptoms. 1. Subjective Symptoms, General Symptoms, and Fever. — 
Mild forms of pericarditis may develop, as in the course of an acute articular rheu- 
matism, without causing any subjective symptoms. They are discovered only by 
a careful physical examination of the heart. In severe cases, however, the peri- 
carditis causes very severe subjective symptoms, which of course have in them- 
selves little that is characteristic. 

Pain may be present in the cardiac region, and often in the epigastrium, but it 
is absent in very many cases. A general feeling of constraint and distress is 
almost constant in all acute cases of any severity, and so is a feeling of dyspnoea, 
which may increase to the highest degree of orthopnoea. The patients often com- 
plain of headache. In severe cases they become stupid and comatose. 

These severe general symptoms are the direct result of the disturbance of the 
circulation. The heart fills with blood with difficulty, and the diastole is incom- 
plete from the increased pressure in the pericardium. Although stasis occurs in 
the veins, there is less blood in the right ventricle than normal. As a result of 
this the pressure falls, and the rapidity of the current in the pulmonary circula- 
tion diminishes. The left ventricle, also, contains too little blood, and the tension 
in the medium-sized arteries falls considerably. This is the explanation of the 
patient's dyspnoea and cerebral anaemia. The former is also increased in large 
pericardial effusions by the mechanical pressure of the distended pericardium on 
the left lung. 

Acute pericarditis is usually associated with fever. This has no special typo, 



PERICARDITIS. 



301 



and usually keeps at a moderate height— 102° to 103*5° (39°-39-8° C.)— but it is 
often broken by considerable variations. In cases of recovery the fever declines 
by lysis. Chronic pericarditis may run its whole course without fever. 

2. Physical Signs — Inspection. — The general hue of a patient with severe 
pericarditis is pale, but also more or less cyanotic. He has an anxious expression. 
He lies with the upper part of the body raised, or he sits up in bed. The breath- 
ing is usually rapid, labored, and somewhat irregular. The veins in the neck are 
swollen and prominent. We very often see marked undulating or pulsating 
movements in the jugular veins, as a result of stasis. The cardiac region seems 
unusually prominent in all cases with much effusion, and the intercostal spaces 
there are flattened out. We sometimes detect a slight oedematous swelling of the 
chest-wall itself. The action of the heart in every large effusion is only faintly 
visible, and is sometimes remarkably diffused. 

Palpation in the milder cases shows the apeK-beat in its normal position and 
of about normal strength ; but, if the amount of the pericardial effusion increases, 
the heart is pushed away from the chest- wall by it, and hence the heart beat 
grows weaker until it disappears entirely. In such cases it is sometimes to be felt 
again if the patient bends forward or lies on his left side. In the- rest of the car- 
diac region we sometimes feel the movements feebly, but they entirely disappear 
as the effusion increases. In some cases, by laying the hand flat on the chest, we 
can feel the rub of the rough pericardial surfaces against each other. 

The pulse is usually accelerated, and in severe cases it becomes irregular. In 
every large effusion, as we have already said, the tension and height of the pulse 
are diminished. In severe cases the pulse sometimes becomes very small and weak, 
but, when the heart is otherwise normal and strong, it may also remain quite 
strong — and indeed this condition of the pulse, in contrast to the great weakening 
of the heart-beat, is sometimes of diagnostic significance. In some cases with a 
large pericardial effusion we have seen a manifest pulsus paradoxus — that is, a 
diminution or a complete disappearance of the radial pulse on every inspiration. 

Percussion shows very characteristic changes if the pericardium is distended 
by the effusion. The cardiac dullness is then increased, and usually assumes a 
triangular form peculiar to pericarditis. The obtuse angle of the triangle is found 
above in the third or second left intercostal space near the left border of the ster- 
num. The lateral boundaries run obliquely to the right and downward to about 
the right parasternal line, and to the left and downward to the left mammillary 
line, or farther. The broad base of the triangle which lies below is usually not to 
be defined by percussion on account of the adjacent left lobe of the liver. On the 
border of the dullness we often find a tympanitic resonance due to the retraction 
of the adjacent lung. The area of the dullness depends, of course, in the first place, 
upon the amount of the effusion, but we must take special notice that in regard to 
this the relation is not constant. In old cases of pericarditis especially we some- 
times find the cardiac dullness very extensive, while the autopsy detects only a 
little fluid in the pericardium. This is explained partly by a secondary dilatation 
of the heart, and partly by a persistent retraction of the lung. 

It is an important diagnostic sign of pericarditis that in many cases the still 
perceptible apex-beat lies within the cardiac dullness, since the pericardial effusion 
extends farther to the left than the heart itself. It is also worthy of note that the 
dullness in pericarditis often shows very great changes when the patient changes 
his position. The dullness is larger when the body is erect than when lying 
down, and when the patient lies on his side it sometimes shows a lateral displace- 
ment of several centimetres. The same changes, however, though rarely so 
marked, also occur in. a hypertrophied heart. 

The characteristic pathognomonic auscultatory sign of pericarditis is the peri- 



302 



DISEASES OF THE CIRCULATORY ORGANS. 



cardial friction-rub. This arises during the movements of the heart from the 
rubbing of the rough and inflamed pericardial surfaces against each other. The 
friction-rub is absent in pericarditis if the rough surfaces of the two layers of the 
pericardium are separated from each other by a fluid effusion, or if they can no 
longer rub against each other from an adhesion of the layers of the pericardium. 
We usually hear the friction-rub the loudest in the neighborhood of the base of 
the heart, but it may also be heard at other parts of the heart. The quality of the 
sound is described as scraping, grating, or creaking. The friction-rub may be 
heard chiefly either during the systole or during the diastole of the heart, but it is 
in general not often closely associated with the phases of the heart's action. We 
sometimes find it intermitting frequently, and jerky. The intensity of the fric- 
tion-rub sometimes varies with the phases of the respiration. It is usually louder 
on inspiration, but sometimes on expiration. If the patient changes his position, 
it sometimes alters the intensity of the sound. It is louder when sitting up than 
lying down, etc. The friction-rub often sounds louder if the stethoscope is pressed 
firmly against the chest, since in this way the layers of the pericardium are 
approximated to each other. 

The heart-sounds, when the valves are intact, may sometimes be heard as well 
as the friction-rub, or they may be completely drowned by the loud rub, at least 
in some parts of the heart. In general, they are weaker in every pericardial effu- 
sion, since their conduction to the ear is impaired. In large effusions where no 
friction-rub is to be heard, we hear the heart-sounds, especially the first, but only 
very low and obscure. This condition in connection with the increase of the car- 
diac dullness is of diagnostic importance. If there is also valvular disease with 
the pericarditis, the pericardial and endocardial murmurs are sometimes hard to 
distinguish from each other, but usually the former greatly preponderate. 

3. Sequelae, of Pericarditis. — A large pericardial effusion may excite special 
symptoms from pressure on the neighboring organs. Thus we have already said 
that compression of the left lung must increase the dyspnoea. In many cases we 
also notice a moderate dullness over the left lower back, from compression of the 
left lower lobe. In rare cases difficulty in deglutition has been observed as a 
result of pressure on the oesophagus, and paralysis of the vocal cords from press- 
ure on the recurrent nerve. 

In cases of long-continued pericarditis the same sequelae may develop as in any 
chronic disease of the heart. The amount of urine diminishes as a result of the 
low arterial pressure. The venous stasis finally leads to general dropsy and to 
symptoms of passive congestion in the liver, spleen, and kidneys. We would also 
state that we have repeatedly met with large effusions in the cavities of the body, 
especially hydrothorax, without any oedema of the skin. All the symptoms of 
stasis mentioned, however, are often much less due to the pericarditis itself than 
to the frequent atrophy and dilatation of the heart which follows it {vide supra). 

Special Forms of Pericarditis. 

1. Pericarditis externa and Mediastino-pericarditis (Pleuro-pericarditis). — 
By pericarditis externa we mean an inflammation of the external surface of the 
pericardial sac, which is usually combined with an inflammation of the mediasti- 
nal connective tissue and the neighboring pleura, especially over the lingula of 
the left lung. This form of pericarditis may exist by itself, or be combined with 
internal pericarditis. It is a rare disease, and is most frequently seen as a result 
of tubercular pleurisy. 

The physical signs must differ so much, according to the localization and extent 
of the process, that we can give few general data in regard to them. There are only 
a few peculiar signs, which must be noted as characteristic of many cases. In the 



PEBICAKDITIS. 



303 



vicinity of the apex-beat, or at the left border of the cardiac dullness, we some- 
times hear a so-called extra-pericardial (pleuro-pericardial) friction-rub. This 
depends both upon the cardiac movements and upon the respiratory movements. 
On holding the breath we hear only the murmur due to the pulsations of the 
heart, while on deep breathing the pleuritic friction-sound is chiefly to be heard. 
In individual cases there are many modifications, which can not all be mentioned. 
Another interesting sign, first found by Grriesinger and Kussmaul in a cicatricial 
mediastino-pericarditis, is the so-called pulsus paradoxus. This consists of a 
diminution of the pulse at each inspiration. This condition arises, in part of the 
cases at least, from the fact that the bands and adhesions of connective tissue at the 
origin of the aorta mechanically nick into and contract its lumen at every inspi- 
ratory movement of the thorax. This explanation, of course, does not suffice for 
all cases, since the pulsus paradoxus also occurs under other conditions, as with 
large pericardial effusions. In some cases there may be seen a marked swelling 
of the jugular veins in the neck at each inspiration, at the same time with the pulsus 
paradoxus, since the large venous trunks also undergo a mechanical nicking 
and constriction at each inspiration. We have ourselves seen a very pronounced 
slowing of the pulse at every inspiration, in a complicated case of extra-pericardial 
adhesions (vagus irritation ?). We must also mention that Riegel observed a dis- 
appearance of the apex-beat on expiration in some cases where there wer? bands 
of connective tissue between the lungs and the outer surface of the heart. At 
every expiration the bands were stretched more tightly, and hence checked the 
movements of the heart. 

2. Obliteration of the Pericardial Cavity (Adhesive Pericarditis ; Adhesions of 
the Layers of the Pericardium; Concretio seu Synechia pericardii). — We may 
have a more or less complete adhesion of the two layers of the pericardium with 
each other as a result of pericarditis. We can sometimes observe this condition 
directly in the course of a pericarditis. Quite frequently, however, we meet with 
extensive adhesions of the two layers of the pericardium on the living subject, or 
at autopsies, without being able to gather any history of a previous acute pericar- 
ditis. The pericarditis must have occurred here in a chronic way, and without 
symptoms from the outset. 

Even extensive adhesions of the pericardial surfaces may develop and remain 
entirely without symptoms, and be met with accidentally at the autopsy. In 
other cases, however, the obliteration of the pericardial sac causes special physical 
signs and severe clinical sequelae. Among the first and most important is the 
retraction of the chest at the apex, or over a greater extent, at the systole. This 
is most comprehensible if there is an adhesion of the pericardium with the heart, 
and also with the chest-wall (Skoda) ; but we certainly find this retraction at the 
systole without co-existing extra-pericardial adhesions. It is not, however, an 
absolutely certain sign of an intra-pericardial adhesion, especially if we have to 
do only with a systolic retraction at the apex, since systolic retractions may some- 
times occur in other disturbances of the heart's motions ; but systolic retractions 
of the whole cardiac region are, in the majority of cases, a certain sign of peri- 
cardial adhesions. The amount of this retraction is often dependent upon the 
respiration, it being usually more marked on inspiration. 

The other symptoms of obliteration of the pericardial cavity are more rare and 
still more uncertain in their diagnostic significance. Friedreich observed a sud- 
den collapse of the jugular veins at each diastole — the " diastolic collapse " — while 
they became well filled again at the next systole. He explained this phenome- 
non by supposing that the conditions for emptying the veins, at the moment 
of the diastole of the ventricle, were especially favorable, since the chest-wall, 
which had previously been drawn in by the systole, went back again quickly. 



304 



DISEASES OF THE CIECULATOEY ORGANS. 



Biess described some cases of pericardial adhesions where the heart-sounds had a 
metallic character from the resonance of the stomach, which had been drawn up. 
All things considered, we must say that although the diagnosis of pericardial adhe- 
sions can be correctly made in many cases, yet the signs given for it are more or less 
uncertain in their significance, since they may be absent in obliteration of the 
pericardial sac, and they may also be caused by other conditions without such an 
obliteration. 

In the cases of pericardial adhesions which give rise to severe disturbances 
of the circulation these are usually not the direct result of the pericardial adhe- 
sions, but are due to the secondary changes which develop in the cardiac muscle. 
Only when extensive extra-pericardial adhesions are also present can there be 
such a restraint upon the systole of the heart, in a purely mechanical way, as to 
cause a diminished filling of the arteries, and stasis in the veins. It is usually, 
however, the secondary atrophy, with fatty degeneration and dilatation of the 
cardiac muscle, that causes the severe disturbances of the circulation. Such cases 
give throughout the general impression of valvular disease. Dyspnoea, general 
oedema, and signs of passive congestion in the liver and kidneys, are the chief 
symptoms of the disease. The diagnosis is often not at all easy. "We can 
sometimes scarcely avoid confounding it with chronic myocarditis, in the absence 
of all heart-murmurs. If the cardiac muscle remains intact, extensive pericardial 
adhesions may exist for years without causing the patient the slightest dis- 
turbance. 

3. Tubercular Pericarditis. — Tubercular pericarditis is an important disease 
clinically, since in many cases it is apparently primary. It may be either quite 
acute or chronic. The patient falls ill quite suddenly, or more gradually with 
indefinite thoracic symptoms, dyspnoea, general weakness, moderate fever, etc. 
If it is of long duration, there is more or less oedema. If we find on physical 
examination, in such cases, the signs of a pericarditis, the diagnosis of tubercular 
pericarditis is probable, if we discover a general " phthisical habit," hereditary 
predisposition, and also co-existing disease of other serous membranes, especially 
pleurisy, or more rarely chronic peritonitis. In the latter case the tubercular 
pericarditis forms one symptom of the so-called tuberculosis of the serous mem- 
branes, but, as has been said before, apparently isolated primary tubercular 
pericarditis does occur (vide supra). We have seen such cases repeatedly, espe- 
cially in old people. In these cases the disease is not easy to diagnosticate. The 
patient gives one the impression of having heart disease, but the physical signs 
in the heart are sometimes of a very indefinite nature. Friction-rubs may be 
entirely absent, on account of adhesions or of large effusions. This is the expla- 
nation of the confusion with myocarditis, or mitral stenosis. In other cases, of 
course, all the physical signs of pericarditis mentioned above may be manifest, 
and a correct diagnosis can be made. 

Diagnosis. — From what precedes, it follows that the diagnosis of pericarditis is 
very easy in many cases, but is very difficult or impossible in others. The most 
unequivocal sign is the characteristic friction-rub. The practiced ear can dis- 
tinguish it from an endocardial sound in many cases by its quality. The pericar- 
dial sound is a rubbing, grating noise, near the ear ; the endocardial is blowing, 
distant from the ear. The following features may serve as marks of distinction 
in doubtful cases : 1. We hear the pericardial sounds at first and also later over 
the base of the heart in the vicinity of the pulmonary valve ; the endocardial are 
often loudest at the apex. 2. The pericardial murmurs are not so closely associ- 
ated with the phases of the heart's action, with systole and diastole, as the endo- 
cardial. 3. We find that the pericardial sounds are not transmitted far. A loud 
rub may be audible at one spot which can not be heard a few centimetres 



- PEKICAKDITIS. 



305 



away. Loud endocardial murmurs, however, are audible over almost the whole 
heart. 4. Sometimes the peculiarity of the pericardial murmur — that it becomes 
louder when the patient sits up, on pressure with the stethoscope, etc. — may be 
of diagnostic value. In many cases, too, the loud, functional, so-called anaemic 
murmurs over the base of the heart may give rise to confusion with pericarditis. 

In the cases where pericardial sounds are absent the diagnosis is rendered pos- 
sible by the relations of the cardiac dullness, and its triangular shape, in connection 
with the character of the apex-beat, the pulse, and the heart-sounds. We have 
already called attention to the ease with which pericarditis may be confounded 
with myodegeneration of the heart and mitral stenosis without any murmur. We 
can not lay down general rules for differentiating these conditions. The more 
careful the examination, and the greater the personal experience, the more easily 
can we avoid a false diagnosis. 

We have already mentioned the determining factors for the diagnosis of the 
different forms of pericarditis and their significance. 

Course and Prognosis. — Many cases of pericarditis in articular rheumatism, as 
a result of pneumonia, or in heart disease, and also many of the rare and appar- 
ently primary forms, may recover completely. The disease lasts, in the mild cases, 
only about a week, in severe cases much longer. 

Many cases of pericarditis, however, terminate fatally. The unfavorable issue 
depends either upon the severity of the primary disease, or upon the intensity and 
form of the pericarditis itself. In extensive croupous pneumonia, in valvular dis- 
ease of the heart, or in severe chronic nephritis, an attack of pericarditis is often the 
terminal affection — the immediate cause of death. In otherwise healthy people, 
however, a severe pericarditis with a large effusion may be the direct cause of 
death, as a result of the impairment of the movements of the heart. The prog- 
nosis of every tubercular pericarditis is absolutely unfavorable. The latter can, 
indeed, run quite a chronic course, but it is hardly ever capable of definite recov- 
ery. The prognosis of pysemic pericarditis is also unfavorable. 

In one class of cases pericarditis takes a chronic course from the start, or 
chronic pericarditis develops from an acute attack. The ultimate prognosis of these 
cases is usually unfavorable, since the secondary atrophy and dilatation of the 
heart gradually lead to severe disturbances of the circulation. We have spoken 
above of the termination of pericarditis in obliteration of the pericardial sac. 

Treatment. — Since pericarditis is a severe affection under all circumstances, we 
must especially see that the patient has perfect rest and care. Extreme caution 
must be enjoined upon him, especially in the cases where at first the subjective 
symptoms are slight. We must keep the patient strictly confined to the bed, and 
not let him leave it even temporarily. 

The remedies which are used against pericarditis aim partly at keeping the 
inflammation in check, and partly at aiding the action of the heart. For the first, 
the continued application of ice to the cardiac region deserves especially to be 
recommended. Local blood-letting, ten or twelve leeches to the cardiac region — 
formerly very often, but now more rarely used — may, in otherwise strong and 
healthy persons, afford great relief in cases with marked subjective symptoms. 
Painting with tincture of iodine and vesicatories, however, deserve little confi- 
dence. Digitalis is our chief means to bring down an accelerated pulse, and to 
strengthen the heart's action. It is the drug which is most active and most fre- 
quently used in pericarditis, and is always indicated when the pulse is frequent 
and of diminished tension. Of course, the action of the remedy must be carefully 
watched, as in all cases where digitalis is prescribed. In its symptomatic relations, 
morphine often does indispensable service where the subjective symptoms are 
marked and the patient is very restless. 
20 



306 



DISEASES OF THE CIECULATOEY ORGANS. 



If the symptoms are threatening, the question arises whether a large fluid peri- 
cardial effusion is the cause of the severe symptoms. In this case the removal of 
the effusion is a necessary vital indication, but the presence of this indication is in 
practice often uncertain, because in the individual case it is very hard, and even 
impossible, to estimate the amount of fluid effusion present. In the first place, we 
must consider the size of the cardiac dullness and the weakening of the move- 
ments of the heart, but both factors may give rise to deception. Hence we always 
first make an exploratory puncture with a Pravaz's hypodermic syringe. The best 
point for insertion is, in general, the sternal end of the fourth or fifth intercostal 
space when the patient is lying on his back. If the exploratory puncture gives a 
positive result, we make a puncture with Billroth's, Fraentzel's, or some similar 
trocar. With regard to the details, we will refer to the description of puncture of 
the pleura. Puncture of the pericardium is always performed by the aid of aspira- 
tion. It is less dangerous than might be feared. Even injuries to the heart dur- 
ing the operation have scarcely ever had severe results, according to experience, 
so far. The temporary relief to the patient, in cases of successful puncture, is 
usually very striking, but the permanent results of pericardial puncture are, of 
course, much less favorable than those of puncture of the pleura, which is chiefly 
due to the character of the underlying disease. In some cases of purulent peri- 
carditis, drainage of the pericardium has also been practiced, after the analogy of 
the treatment of empyema, but experience on this point is not yet very extensive. 

[The experiments of Botch show that pericardial effusion causes dullness in the 
fifth right interspace, a sign which he thinks is not produced in cardiac enlarge- 
ment. This observation has diagnostic as well as therapeutic value, though, as 
far as I know, puncture has never yet been practiced at this point in the living 
subject. 

Roberts has tabulated sixty cases of paracentesis of the pericardium, with 
twenty-four recoveries. 

In purulent effusion, free incision with drainage has been successful in several 
cases.] 

If there is a condition of cardiac weakness, stimulants are indicated — strong 
wine, subcutaneous injections of ether or camphor, or wine of musk. We try to 
keep up the patient's strength by the best of nourishment. 

The resulting conditions of disturbance of the circulation, like oedema, in 
chronic pericarditis, are treated in the same way as in valvular disease {vide supra). 
Digitalis, in small doses, and diuretics, are the chief remedies. 



CHAPTER II. 

HYDRO-PERICARDIUM. 

{Dropsy of the Pericardium.) 

The collection of a serous transudation in the pericardial sac, without any 
inflammatory symptoms in the serous membrane itself, we term hydro-pericar- 
dium, or dropsy of the pericardium. Dropsy of the pericardium, which formerly 
played quite a great role in pathology, is never a disease of itself, but is always 
a secondary condition. It may occur in anaemic and cachectic people as a result 
of hydraemia, but it usually depends upon a local or general venous stasis in the 
pericardium. In the latter case the hydro-pericardium is one symptom of general 
dropsy, and hence is found chiefly in heart disease, renal disease, or pulmonary 
emphysema. 



HiEMO-PERICARDIUM. —PNEUMO-PERICARDIUM. 307 



The clinical symptoms of hydro-pericardium are only exceptionally distinct in 
the whole picture of the disease, which is filled by the underlying affection. Large 
amounts of fluid in the pericardial sac, which may collect up to a quart (a litre) or 
more, must of course impair the action of the heart, weaken the heart-beat object- 
ively, and cause an increase in the cardiac dullness. The distinction from peri- 
carditis is rendered possible by the absence of a friction-rub, but especially by 
attention to the existence of an underlying disease. In other respects the distinc- 
tion between a pericardial transudation and an effusion during life is not always 
easy. 

The prognosis and treatment depend wholly upon the nature of the underlying 
disease. Only exceptionally do we need to remove a transudation by puncture 
when it is very large. 



CHAPTER III. 

HiEMO-PERICARDIUM. 

{Blood in the Pericardial Sac.) 

In rare cases haemorrhages occur into the pericardial sac. The source of the 
haemorrhage is most frequently an aneurism of the aorta, which perforates into 
the pericardium. Other causes of haemorrhage are the bursting of aneurisms of 
the coronary arteries and rupture of the heart. The latter has been seen after 
injuries, and also as a result of cardiac aneurism and the cicatricial formations in 
myocarditis (see myocarditis). Finally, direct injuries to the heart, especially 
bullet- wounds, may also cause haemorrhages into the pericardial sac. 

In most cases death occurs in a few moments, from compression of the heart, 
when a haemo-pericardium comes on. Hence the amount of blood poured out into 
the pericardial sac is usually not very considerable. Only in the cases where the 
blood oozes out more slowly can a great distention of the pericardial sac be reached. 
The diagnosis is only rarely possible. With regard to treatment we can merely 
note that, in some traumatic cases, the aspiration of the blood has been performed 
with success. 



CHAPTER IV. 

PNEUMOPERICARDIUM. 

{Air in the Pericardial Sac.) 

The entrance of air or gas into the pericardial sac has been observed in rare 
cases, apart from external wounds, as a result of the perforation of a pyopneumo- 
thorax, or of some other suppurating process in organs that contain air. Thus 
cases are known where the rupture into the pericardial sac comes from the 
oesophagus, as in cancer ; from the stomach, in cancer or ulcer ; or from the lungs, 
in tubercular or gangrenous cavities. Since the agents of inflammation enter the 
pericardium along with the air, a purulent pericarditis almost always develops, 
beside the pneumo-pericardium, or it may rarely be simply a sero-fibrinous peri- 
carditis. 

The most characteristic and striking sign of pneumo-pericardium is the pres- 
ence of a metallic sound, due to the movements of the heart. Either the heart- 
sounds themselves, or some existing friction-rub, acquire a metallic timbre from 
the change of resonance, or splashing metallic sounds are produced in the peri- 



308 



DISEASES ' OF THE CIRCULATORY ORGANS. 



cardial sac from the movements of the air and the fluid, which may even be heard 
at a great distance from the patient. In regard to diagnosis, however, it is impor- 
tant to know that signs similar to those of metallic resonance in the heart may 
arise from the stomach, when it is drawn or pushed upward. 

In true pneumopericardium percussion gives a more or less complete absence 
of the cardiac dullness. On rod-percussion (see page 252) a metallic sound is some- 
times heard, whose pitch may vary somewhat with the phase of the heart's action. 
If fluid is also present in the pericardial sac beside the air, the dullness caused by 
this will rise on raising up the patient. 

The other symptoms of the disease and the treatment are the same as in a 
severe pericarditis. The prognosis, however, corresponding to the primary dis- 
ease, is wholly unfavorable. 



SECTION III. 
Diseases of the Vessels. 
CHAPTER I. 

ARTERIO-SOLEROSIS. 

{Endarteritis chronica deformans. Atheroma of the Vessels.) 

JEtiology. — Atheromatous degeneration of the arteries is chiefly a disease of 
advanced life, in persons over forty. It is often to be regarded, especially in old 
people, not as a disease, but as attributable to conditions of senile involution. 

Beside age there are also a number of setiological factors which favor the 
earlier occurrence and a greater extension of the atheroma. Among these are, 
first of all, chronic alcoholism ; also syphilis, gout, chronic nephritis, articular 
rheumatism, and chronic lead-poisoning. It is, however, hard to find more positive 
evidence for the connection between atheroma and the conditions mentioned, 
although the special connection between alcoholism, and perhaps syphilis, and 
arterio-sclerosis is made probable by many observations. We must mention that 
in many families there is a pronounced hereditary tendency to atheroma of the 
vessels and its results. Men are decidedly more disposed to the disease than 
women. 

Pathological Anatomy. — Atheroma is almost exclusively confined to the arte- 
ries ; only exceptionally do like processes occur in the veins. Among the arteries 
the aorta is almost always the most intensely and extensively diseased ; we also 
find disease in the iliac and femoral arteries, the brachial, radial, and ulnar, the 
coronary arteries of the heart, and the arteries of the brain. In some of the other 
arteries, however, like the gastric artery, the hepatic, and the mesenteric, we very 
rarely find atheromatous changes. 

The atheromatous process is easy to recognize macroscopically. Instead of the 
smooth internal surface of the arteries we find more or less numerous irregulari- 
ties and thickenings on the intima, which appear either more or less gelatinous 
and translucent, or dense and fibrous, or ossified as a result of calcification, in 
which case they also feel perfectly hard. In extensive calcification the whole 
artery is changed to a hard, stiff tube. In many cases we find the surface of the 
thickenings destroyed — atheromatous ulcers — and covered with masses of thrombi. 

Microscopic examination shows that the chief changes are situated in the 
intima of the arteries. This appears three or four times as thick as normal, 



ARTERIO-SCLEROSIS. 



309 



partly from the swelling of its elements and partly from the new growth of con- 
nective tissue and the deposit of round cells. In the connective-tissue cells of the 
intima, and in the endothelial cells of its surface, we usually find a marked fatty 
degeneration, to which the yellowish, translucent appearance of the surface is due. 
Finally, in the deeper layers, there is a complete breaking down of the tissue into 
a mixture of fat, detritus, and cholesterine crystals, which has given the whole 
process the name of atheroma. If this destruction extends to the surface, an 
atheromatous ulcer is formed. In other places, however, it does not reach ulcera- 
tion, but the superficial layers of the intima become sclerosed, and are finally 
changed to lamellae of bony hardness from the deposition of lime-salts. The 
atheromatous spots on the intima of the vessels often give rise to the formation of 
parietal thrombi. 

The media and adventitia of the arteries also show changes in the later stages 
of the process. Here, too, we may finally get fatty degeneration and calcification. 
In other cases, however, there is a marked atrophy of the media. 

The immediate result of the atheromatous changes is a loss of elasticity in the 
walls of the vessels. The ability to resist the blood-pressure is reduced, and this 
is why diffuse or circumscribed aneurismal dilatations of the vessels so often arise 
as a result of arterio-sclerosis (see the following chapters). 

Another result of the extensive atheromatous degeneration of the vessels is an 
increase of the resistance to the blood-current, and a consequent elevation of the 
arterial pressure. The latter is also increased by the loss of elasticity in the 
medium-sized and smaller arteries, whereby an important impelling force for the 
blood-current is lost. Hence the left ventricle is almost always hypertrophied in 
extensive arterio-sclerosis, in case the general state of the patient's nutrition is suffi- 
cient for it. 

The thickening of the intima in the smaller vessels often causes so marked a 
diminution of the blood-supply that secondary disturbances of nutrition are not 
wanting in the various organs. The lumina of the vessels may be still further nar- 
rowed, or even completely closed, by the formation of thrombi on such portions 
of the wall of the vessels as have undergone atheromatous changes. We have 
already in part learned to recognize the sequelae which necessarily arise in the 
various organs, such as indurations in the heart as a result of atheroma of the 
coronary arteries, and we will return later on to the analogous changes in some 
other organs, like cerebral softening and certain forms of contracted kidney. 

Clinical Symptoms. — In order to decide whether an arterio-sclerosis is present 
in the living subject, we are of course exclusively restricted to the examination of 
those peripheral arteries that are accessible to palpation. We must examine, first 
of all, the radial, brachial, femoral, and temporal arteries. If there is atheroma, 
we feel the hard and partly bony vessel- wall. In marked cases we have a feeling, 
especially in the radial, as if we had hold of a goose's neck. We sometimes 
notice a diffuse dilatation in the femoral arteries. In many cases the marked spiral 
form of the vessels is very striking, and it is a direct result of the loss of elasticity 
of their walls and of the increased blood-pressure. The spiral form is most fre- 
quently observed in the temporal arteries, in the brachial, and in the radial. 

Although we can often directly and certainly discover atheroma in the ves- 
sels mentioned, we must always be cautious in deciding from this that there is 
also an atheroma of the internal arteries, for the radial arteries often feel very 
rigid, while the autopsy later on shows only a little or absolutely no atheroma of 
the internal arteries. In other cases, however, we find at the autopsy marked 
atheromatous changes in the arteries of the brain, the kidneys, the heart, etc., 
although the external arteries during life felt perfectly normal. We see from 
this how hard it is to make a sure diagnosis of general arterio-sclerosis. 



310 



DISEASES OF THE CIECULATOEY OEGANS. 



It is impossible to give a uniform picture of arterio-sclerosis, since its results 
appear now chiefly in this organ, and now chiefly in that, whereby entirely dis- 
tinct types of disease may arise. Hence we must confine ourselves here only to 
mentioning briefly the most important sequelae, which demand, generally, a sepa- 
rate description. 

In the heart we find a hypertrophy of the left ventricle as a result of the 
increased resistance to the arterial circulation. This is often apparent during life 
from the strength of the apex-beat and its displacement to the left, and also from the 
extension of the area of cardiac dullness to the left. On auscultation, the increased 
tension in the aortic system is made manifest by the strength of the aortic second 
sound. The examination of the heart, however, is often rendered difficult by the 
presence of pulmonary emphysema. On the other hand, we sometimes can not 
decide how far a manifest hypertrophy of the left ventricle is due to an arterio- 
sclerosis and not to other co-existing processes, like contracted kidney. We often 
find other anatomical changes in the heart beside hypertrophy of the left ven- 
tricle. We have already spoken of the important and interesting results of 
atheroma of the coronary arteries, the formation of the so-called indurations of 
myocarditis in the heart (see page 287, et seq.). Sometimes, from an invasion of 
the aortic valves by the atheromatous process, we get an insufficiency, or much 
more rarely a stenosis of the aortic orifice. Finally, we may also mention here 
that atheroma, especially of the ascending aorta or the arch, is the commonest 
cause of the formation of aneurism of the aorta. 

We have already described the character of the peripheral arteries. The 
radial pulse is hard and tense, and the wave is either quite high, or, where the 
tube is more contracted, small. Since the wall of the vessel contracts only 
slowly, in consequence of its loss of elasticity, the radial pulse is usually sluggish — 
a pulsus tardus. This condition is also pronounced in the sphygmographic 
tracing, which shows a slow ascent, and a still slower descent, of the pulse-curve, 
and an absence of the elevation in the descending limb of the curve, due to the 
normal elasticity. The frequency of the pulse is quite different in different cases ; 
it is often rather slow as a result of sclerosis of the coronary arteries (q. v.). The 
pulse is very often irregular as a consequence of changes in the heart. We some- 
times find an abnormal delay in the radial pulse, or in the pulse in other arteries, 
in comparison with the heart-beat, from the lessened rapidity of transmission of 
the pulse-wave. 

Beside the heart, the brain is the chief place in which we observe defi- 
nite results of arterial sclerosis. The increased tendency to rupture which the 
atheromatous vessel-walls show, and the co-existing heightened blood-pressure, 
explain the comparatively frequent occurrence of cerebral haemorrhages. Cere- 
bral haemorrhages very often (always, according to some authors) result from 
little miliary aneurisms, which have formed in the atheromatous cerebral arteries. 
Atheroma is also the most frequent cause for the formation of foci of softening in 
the brain, since the arterial changes may give rise to a closure of the cerebral 
arteries both from thrombosis and embolism. We will later describe in full the 
clinical symptoms of the affections mentioned. 

In the kidneys, too, atrophic processes often develop from the diminution of 
the blood-supply by the narrowed lumina of the vessels, and they lead to a special 
form of contracted kidney. The origin of the granulated "senile kidney" is in 
large part due to atheroma of the renal arteries. 

Gangrene of the extremities may arise from a plugging of their arteries by 
thrombosis, or more rarely by embolism. The so-called "senile gangrene" almost 
always depends upon arterio-sclerosis. 

From all this it follows that the type of the disease may appear very different 



ANEURISM OF THE THORACIC AORTA. 



311 



in different cases. The symptoms in the vascular apparatus often predominate 
over all others. The heart, which is simply hypertrophied, or has undergone in 
part cicatricial degeneration, is finally paralyzed, and then all the symptoms of a 
chronic heart disease develop — dyspnoea, oedema, etc. If there is also albuminuria, 
a type of disease is produced which resembles that of contracted kidney. In other 
cases, however, the symptoms in the brain are especially manifest, either alone or 
in combination with the other symptoms mentioned. 

We must mention, however, in conclusion, that all the results of arterio- 
sclerosis mentioned may be absent for a long time or altogether. Many people 
have practically no symptoms at all from their arterio-sclerosis, and reach an 
advanced age, but we must always consider the possibility of the sudden occur- 
rence of severe symptoms, and make our prognosis accordingly. 

There is no question of a special treatment of arterio-sclerosis, since we are not 
in a position to affect the process by any remedy. In the individual case the 
treatment is directed according to the symptomatic indications resulting from the 
sequelae. Prophylaxis, by avoiding the injurious influences mentioned which are 
regarded as aetiological factors, is more important, as this may perhaps prevent, 
or at least delay, the development of the process. 



CHAPTER II. 
ANEURISM OF THE THORACIC AORTA. 

iEtiology and Pathological Anatomy.— The circumscribed dilatation of an 
artery is termed an aneurism. The cause of its formation is almost always to 
be sought in a primary disease of the vessel-wall, which causes it to yield abnor- 
mally to the blood-pressure. As we have already said in the previous chapter, it 
is chiefly arterio-sclerosis which lies at the foundation of the formation of aneu- 
risms in many cases. The same factors, therefore, which favor the origin of 
arterio-sclerosis are also mentioned in the aetiology of aneurisms. It is also 
repeatedly asserted that severe physical exertion plays a part in the aetiology of 
aneurism of the aorta. 

[The occurrence of aneurism in early middle rather than in advanced life shows 
that too much stress can be laid on atheroma as a cause. That sudden strain often 
plays an important part in the aetiology can scarcely be doubted, though the cases 
in which a perfectly healthy aorta yields locally to internal pressure must be very 
rare. It is highly probable that violent exertion tends to produce changes in the 
walls of the aorta. The far greater frequency of aneurism in the male sex is 
notable. Syphilis, gout, alcoholic excess, and lead-poisoning appear to be factors 
in some cases.] * 

The size of aneurisms of the aorta varies very much, of course, in different 
cases. They most frequently are about the size of an apple or the fist ; but in rare 
cases much larger aneurisms are observed. According to their shape we distin- 
guish the more diffuse or spindle-shaped dilatations from the saccular aneurisms 
(aneurisma diffusum sen cylindricum, aneurisma fusiforme, et aneurisma sac- 
ciforme). Intermediate forms and combinations of the different forms occur in 
manifold ways. 

We never find the wall of the aneurism, corresponding to its origin, formed of 
a normal vessel-wall. The intima almost always shows the same changes as are 
characteristic of arterio-sclerosis, only in a much higher degree. The media, too, 



312 



DISEASES OF THE CIRCULATORY ORGANS. 



is usually changed, and its muscular structure is often fatty degenerated. The 
adventitia is usually thickened by chronic inflammatory processes. The media, 
and sometimes the intima, are in many cases so much atrophied that the wall of 
the aneurism, at least in part, is formed only of the adventitia. 

In the cavity of the aneurism the blood is only partly fluid. We usually find 
it more or less full of fresh and old masses of thrombi. The oldest thrombi, which 
lie upon the wall of the aneurism, are firm, yellowish, adherent to the wall, and 
sometimes calcified. At other points the thrombi are softened and broken down. 
The most marked coagulation is usually found in the saccular aneurisms with a 
narrow entrance, because in this form of aneurism the blood is almost completely 
stagnant in the aneurismal sac. 

Aneurisms of the aorta usually have their seat in the ascending aorta, or in the 
arch. Aneurisms of the descending thoracic and of the abdominal aorta are far 
more rare. The following description refers principally to aneurisms at the begin- 
ning of the aorta. The other aneurisms will demand a brief separate description 
farther on. 

Clinical Symptoms. — The symptoms of aneurism fall into two groups. The 
first group embraces those symptoms which are directly excited by the aneurism 
itself — first of all its physical signs. The subjective sensations of the patient, 
relating directly to the aneurism, are of a very uncertain nature, and are often 
entirely absent. In other cases there is pain in the region of the aneurism, either 
only slight and pressing, or very severe and subject to paroxysmal increase. 
Sometimes, too, the patient feels the beating and pulsation of the aneurism. The 
second group of symptoms concerns the results which the aneurism produces in 
the circulatory apparatus, and by pressure on the neighboring organs. 

1. Physical Signs. — It depends entirely upon the position of an aneurism of 
the aorta whether it causes physical signs or not. Deep aneurisms, wmich nowhere 
approach the chest- wall, may of course be quite inaccessible to direct examination. 

Aneurisms of the ascending aorta, however, and of the arch, often extend so 
near to the anterior wall of the chest that they cause an abnormal pulsation. We 
feel this most frequently at the sternal end of the second right intercostal space, 
or over the upper part of the sternum. The pulsation of an aneurism of the arch 
of the aorta may sometimes be felt in the jugular vein. It often occurs a moment 
later than the systole of the heart. In many cases the pulsation is clearly double, 
analogous to the normal dicrotism of the pulse. We sometimes feel a slight sys- 
tolic thrill with the flat of the hand. In the rare aneurism of the descending 
thoracic aorta the pulsating swelling may make its appearance in the back, between 
the vertebral column and the left scapula. If the aneurism has a certain size, the 
pulsating part protrudes as a tumor. The protrusion is either merely slight, or in 
many cases it forms a large, prominent swelling. It then shows usually a marked 
pulsation, not only from below upward, but also in a lateral direction, which is 
of diagnostic significance. In large aneurisms, however, the pulsation sometimes 
is only very weak, and feels obscure, from the formation of many coagula. 

The marked prominence of large aneurisms is possible only because the cover- 
ing parts, not only the muscles and skin, but also the cartilages and bones, the 
ribs and sternum, are brought to a gradual atrophy and wasting by the persistent 
pressure. The skin over large aneurisms gradually becomes thinner and thinner, 
until finally it may even become necrotic. 

In many cases percussion gives a positive result, since the resonance over the 
aneurism is necessarily more or less dull. The dullness is usually evident in the 
upper right intercostal spaces, or the adjacent parts of the sternum. Sometimes 
it even precedes the palpable pulsation, although then its significance is usu- 
ally still very uncertain. In rare cases of aneurisms of the ascending aorta and 



ANEURISM OF THE THOEACIC AORTA. 



313 



of the arch, dullness and abnormal pulsation have been observed to the left of the 
sternum. 

Auscultation gives varying results. In some cases (probably chiefly when 
many coagula form) we hear nothing at all over the aneurism. In other cases we 
hear one or two sounds, which are usually the audible heart-sounds transmitted. 
Perhaps a systolic sound may also arise from vibration of the wall of the aneu- 
rism. In other cases, we hear a murmur over the aneurism. A dull and usually 
not very loud systolic murmur often arises from the formation of eddies in the 
aneurismal sac. If we also hear a diastolic murmur, it is almost always due to a 
co-existing insufficiency of the semilunar valves of the aorta (vide supra). 

2. Sequelae. — An aneurism of the aorta by itself probably never causes such an 
increased resistance to the blood-current as to give rise to the development of 
a hypertrophy of the left ventricle. In the quite frequent cases where hyper- 
trophy of the left side of the heart exists, it may almost always be referred to a 
co-existing insufficiency of the aortic valves, and sometimes to very extensive 
atheroma of the arteries. During life a hypertrophy of the heart may be simu- 
lated, because the heart is pushed to the left by the aneurism. 

In many cases the signs in the peripheral arteries are important. Marked ine- 
quality of the pulse in symmetrical arteries is often an especially valuable diag- 
nostic sign. Either the trunk of an efferent vessel in the neighborhood is com- 
pressed by the aneurism, or the lumen of the exit of the vessel is itself involved in 
the aneurism, and hence the opening of the vessel is distorted or contracted, or 
partly stopped by a coagulum. This readily explains why, in aneurism of the 
ascending aorta, the radial, and sometimes the carotid pulse, are plainly weaker on 
the right than on the left, as a result of implication of the trunk of the innomi- 
nate, while in aneurism of the arch or of the beginning of the descending aorta 
the opposite condition may obtain. Abnormal differences, too, in the intensity of 
the pulse in the upper and lower halves of the body may arise under some cir- 
cumstances. 

A marked delay of the pulse in the arteries arising below the aneurism is a 
symptom that is occasionally seen. Thus, we see in aneurism of the arch of the 
aorta that the left radial pulse is later than the right, and that in aneurism of the 
descending aorta the pulse in the lower extremities is later than the radial pulse. 

We see very striking signs in the veins if the large venous trunks in the tho- 
rax, the superior vena cava, or an innominate vein, are compressed by the aneu- 
rism. The veins swell in the neck, in the upper extremities, or upon the surface 
of the thorax, according to the seat of the compression. Local oedema may also 
be produced in this way. 

The respiratory organs are exposed to the pressure of aortic aneurisms in many 
ways. Compression of the lungs by large aneurisms actually contributes toward 
increasing the dyspnoea in many cases. This may be still more distressing if the 
trachea be compressed. Of the two main bronchi, the left bronchus, which lies 
beneath the arch of the aorta, is sometimes compressed, which produces the symp- 
toms of a unilateral bronchial stenosis (vide supra). The comparatively frequent 
compression of one recurrent nerve, especially the left, is also of diagnostic impor- 
tance, as it results in paralysis of one vocal cord. We refer the occasional par- 
oxysms of severe dyspnoea to a compression of the branches of the vagus, but no 
satisfactory coarse anatomical cause has been found for them. 

Very prominent symptoms sometimes arise from compression of the intercostal 
nerves or branches of the brachial plexus by the aneurism. As a result of this 
pressure, extremely severe and distressing neuralgias arise in the nerve territories 
affected, and sometimes we see motor paresis in the arm. 
« Finally, disturbances of deglutition arise in many cases from compression of the 



314 



DISEASES OF THE CIRCULATORY ORGANS. 



oesophagus. If this be falsely interpreted, it may lead to a mischievous use of the 
oesophageal sound. Cases have repeatedly occurred where perforation of the 
aneurism was caused by passing a sound into the oesophagus. Hence we must 
always remember the possibility of aneurism in practice. 

Course and Termination of the Disease— Aneurisms may remain latent for a 
long time without causing the patient any symptoms. In such cases a sudden 
perforation may lead to a speedy and unexpected death. 

In the cases which have shown the above symptoms to a greater or less 
extent for a long time, and often for years, sudden death quite frequently results 
from rupture of the aneurismal ' sac and perforation into a neighboring organ. 
In perforation into the pericardium death follows almost instantly from cessation 
of the heart's action. In perforation into the oesophagus a fatal haemorrhage 
occurs. In perforation of the aneurism into the air-passages, the trachea or 
bronchi, or into one pleural cavity, two factors, haemorrhage and suffocation 
unite in causing death. In aneurisms which gradually erode the anterior wall of 
the chest, the perforation is in rare cases external ; but here a sudden, immediately 
fatal haemorrhage rarely ensues ; much more commonly a slowly increasing 
anaemia develops as a result of repeated slight haemorrhages which may some- 
times go on for weeks. Death then ensues from the gradually increasing weakness, 
or from a final severe haemorrhage. Perforation of an aneurism into the right 
side of the heart, into the pulmonary arteries, or the vena cava, is a rare termina- 
tion. Here death does not follow at once, but severe general disturbances of the 
circulation, like dropsy, soon arise. In many of these rare cases peculiar phys- 
ical signs also appear — a venous pulse, a loud systolic murmur over the point 
of perforation, etc. 

If, in patients with aneurism of the aorta, death does not ensue from a sudden 
perforation, the general type of the disease takes a form similar to chronic heart 
disease. The aneurism, as we have said, is often also combined with aortic insuffi- 
ciency. The left ventricle gradually becomes paralyzed, and the well-known dis- 
turbances of compensation set in — increasing dyspnoea, oedema, etc. In other cases 
the patient gradually becomes duller and weaker from the distressing pain, the 
sleeplessness, and the other symptoms, and dies with the signs of increasing 
general weakness. 

Recovery from aneurism of the aorta does not occur. 

Diagnosis. — The diagnosis of aneurism of the aorta can in many cases be made 
with great ease and certainty, but in other cases it is very difficult and even 
impossible. If the direct physical signs are plain, especially if we feel an abnor- 
mal pulsation, we shall not be apt to commit an error ; but the diagnosis presents 
great difficulties in those cases where the aneurism is not accessible at all, or acces- 
sible only with great difficulty, where it merely causes indefinite symptoms, pain 
in the chest, occasional oppression, symptoms of pressure on neighboring organs, 
etc. A very stubborn intercostal neuralgia, which no remedy can remove, may 
be for a long time the only symptom, often misinterpreted, of a latent aneurism. 
The disease is often not recognized, however, because in such cases we do not gen- 
erally think of the possibility of an aneurism, and hence we neglect a careful 
examination of the heart and the arteries, and also the search for other symptoms 
of compression, like paralysis of the vocal cords ; but sometimes, even with the 
most careful examination, the diagnosis can not amount to more than a suspicion. 

The distinction between aneurism and other tumors in and about the thorax 
sometimes presents difficulties in diagnosis. Mediastinal sarcomata and abscesses, 
circumscribed empyemas, tumors arising from the sternum, or new growths in 
the lungs and bronchial glands, may all give rise to confusion. We can scarcely 
lay down any general rules for diagnosis, since the conditions differ in almost 



ANEURISM OF THE THORACIC AORTA. 



315 



every case. If we feel a swelling, its pulsation is the symptom which points most 
to an aneurism, but we must be certain that the pulsation is not merely partial, 
but that it really takes place in all directions within the. swelling- itself. We must 
also consider the auscultatory symptoms, the condition of the heart and the arte- 
ries, and also any symptoms of compression ; yet in such cases we can not always 
make a definite diagnosis. 

Treatment. — Many attempts have been made to bring about an obliteration of 
the aneurism, and thus a recovery. Although the methods of treatment aiming 
at this have obtained decisive results in the aneurisms of peripheral arteries, their 
results in aneurism of the aorta are still of a very doubtful character ; yet we are 
always justified in any given case in trying one of the methods recommended. 

Persistent compression by a pad can of course be employed only in those cases 
where the aneurism projects at one part of the chest- wall. The pressure, how- 
ever, usually causes great pain, and hence is ill borne. 

Tying the carotid, the subclavian, or both vessels, has also been repeatedly 
performed in aneurism of the arch of the aorta, sometimes with apparent success, 
but oftener without any result. 

" Acupuncture " of the aneurism (V elpeau) consists in inserting a needle or an 
iron wire into the aneurismal sac in order to excite coagulation in it by this 
means. The results obtained by it in aneurism of the aorta are not very encour- 
aging. 

Better results are reported from galvano-puncture. Two needles inserted into 
the aneurism are connected with the poles of a galvanic battery, by which a weak 
current is passed through the aneurism. Here we must regard the chemical and 
electrolytic action of the current as well as the mechanical action of the needles. 

Injections of chemical substances into the aneurismal sac, in order to produce 
coagulation, are dangerous, since the coagula caused by it may give rise to emboli. 
Hence we have abandoned making trial of liquor ferri sesquichloridi and similar 
substances. We can better recommend a trial of injections of ergotine into the 
vicinity of the sac, two to five grains (grm. O^l-O^) of the aqueous extract of 
ergot dissolved in water or glycerine, injected every day or two. This method 
was first employed with success by Langenbeck in peripheral aneurisms. Its 
action depends upon a contraction of the smooth muscles in the wall of the aneu- 
rism, caused by the ergotine. 

We can expect little action on an aneurism from the use of internal remedies, 
although favorable results have been repeatedly reported. Acetate of lead, five 
to ten grains (grm. 0*3-0 '6) a day, and iodide of potassium, half a drachm to a 
drachm (grm. 2-4) a day, are most praised. 

The symptomatic treatment of aneurism, which tries to relieve the patient's 
sufferings, and the dietetic measures prescribed, follow the generally customary 
principles. In a rupture of the aneurism externally we try to avert the fatal 
catastrophe by absolute rest, ice-bags, styptic cotton, etc. Treatment is powerless 
against internal perforations. 

[Tufnell's method, so called, which has given good results in abdominal and 
peripheral aneurisms, proves sometimes useful in palliating the symptoms and 
lengthening the course of aortic aneurism. The aim of this method is to diminish 
the force and rapidity of the circulation, and, if possible, to increase the fibrinous 
deposit. It is carried out by enforcing absolute rest in the recumbent position, 
and by limiting the amount of food, especially of liquids. About ten ounces of 
solid food and eight of liquid are allowed daily, divided into three meals.] 



316 



DISEASES OF THE CIRCULATORY ORGANS. 



CHAPTER III. 
ANEURISMS OF THE OTHER VESSELS. 

Aneurism of the Abdominal Aorta. — Its favorite seat is the vicinity of the 
cceliac axis. In many cases it may be felt through the abdominal wall as a pul- 
sating tumor, over which a systolic sound or a whirring murmur can be heard. 
The possible symptoms of compression are very numerous. The stomach, intes- 
tine, and liver (jaundice) may be implicated. Pressure of the aneurism upon the 
nerve-trunks, or even pressure on the spinal cord after gradual erosion of the 
vertebras, with consequent severe neuralgia, paralysis, etc., has been repeatedly 
observed. Death usually ensues from rupture of the aneurismal sac and internal 
haemorrhage. 

Aneurism of the trunk of the innominate is rare. Its symptoms are very 
much like those of an aneurism of the arch of the aorta. If we feel a pulsating 
tumor, it is usually situated somewhat higher up than the aneurism of the aorta, 
in the first right intercostal space, or the tumor even extends into the supra- 
clavicular fossa. In rare cases aneurisms of the subclavian and of the carotid have 
been observed. We have ourselves seen an aneurism of the internal carotid the 
size of a cherry pressing on the Gasserian ganglion, which caused an extremely 
severe trigeminal neuralgia lasting for years. 

Aneurism of the pulmonary artery may appear as a pulsating tumor in the 
second left intercostal space. It is usually impossible to distinguish it with cer- 
tainty from an aneurism of the aorta. 

We have already mentioned, in the description of pulmonary tuberculosis, the 
great importance of small aneurisms of the branches of the pulmonary artery in 
pulmonary cavities, as a frequent cause of haemorrhage. 

Aneurisms of the arteries of the brain, which are relatively most frequent in 
the basilar artery and the artery of the fissure of Sylvius (the middle cerebral 
artery), may cause severe cerebral and bulbar symptoms (see page 654). As has 
already been mentioned, miliary aneurisms of the cerebral arteries play an impor- 
tant part in the aetiology of cerebral haemorrhage (q. v.). 

The symptomatology and treatment of aneurisms of the peripheral arteries 
belong to the domain of surgery. 



CHAPTER IV. 
RUPTURE OF THE AORTA. 

A rupture of a previously healthy aorta, with fatal haemorrhage, after violent 
traumatic influences, has been seen only in a very few cases. In the majority of 
the very rare cases of rupture of the aorta we have to do with a vessel that is 
already atheromatous. In some cases a special exciting cause is present and in 
others it is absent. We once saw sudden death caused by rupture of the ascend- 
ing aorta in a young man about twenty-five, who before that seemed perfectly 
healthy. No trace of atheroma was found ; but at the point of rupture there was 
a slight protrusion and a decided thinning of the wall, which was probably con- 
genital. The formation of a so-called dissecting aneurism, which has often been 
seen in the aorta, is of anatomical interest. Here only the intima and media are 
torn. The blood burrows between them and the adventitia or between the layers 



N AERO WING OF THE AORTA. 



sir 



of the media. Most of the cases of dissecting aneurism of the aorta also result, 
like rupture of the aorta, in sudden death, but sometimes the blood-sac formed 
may exist for a long- time, and produce the same type of symptoms as ordinary 
aneurism of the aorta. 



CHAPTER V. 
NARROWING OF THE AORTA. 

Congenital narrowness of the aorta and its branches is a condition to which 
Rokitansky first, and later Virchow, have directed attention. We find this 
anomaly especially in people, mostly women, who during life have shown the 
signs of persistent chlorosis. Sometimes such people are backward in their whole 
development ; they retain a puerile habit, and show a defective development of the 
genitals. They often suffer from palpitation, faintness, and a tendency to haem- 
orrhages. In many cases the heart is also small, but in others it is dilated and 
hypertrophied. Valvular disease of the heart has been repeatedly found com- 
bined with general narrowness of the arterial system. During life the anomaly 
of the vascular system in question may sometimes be suspected, but it can never 
be recognized with certainty. 

Narrowing of the aorta at the point of insertion of the ductus arteriosus is a 
disease observed in rare cases, whose origin probably always falls in the period 
directly after birth and is associated with obliteration of the f cetal ductus arteriosus. 
Other congenital anomalies of the heart are often present at the same time. If 
the narrowing of the aorta is not very marked, it may be completely equalized by 
a secondary hypertrophy of the left ventricle and the development of a collateral 
circulation. The latter arises from a marked dilatation of the anastomoses 
between the first intercostal artery, the dorsalis scapulae, the subscapularis, and the 
transversalis colli on one side, and the lower intercostal arteries, which come off from 
the descending aorta below the narrowing, on the other. Anastomoses are also 
formed between the mammary and the superior epigastric on one side and the 
lumbar and femoral arteries on the other. During life the dilated arteries are 
prominent, in part abnormally distorted, and perceptibly pulsating, especially the 
dorsales scapulae, the subscapulars, the mammaries, and the epigastrics. In some 
cases a systolic murmur has been heard over some of these vessels. The pulse in 
the arteries of the lower extremities, the femoral and popliteal, is very weak and 
scarcely perceptible. 

In many cases the collateral circulation is so complete that the person 
affected may feel no subjective disturbance at all, and may attain an advanced 
age, but in other cases disturbances of the circulation appear sooner or later, and 
the patient finally succumbs to dropsy. Sudden death from rupture of the heart 
or of the aorta has also been observed. 



DISEASES OP THE DIGESTIVE ORGANS. 



SECTION I. 

Diseases of the Mouth, Tongue, and Salivary Glands. 

CHAPTER I. 

STOMATITIS. 

{Inflammation of the Mouth.) 

iEtiology. — Inflammation of the buccal mucous membrane is not infrequently 
the direct result of mechanical or chemical causes. As mechanical causes we 
may mention particularly the sharp edges of broken or carious teeth. Chemical 
irritation may come from highly spiced food, or from tobacco-chewing or exces- 
sive smoking. Very intense inflammation is caused by acids, alkalies, and the 
like, attacking the mucous membrane. Mercurial stomatitis is also of practical 
importance, caused by mercurial poisoning, or not infrequently by the therapeu- 
tic employment of the drug. The stomatitis attendant upon the cutting of teeth 
in children will be discussed below. 

In many instances stomatitis comes from a direct propagation of inflammation 
from neighboring parts. It thus forms a frequent complication of pharyngeal 
catarrh and less often of rhinitis. 

Infection plays an important part in the aetiology of stomatitis. The local 
inflammation may be merely part of a constitutional infectious disease, as in mea- 
sles, variola, and syphilis. Stomatitis is still more frequently a complication of 
some severe and protracted illness, where the mouth is not properly attended to 
and cleansed. The bits of food and the mucus quickly begin to decay. Great 
numbers of fungi and bacteria invade the buccal cavity, and excite inflammation 
in its mucous membrane. 

Scorbutic stomatitis will be considered under scurvy. 

Clinical History. — The usual symptoms of an inflammation of mucous mem- 
brane — namely, redness, swelling, and increased secretion — are exhibited in stoma- 
titis. The redness is usually most intense on the inside of the cheeks and on the 
gums. Indeed, we have the special name — gingivitis — for inflammation of the 
latter. The swelling is best shown by the indentations made by the teeth in the 
cheeks and the edges of the tongue. The tongue and gums are smeared with 
mucus. There is often considerable salivation. If the inflammation is more 
active, we find a purulent coating on a greater or less portion of the membrane. 
The tongue is almost always thickly coated. If we scrape off a little of the coat- 
ing and put it under the microscope, we find a great abundance of pavement epi- 
thelium, in part fatty-degenerated, pus, micrococci, the bacterium called leptothrix 
bnccalis, and remains of food. Whit© spots made up of epithelium may also be 



ULCERATIVE STOMATITIS. 



319 



formed elsewhere than on the tongue. Here and there little vesicles appear which 
burst and leave superficial ulcers. 

The local discomfort of severe stomatitis is by no means trifling". There is 
burning pain which interferes with taking food, and usually the processes of 
decomposition occasion a constant bitter or disgusting taste in the mouth, as well 
as a foul and offensive breath. 

The duration of the disease depends on the nature of the immediate cause or 
the character of the primary disorder. Usually a stomatitis which gets well in 
one or two weeks is called acute, and a more tedious attack, chronic. The chronic 
form is seen in topers and inveterate smokers. It may last for years, with the 
symptoms described above, only milder. For lingual psoriasis, vide infra. 

Treatment. — If the inflammation is considerable, the diet must be liquid. 
Sometimes cold drinks are most agreeable, sometimes lukewarm. Often the pain 
is relieved by taking from time to time a sip of iced water or a bit of ice ; but it 
may happen that the patient will prefer to rinse the mouth with lukewarm water. 
The important indication, to keep the mouth as clean and pure as possible, is best 
met by having the mouth frequently rinsed out with a one- or two-per-cent. solu- 
tion of carbolic acid, a two-per-cent. solution of chlorate of potash, or one or two 
teaspoonfuls of a one-per-cent. solution of permanganate of potash to a glass of 
water. In children who can not do this, the mouth is to be carefully washed or 
sprayed. If the gams are spongy, they should be painted with a mixture con- 
taining equal parts of tincture of myrrh and tincture of rhatany. If there are 
superficial ulcers scattered about, it is sometimes an excellent plan to touch them 
lightly with lunar caustic, to hasten their healing. 

Chronic stomatitis is often very obstinate, resisting all sorts of treatment for a 
long time. The first thing is to remove any such injurious agencies as tobacco 
or bad teeth. It is recommended to swab out the mouth with a solution of cor- 
rosive sublimate (1 to 5000), or of lunar caustic (1 to 30-50). A well-known 
household prescription is to chew bits of rhubarb. 



CHAPTER II. 

ULCERATIVE STOMATITIS. 

(Stomacace.) 

JEtiology. — By ulcerative stomatitis is meant a severe disease of the buccal 
mucous membrane, with superficial necrosis and the consequent formation of 
ulcers. The abnormal processes are not in all cases identical, and their cause may 
vary. Still, it is probable that infection is the important factor, at least in most 
cases. The disease has repeatedly been epidemic, chiefly among soldiers in bar- 
racks or on a campaign, and among the inmates of jails. It also occurs in 
children, principally at the time of the second dentition ; and in such cases, also, 
the evidence of contagion and of endemic influences is often very striking. 
Mercurial stomatitis, if severe, always assumes the form of ulcerative stomatitis. 
(For the scorbutic form see page 904.) 

Symptoms. — The disease usually attacks the gums of the lower jaw first, gradu- 
ally spreading thence to neighboring portions of the lips and cheeks. The 
tongue and palate are generally not very much affected, though often the seat of 
a simple catarrhal inflammation. 

Inspection shows that the mucous membrane in the places mentioned has a 
thick, soft, purulent coating. The gums are swollen, spongy, and red, and bleed 



320 



DISEASES OF THE DIGESTIVE OKGANS. 



easily. In severe cases the incisors become loose, and may fall out. There is 
usually profuse salivation. The lymph-glands at the angle of the lower jaw and 
on the chin are generally swollen. The breath is very offensive, poisoning the 
air of the whole room. 

The local discomfort of the patient is the same as in simple stomatitis, only 
much worse. It is very -difficult to take nourishment. In many cases there are 
marked constitutional symptoms. The patient feels very weak and languid. 
There may be moderate elevations of temperature, particularly in children. Now 
and then severe symptoms of constitutional sepsis have followed the disease. 

The course of ulcerative stomatitis is favorable in the great majority of cases. 
With good treatment and nursing, the ulcers gradually clean up, and at the end 
of one or two weeks recovery is complete. Exceptionally, the disease may be 
more chronic. The most frequent way in which recovery is delayed is that the 
disease extends to the periosteum of the lower jaw, causing necrosis of small 
portions of the bone, which must be expelled before the patient is well. 

The treatment does not differ essentially from that of the milder forms of 
stomatitis. The mouth must be still more carefully cleansed and disinfected. A 
solution of potassic chlorate (1 to 30) is the favorite mouth-wash. Some authors 
strongly recommend the simultaneous internal administration of this remedy ; 
but we must employ it cautiously in children, as it has repeatedly caused poison- 
ing. For children two or three years old we ought not to give over fifteen to 
thirty grains (grm. 1-2) in a day. 

As to prophylaxis, we should mention that all patients who are using mercury 
should employ a gargle of potassic chlorate faithfully from the beginning of 
treatment, in order to prevent the occurrence of mercurial stomatitis. If saliva- 
tion occurs, the mercury must be stopped. 



CHAPTEE III. 

APHTHiE. 

(A])ht7ious Stomatitis.) 

Aphthje is a name given by physicians to several entirely distinct things. 
Many doctors call every disease aphthae in which there are white spots upon the 
buccal mucous membrane. It is thus frequently confounded with thrush. Ger- 
man mothers often apply the same name (Schwammchen, or fungus) indifferently 
to thrush and to aphthae. 

There is a special form, known as Bednar's aphthae. In new-born children 
white patches are not infrequently found lying symmetrically on both halves of 
the hard palate near the alveolar processes, and persisting till about the third 
month. These plaques are not syphilitic, although often thought to be. They 
are probably merely due to the tongue pressing upon the thin mucous membrane 
during nursing. Generally they do no harm ; but in marantic, ill-cared-for 
children, they may develop into quite deep ulcers. In that case, repeated cauteri- 
zation with a five-per-cent. solution of argentic nitrate is required. 

The genuine aphthae are roundish spots upon the mucous membrane, grayish 
white and of small size, unless made larger by the confluence of several into one 
another. They usually have a narrow, red areola. They are most numerous on 
the edges and dorsum of the tongue and on the fraenum, but they also occur 
on the lips and cheeks. The attempt to remove the white spot with forceps 



THRUSH. 



321 



never succeeds, but does cause bleeding. In addition to the genuine aphthae 
there are almost always the signs of a common stomatitis, which may be mild or 
severe. The white spots are in part due to a thickening and opacity of the epithe- 
lium, and in part are said to be caused by the formation of a fibrinous exudation, 
which penetrates the most superficial layers of the mucous membrane. 

The disease occurs chiefly in children, and at the time of the first dentition. 
The child is usually restless, often somewhat feverish, and evidently suffers pain 
when nursing. Generally there is considerable salivation. The lymph-glands 
may be a little enlarged. Herpetiform vesicles may appear on the lips. The dis- 
ease is not rare in adults. Many individuals seem especially liable to it, and very 
frequently have little, white, and often very painful spots here and there on the 
tongue or elsewhere in the mouth. 

The prognosis is always favorable. There is usually complete recovery in a 
week or two. The treatment of children consists in carefully washing out the 
mouth with cold water, and in administering potassic chlorate. Of a mixture 
consisting of three parts of potassic chlorate, twenty of syrup, and a hundred of 
water, we may give a dessertspoonful every two hours. If the spots do not dis- 
appear, we can paint them with a five-per-cent. solution of sulphate of zinc, or a 
solution of borax (1 to 30). If some of the places are especially painful, particu- 
larly in adults, we may touch them with lunar caustic, when they usually are 
soon cured. 

In conclusion, as to aetiology, infection is a not unlikely cause, if we consider 
that small epidemics or endemics have repeatedly occurred. Lately attention has 
been called to the possibility that the milk of cows, suffering from hoof-and- 
mouth disease, may be a source of infection. That this may happen seems 
indubitable ; but how frequently it occurs, future observations must determine. 



CHAPTER IV. 

THRUSH. 

(Soor. Muguei.) 

iEtiology. — Weak and artificially nourished children are particularly liable to 
this disease ; but it also attacks adults who are suffering from phthisis, carcinoma, 
and severe typhoid or typhus fever. In it, grayish-white deposits are developed 
upon the buccal and pharyngeal mucous membrane. The microscope shows these 
collections to be fungi ; there are a multitude of oval spores, or coniclia, and a 
tangled mass of long mycelium threads. Until lately the fungus of thrush was 
called oidium albicans, and was held to be identical with the oidium lactis found 
in sour milk. More recent investigations, however, made by Grawitz, have 
rendered it very probable that the thrush fungus is of the budding variety. 
Grawitz regards it as the mycoderma vini, Rees as the saccharomyces albicans. 
The mycoclerma vini is the fungus present in the acetic fermentation of alcohol 
when alcoholic drinks " sour." At any rate, the thrush fungus is widely dissemi- 
nated, for thrush is often seen. 

Symptoms.— The mucous membrane of the tongue, cheeks, and soft palate is 
usually somewhat red and swollen. Upon it we see at first small white spots, 
which may gradually spread. Microscopic investigations have shown that the 
fungus develops first in the middle layers of the epithelium. From this starting- 
point it grows not only upward, but also downward into the mucous membrane. 
21 



322 



DISEASES OF THE DIGESTIVE ORGANS. 



If the growth is abundant, it is easy to scrape off the upper layers, and make a 
diagnosis by aid of the microscope. In exaggerated cases the growth may even 
extend from the pharynx into the upper part of the oesophagus and the entrance 
of the larynx. But we never find thrush in the larynx itself, or the nostrils, or 
the stomach — briefly, in no place where there is cylindrical epithelium. 

As a rule, thrush is accompanied by a more or less severe stomatitis. The fluids 
of the mouth have an acid reaction. Nursing, or chewing, and swallowing, are 
painful. Still, it is a question whether the stomatitis is due to the fungus, or 
whether it prepares the territory for the fungus to settle in. Nursing infants, who 
suffer from thrush, often have diarrhoea or marasmus at the same time, which 
latter affections are more probably the cause than the result of the thrush. If 
vigorous and healthy sucklings are attacked by thrush, the disease is usually 
quite harmless, quickly vanishing if proper cleanliness is maintained. In sickly 
children, particularly if bottle-fed, the appearance of the disease is very ominous. 
In adults, thrush is seldom seen except when there is great general prostration ; 
and it is therefore, to a certain extent, an unfavorable symptom. 

Treatment. — To prevent the development of thrush in children, the mouth 
must, if possible, be wiped out, each time they drink, with a cloth wet in cold water ; 
and if adults are very ill, they require equal attention in this regard. As soon as 
we see the first traces of the disease, we should touch the parts attacked with a 
brush wet in aqueous solution of borax (1 to 30) or. of sodic carbonate (1 to 20). 
Honey should not be added to the borax solution, as is often unwisely done. If 
the thrush has once got a vigorous start in the mouth of marantic children or of 
adults suffering from an incurable disease, it must be confessed that we often fail 
to check its growth. 



CHAPTER V. 

GLOSSITIS. 

{Parenchymatous Inflammation of the Tongue!) 

Inflammation of the true lingual parenchyma is rare, although the tongue's 
mucous surface is frequently involved in the various diseases of the mouth. 

1. Acute parenchymatous glossitis is the name given to an inflammatory infil- 
tration of the whole or a part of the tongue, usually ending in abscess. The most 
frequent cause is the sting of a bee or wasp, or it may follow burns or severe cau- 
terization. In the rare instances where it is apparently spontaneous, it is probable 
that some little wound has afforded ingress to the inflammatory poison. 

The symptoms of acute glossitis are very violent in the severer cases. The 
tongue is enormously swollen, so as sometimes to protrude from the mouth. It 
has a thick, soft, purulent coating, and often presents excoriations and ulcerations. 
The subjective symptoms are very disagreeable. The patient has violent pain. 
Talking and eating are almost impossible. There is usually catarrhal inflamma- 
tion of the rest of the mouth. The cervical lymphatic glands are swollen. The 
salivation is profuse and very annoying. In many cases the tongue swells so 
much as to cause dyspnoea and more or less suffocation. There is usually fever. 

Treatment consists in the employment of ice, which the patient should keep 
constantly in his mouth, if possible. Very great relief follows deep scarification 
in a few places, where the swelling is greatest. As soon as fluctuation is obtained, 
we must give exit to the pus. This is usually followed by a rapid abatement of 



NOMA. 



323 



the discomfort, and complete recovery. It is the exception that the increasing 
dyspnoea necessitates tracheotomy. 

2. Glossitis Dissecans. — This is a chronic disease, of rare occurrence and 
unknown aetiology. It causes the gradual development, upon the surface of the 
tongue, of a number of deep fissures and indentations, giving the organ an uneven 
and ragged look. The pain is due to the frequent presence of excoriations and 
ulcers in these fissures. 

The trouble is not intrinsically dangerous, nor does it need special treatment. 
We should prescribe cleanliness and the use of some disinfectant mouth-wash. 
Ulcers, if present, must be touched with lunar caustic. 

3. Lingual Psoriasis. Leucoplacia. (Tylosis ; Ichthyosis Unguceet oris.) — This, 
again, is a superficial disease, the aetiology of which is unknown. It consists in 
localized hyperplasias of the epithelium of the tongue, sometimes conjoined with 
similar spots upon the cheeks and lips. Usually the tongue gets to look like a 
map ("lingua geographical). The disease generally lasts years, but causes dis- 
comfort only when extraordinarily severe. Still, it may cause a hypochondriac 
endless anxiety, especially if he takes it to be syphilitic. 

This last statement applies still better to a peculiar disease allied to psoriasis. 
It is called leucoplacia, and affects the mucous membrane of the tongue and mouth. 
Usually it causes the appearance, on the lateral borders of the tongue, of dull- 
whitish spots, which have the look of scars, and are generally somewhat notched. 
As a rule, the cheeks display at the same time similar white spots, which are evi- 
dently due merely to thickening of the epithelium. Certain spots may disappear, 
but are sure to be replaced by others, so that, as far as has yet been observed, the 
disease must be regarded as incurable. Still, it is not of great importance, for, in 
many cases, the local discomfort is very slight. If the indentations along the 
sides of the tongue become cracked or ulcerated, then there may be great pain. 
The cause of leucoplacia is not yet known. It certainly is not syphilitic, although 
the disease is said to be especially prone to attack those who have at some former 
time been infected with syphilis. This certainly does not apply to all cases. Nor 
is excessive smoking connected with the disease ; we have seen leucoplacia in 
women. Treatment is, as we have said, usually unsuccessful. Still, thorough 
cleanliness and good care of the mouth may avert any great discomfort. We may 
try the effect of painting the spots with a five-per-cent. solution of chromic acid. 
The chief importance of knowing the disease is to prevent our confounding it with 
syphilitic affections, and thus to save the patient needless apprehension and need- 
less mercurialization. 



CHAPTER VI. 

NOMA. 

( Water- Cancer. Cancrum oris.) 

Noma is a gangrene of the cheek, apparently of spontaneous origin, and attack- 
ing chiefly feeble and sickly children. The disease is rare. It may be primary, but 
is usually a sequel of severe diseases, like measles, scarlet fever, typhus and typhoid 
fevers, and pneumonia. Now and then it has been observed in adults. A priori, 
it is extremely probable that noma is due to some parasitic micro-organism ; but 
the matter has not yet been minutely investigated. It deserves mention, that 
noma is said to occur with much greater relative frequency in moist regions along 
the coast— for example, in Holland— than among us in Germany. 



324 



DISEASES OF THE DIGESTIVE OEGANS. 



The disease begins, without any evident occasion, in an insignificant spot of 
gangrene on the inner surface of the cheek — that is, in the mucous membrane. It 
is usually situated near the corner of the mouth. Externally, the parts are soon 
swollen by collateral oedema, and the whole cheek gradually becomes hard and 
infiltrated. At first, all we see upon the mucous membrane is a dirty-greenish 
spot, not much larger than a silver dime ; but soon the whole cheek and the 
neighboring parts are one mass of gangrene. Bits of dead tissue come away, and 
foul-smelling ichor flows continuously into the mouth. The collateral oedema 
may finally pervade that entire half of the face. The neighboring lymph-glands 
are always greatly swollen. 

This condition is almost always accompanied by fever, often reaching or 
exceeding 104° (40° C). The general health may indeed for a time be astonish- 
ingly little affected ; but gradually prostration comes on, or even general sepsis 
develops, with fever, stupor, and delirium. Frequently lobular pneumonia, which 
may have a gangrenous character, is produced by the inhalation of sloughing bits 
of tissue ; and often the ichor, being swallowed, excites violent and offensive 
diarrhoea. The local discomfort is not really very considerable in most cases, 
compared to the severity of the disease. There may even be no pain felt what- 
ever. 

The prognosis is almost always fatal. Death sometimes occurs suddenly from 
collapse. Sometimes it comes at the end of three or four weeks, from a gradual 
sinking of the bodily powers. Recovery has been seen in only a few cases : there 
is a line of demarkation formed, the sloughs come away, and, a slow convalescence 
follows, leaving extensive and usually very disfiguring scars behind. 

Treatment must have for its chief object to check further extension of the 
gangrene, by removing all parts that are already destroyed. Local cauterization 
with concentrated hydrochloric acid, or fuming nitric acid, or lunar caustic, or 
chloride of iron, is usually futile. It is probably the best way to remove all the 
gangrenous portion by means of Paquelin's thermo-cautery. At least in the early 
stages of noma we may hope something from this method of treatment ; but if the 
case is far advanced, we can hardly expect to accomplish much. 

We should also disinfect the mouth as thoroughly as possible. The most 
efficient means is to syringe it out with solutions of salicylic or carbolic acids, or 
permanganate of potash, and to dust it with iodoform. We should do our best to 
maintain the patient's strength. 



CHAPTER VII. 

PAROTITIS. 

(Mumps.) 

Parotitis, or inflammation of the parotid gland, appears not only as a peculiar, 
primary, infectious disease, usually epidemic, but also as a secondary complication 
of numerous other severe diseases. These two forms should be considered sepa- 
rately. 

1. Idiopathic, Primary Parotitis (Epidemic Mumps). 

Etiology. — The disease occurs in epidemics that, although not very frequent, 
may be quite extensive. Here and there a sporadic case is seen. Children and 
young adults are most liable to it. Nursing infants enjoy a marked immunity, as 
well as elderly persons. Males are much oftener attacked than females. 

There can be no doubt that mumps is a specific infectious disease ; but we pos- 



PAROTITIS. 



325 



sess no minute knowledge of the infectious agent. Still, it is natural to suppose 
that the infectious matter reaches the gland by way of Steno's duct. 

Numerous observations support the view that the disease is directly contagious. 
The period of incubation seems to vary. On the average, it is about fourteen 
days. 

Clinical History. — There may be a prodromal stage of one or two days, with 
mild feverish symptoms. The disease itself begins with swelling of one parotid 
gland. The swelling is directly below and in front of the lobe of the ear, which 
is gradually pushed upward. In the next few days the swelling rapidly 
increases, and it and the collateral oedema of the cheek and floor of the mouth 
may become very considerable. The face is much distorted, but often makes a 
very comical impression, especially as everybody knows how harmless the disease 
is. In many cases the other gland also swells later. 

An abscess hardly ever forms in genuine mumps ; nor does the swelling often 
become very hard. Generally it has a somewhat doughy consistence. The cor- 
resx3onding portion of skin is usually pale and shiny. 

The local discomfort is moderate in most cases. There is difficulty in chewing, 
swallowing, and talking. Often quite a severe stomatitis develops, with foul 
breath. 

There is usually fever, but seldom over 102° (39° C). Only occasionally has 
there been a case with grave typhoidal symptoms. 

Complications. — It is not rare for men to have a swollen testicle, which may be 
quite painful, but usually subsides in a few days. Double orchitis is rare. In 
boys this complication is much rarer than in adults. Some observers have men- 
tioned analogous swellings of the female genitals and mammas, but this is 
doubtful. 

It should be mentioned that Penzoldt observed cases with swelling of the sub- 
lingual and submaxillary glands during an epidemic of mumps, the parotid 
escaping. 

The prognosis of epidemic parotitis is, as we have said, almost always favora- 
able. The trouble seldom lasts more than a week or ten days, when the swelling 
goes down, and the patient completely recovers. 

The diagnosis is easy. The only thing to exclude is swelling of the lymph- 
glands, and they never have exactly the same location as the parotid. 

Special treatment is hardly necessary. Children should be kept in bed. 
Usually some salve, like vaseline, is applied to lessen the feeling of tension. If 
resolution is tedious, we may paint the swelling with iodoform collodion (1-15), 
or with tincture of iodine ; or we may prescribe iodoform ointment (1-15). If 
there is orchitis, the testicle must be elevated, as by a suspensory bandage. If the 
pain and swelling are marked, an ice-bag should be applied. 

2. Secondary Parotitis, or "Metastatic Parotitis." — This secondary form may 
be a complication of any grave disease. In most cases it is due to inflammatory 
agents generated by decomposition of matters in the mouth, which agents reach the 
gland through Steno's duct. It was formerly the universal belief that the infec- 
tion was metastatic, being conveyed through the blood-vessels ; but it is doubtful 
whether this does occur. It is probable that the pyaemic form is in many instances 
thus produced. Secondary parotitis is most frequently observed in typhus and 
typhoid fevers. It also is seen occasionally in all other severe acute diseases, and 
in phthisis, and carcinoma. 

The parotid gland swells, just as in the primary disease. It is, however, much 
oftener of excessive size, and in the majority of cases suppurates. If one has an 
opportunity to make an autopsy on such a case of secondary parotitis in its early 
stages, the cross-section of the swollen gland presents a large number of rather 



326 



DISEASES OF THE DIGESTIVE OEGANS. 



small discrete abscesses. These finally unite to form one larger abscess, which 
usually discharges outward, or into the external auditory meatus. Sometimes 
the parotid suffers from gangrenous inflammation, and there is extensive slough- 
ing. If such a case finally gets well, still, as a rule, some permanent injuries have 
been inflicted : there is facial paralysis, due to destruction of the facial nerve, or 
deafness, caused by an extension of the inflammation to the middle ear. 

The treatment of secondary parotitis is that of any phlegmonous inflammation. 
We may at first try to scatter the swelling by ice or iodoform ointment, but this 
usually fails. As soon as fluctuation is detected, the spot must be incised, and a 
drainage-tube inserted. The prognosis depends chiefly on the nature and course 
of the original disease. 



CHAPTER Yin. 
ANGINA LUDOVICI. 

The name angina Ludovici is applied to a rather rare phlegmonous inflam- 
mation of the floor of the mouth. Its starting place seems to be the submaxillary 
gland, at least in most cases. It may be primary, or a complication of other severe 
acute diseases. 

Angina Ludovici usually begins with swelling in the neighborhood of the sub- 
maxillary gland. The swelling rapidly increases, and comes to involve the whole 
floor of the mouth and the anterior surface of the throat. It causes great discom- 
fort. Talking, chewing, and swallowing are almost impossible. There is usually 
fever, and in many cases we even find the symptoms of general sepsis. There 
may be great dyspnoea, due either to compression of the larynx or to oedema of 
the glottis. The final result in some cases is an extensive sloughing of the soft 
parts. This has the special name of cynanche gangrenosa. In other cases an 
abscess forms, and points outward or into the oral cavity. The swelling is some- 
times, though seldom, reabsorbed. 

The prognosis should always be guarded, for severe constitutional symptoms 
and a fatal ending are not infrequently seen, particularly if the patient has a 
weakly constitution. There may also be repeated exacerbations and relapses. 

Treatment. — At the commencement of the disease we may make the attempt, 
in suitable cases, to check the process by local depletion and by ice ; but, as soon 
as suppuration or gangrene begins, the case becomes a surgical one. Now and 
then the threatening asphyxia demands tracheotomy. 



CHAPTER IX. 

ANOMALIES OF DENTITION. 

{Difficult Dentition.) 

The processes of dentition play so important a role in the disorders of child- 
hood that we feel obliged to discuss the subject, at least briefly. 

The first appearance of any of the milk-teeth usually takes place when the 
child is seven to nine months old. It may, however, occur either earlier or later 
than this period. As a rule, the two lower central incisors are cut first. Then the 
upper central incisors appear, a few weeks later, and next the lateral incisors of 
the upper jaw. In the beginning of the second year come the lower lateral inci- 



ANOMALIES OF DENTITION. 



327 





sors, and almost simultaneously the four anterior molars. The four canine, or 
" eye " and " stomach " teeth, are cut in the second half of the second year ; and last 
of all comes the eruption of the four posterior molars. The first dentition is, there- 
fore, completed by the end of the second or in the beginning' of the third year, 
with the development of all the twenty milk-teeth. The accompanying diagram 
(Fig. 31), after Vogel, represents the order in which the separate teeth appear. In 
the fifth or sixth year the milk-teeth begin to be replaced by the permanent teeth 
of the second dentition. "Trouble with 

teething," however, almost invariably refers ^rj^ fllUlJIj y 
to anomalies of the first dentition. 

Noticeable delay in teething is frequent 
in weakly, and particularly in rachitic chil- 
dren. In such cases, sometimes, all the teeth 

are not cut till the end of the third year. ^^QADILQDj^ 

On the other hand, it sometimes happens Fig 3J 

that certain teeth appear every year, or even 

are present at birth. If such an abnormally early tooth is only loosely inserted 
in the gums, it should be removed with the forceps ; for it interferes with nursing, 
and injures the opposing surface of the mouth. But if the tooth is firm in its 
place, we let it be. 

During the eruption of the teeth there is in every child considerable redness of 
the mucous membrane and an increased flow of saliva. The child evidently feels 
an itching in the mouth, and therefore a constant desire to bite something. This 
simple catarrh is sometimes accompanied by a slight rise in temperature. Occa- 
sionally there is a severe stomatitis, with which thrush may be associated. 
These troubles should be treated as already described. 

In consequence of the salivation, and the large amount of saliva which is swal- 
lowed, in which the various processes of decomposition are apt to develop, we 
often see gastro-intestinal diseases in teething children. In most children a tem- 
porary and mild diarrhoea occurs. We should be particularly careful at this 
period about the child's nourishment and in treating any marked gastro-intestinal 
symptoms. Experience shows also that teething children are unusually liable to 
simple or even capillary bronchitis, and catarrhal pneumonia. 

Nervous disturbances are often referred to dentition. The most important 
symptom of this kind is eclampsia. The attacks are sometimes called " teething- 
convulsions." Although the laity go too far in ascribing all sorts of nervous dis- 
orders to teething, still experienced specialists do recognize the possibility of such 
an origin for many cases. Some of the convulsions may in fact be regarded as 
reflex (vide infra the chapter on the convulsions of children, page 737). 

When the upper canines, or '* eye-teeth," are being cut, there is sometimes a 
unilateral purulent conjunctivitis, which is perhaps to be explained as an exten- 
sion of the inflammation by way of the antrum of Highmore and the nostrils. 

Eczema and other cutaneous eruptions have been often ascribed to dentition ; 
whether justly, is doubtful. 

There is of course no special treatment for difficult dentition ; and the various 
disturbances which it may indirectly produce are to be treated on general princi- 
ples. 



328 



DISEASES OF THE DIGESTIVE ORGANS. 



SECTION II. 

Diseases of the Soft Palate, Tonsils, Pharynx, and Naso- 
pharynx. 

CHAPTER I. 

SORE THROAT. 

(Tonsillitis. Angina.) 

iEtiology. — Acute inflammation of the soft palate and tonsils, in its various 
forms, is one of the commonest of diseases. Almost everybody has had personal 
experience with it. It is chiefly a disease of early life, being infrequent after the 
thirty-fifth year. Individual predisposition to it varies greatly. There are per- 
sons who have one or more attacks almost every year, while with others attacks 
are rare and insignificant. In many instances exciting causes have evidently 
been potent. Chief among these is catching cold ; the sufferer had got wet feet, 
or had been talking in a damp, cold atmosphere. Most cases, therefore, occur in 
cool weather, although now and then attacks may occur in the hottest days of 
summer. Again, direct injuries of the pharynx may produce the disease, e. g., 
the smoky atmosphere of inns, combined with loud talking or shouting ; the 
inspiration of poisonous vapors ; cauterization of the mucous membrane with 
concentrated acids, alkalies, and other chemical agents ; and burns. 

[Especially when tonsillitis recurs in an individual, or attacks several members 
of the same household about the came time, it is well to have the drainage care- 
fully examined. The precise connection between bad drainage and sore throats 
we do not know, but that they are often connected there seems to be no doubt.] 

Frequently the inflammation is due to extension from neighboring parts, as 
in coryza, laryngitis, and stomatitis. In many cases both affections are simul- 
taneous results of one common cause. 

Finally, sore throat may be a symptom of many acute infectious diseases, 
such as scarlet fever, measles, small-pox, and erysipelas. It is also very probable 
that at least some of the primary cases of sore throat are to be regarded as acute 
infectious diseases ; but this has not yet been really proved. 

To distinguish between an inflammation of the soft palate by itself and affec- 
tion of the tonsils is not practicable. In most cases the tonsils are the stronghold 
of the disease ; less often we find the inflammation limited to the soft palate. 

Clinical History. — The most important subjective symptom of sore throat, and 
that by which it is usually first recognized, is the difficult and painful deglutition. 
The pam is sometimes manifest before any objective changes are to be seen. It 
may in a severe case be very violent and distressing. The pain has a " darting " 
character, or sometimes is " burning " ; and it is most acute whenever the patient 
swallows, although in well-marked cases it seldom entirely intermits. Swallow- 
ing is not only painful, but it is laborious ; it requires more than usual effort and 
time. The patient feels constantly as if he had to swallow a big lump. This sen- 
sation is worse if the tonsils are swollen. It is a matter of experience that not 
infrequently an " empty " swallowing hurts more than swallowing a liquid or 
some half -solid substance. 

Talking is also difficult. Every word may be painful, so that the patient 
expresses his wishes as briefly as possible. Even in a mild case, speaking for any 
length of time will produce a burning pain in the throat. The impaired mobility 



SORE THROAT. 



329 



of the soft palate often prevents the complete cutting off of the nasal passages in 
talking, so that the voice has a nasal twang ; and often it sounds as if the patient 
were talking with his mouth full : he has the " voice of sore throat." 

Further local discomfort results from the mucus and saliva collecting in the 
mouth. Salivation is not infrequent, probably as a result of the stomatitis usually 
present. In other cases the patient complains that his mouth feels dry and sticky. 
Frequently there is a persistent bad taste in the mouth, and the breath is dis- 
agreeable. 

With these local disturbances more or less severe constitutional symptoms are 
almost always conjoined. Indeed, these latter may begin a day or two earlier 
than the local symptoms. The patient is indisposed, languid, has anorexia and 
headache. The general disturbance may be surprisingly great in comparison 
with the slight objective changes in the tonsils. 

There is fever in most of the well-marked cases ; it may even be quite high. 
Temperatures of 103° or 104° (39 'S 0 -^ 0 C), or even higher, are not rare. Sore 
throat can not be said to have one particular type of fever. Usually the fever 
appears rather abruptly, remains high for several days, with an occasional slight 
interruption, and then falls with equal abruptness to normal again. 

The entire attack usually lasts only a few days, seldom more than a week. 
Even where a person is quite ill for several days, convalescence is almost always 
rapid and complete, that is, if the patient has a good constitution. 

Special complications are very infrequent, except that the neighboring parts — 
the larynx, mouth, and throat — are not seldom involved. Herpes labialis is quite 
frequent. Beyond this there is nothing to mention. 

Various Forms of Sore Throat. 

The symptoms thus far mentioned are much the same in all cases of sore 
throat, varying only in intensity and duration. But the objective changes to be 
observed in the soft palate and tonsils are noticeably different in different cases. 
Whether the aetiology differs also we have no certain information. In some 
instances it seems probable that it does. 

We shall distinguish five chief varieties of acute sore throat. Transitional 
forms are, however, by no means rare. Genuine diphtheria, which is a specific, 
acute, infectious disease, and has already been discussed, does not need to be 
brought up again here. 

1. Catarrhal Sore Throat {Simple Catarrhal Inflammation of the Mucous 
Membrane of the Soft Palate). — There is a more or less vivid reddening of the 
mucous membrane, either uniform or in patches. The swelling is most marked 
in the pillars of the fauces and the uvula. The surface of the tonsils is likewise 
reddened ; their size may be somewhat increased or remain unchanged. The 
mucous membrane of the palate and uvula may be covered here and there with a 
thin layer of muco-pus, which can easily be wiped off. The tonsils may present 
small, superficial erosions, scattered about. These little ulcers are apt to lie at the 
openings of the follicles. The small " blisters " which are often seen on the 
mucous membrane of the soft palate may be caused in various ways. Either they 
are mucous glands or solitary follicles, swollen ; or, rarely, they are real vesicles 
filled with a clear fluid and produced by a raising up of the epithelium. The cer- 
vical lymph-glands are usually but slightly swollen, if at all. 

This is the common and mildest form of sore throat. It may be over in a day 
or two. In other instances, however, it causes considerable local and general 
discomfort. The disease seldom lasts longer than five to eight days. 

2. Follicular Tonsillitis.— In this form there is not only more or less catarrhal 
inflammation of the soft palate, but a decided swelling of one or both tonsils. 



330 



DISEASES OF THE DIGESTIVE ORGANS. 



On the reddened surface of these swollen bodies are whitish-yellow spots, varying 
in number from two or three to ten or more, and corresponding to the follicles. 
These spots are often seen to be plugs projecting from the openings of the folli- 
cles. It is usually easy to press out the pasty contents of the follicle, represented 
by the white speck, with a spatula. The microscope shows it to consist of numer- 
ous epithelial cells and pus-corpuscles, bacteria, and detritus, and sometimes there 
are also crystals of the fat acids and cholesterine. The pus-corpuscles may so 
predominate that we may have small follicular abscesses, which, on being opened, 
leave superficial ulcers behind. The parenchyma of the tonsil is swollen with a 
serous and cellular infiltration, increasing the bulk of the part. The trouble is 
usually bilateral, though often more marked and extensive on one side than on 
the other. In the severer cases the cervical lymph-glands are swollen. 

The clinical symptoms do not differ essentially from those of the other forms. 
The attack may be mild or severe. Usually the contents of the follicles are dis- 
charged after a few days, and the tonsils become normal again. Yet the con- 
tents may be retained some time, and become calcified. It is not a rare thing to 
find such plugs in the tonsils of those who are subject to sore throat. Timid and 
hypochondriacal individuals are sometimes badly frightened by expectorating 
these old chalky plugs, which they believe to be " tubercles " ! 

3. Tonsillar Abscess {Parenchymatous Sore Throat). — In this form the swell- 
ing of the tonsils is the most striking symptom. They may be more than twice 
their natural size. The anterior pillars of the fauces are pushed forward, and 
become convex. The swelling extends so far toward the median line that the 
tonsil touches the uvula ; or, if the affection is bilateral, the two tonsils press 
against each other, grasping the uvula between them, or pushing it forward. 
The soft palate is very much reddened, particularly at first. Its surface is usually 
thickly covered with mucus. If this be wiped off, the mucous membrane is seen 
to have a moist, cedematous luster. The mucous membrane of the tonsils not 
infrequently suffers a superficial necrosis. Follicular and parenchymatous ton- 
sillitis are often combined. 

In well-marked cases of abscess the local discomfort is usually great. The 
patient is in a pitiable condition : he can neither talk, nor swallow, nor gargle. 
The few words which he painfully utters have in an extreme degree the nasal 
quality of the "voice of sore throat." 

In the milder cases the trouble seldom lasts but a few days before the swell- 
ing goes down and the discomfort and usually rather high fever gradually abate. 
In other cases, however, a tonsillar abscess forms, usually on only one side. 
The mucous membrane bulges out more and more in one spot ; fluctuation is 
detected ; and, finally, the abscess breaks. With the discharge of the pus the 
pain is relieved very rapidly, or it may vanish at once. The rest of the tonsil 
soon regains its former size, and in a few days the patient is well. Relapses are 
possible, but rare. 

Parenchymatous, or (as it is called) phlegmonous sore throat, in which the soft 
palate and not the tonsil is chiefly affected, is infrequent. Its usual cause is some 
severe external injury, like burns, and cauterizations with concentrated acids or 
alkalies. The swelling extends deep down into the submucous tissue. The uvula 
may have the diameter of one's finger. There is intense hypersemia. Sometimes 
there are haemorrhages into the mucous membrane : this is called hemorrhagic 
sore throat.* 



* Another form with the same name occurs where there is violent tonsillitis with necrosis or gan- 
grene. There is also a necrotic, hseinorrhagic sore throat accompanying scurvy and analogous dis- 
eases. 



SORE THROAT. 



331 



There are also a peri-tonsillar and a retro-tonsillar abscess, which from a clin- 
ical standpoint are not essentially different from the more common form. They 
are almost always unilateral, and are due to a suppurative inflammation of the 
peri-tonsillar connective tissue, lying between the tonsil and one of the pillars of 
the fauces, usually the anterior one. 

4. Necrotic Tonsillitis, or Necrotic Sore Throat. — In this form the tonsils are 
chiefly affected. The pillars of the fauces and the uvula are but slightly affected 
with simple catarrhal inflammation. The tonsils are, as a rule, moderately swol- 
len, seldom attaining great size. The mucous membrane covering them presents 
a whitish or grayish- white discoloration, often quite extensive, and most marked 
on the side toward the uvula. These spots are often erroneously said to be a 
white " coating " ; but a more careful investigation shows that there is in reality 
a necrosis. The process may be superficial ; sometimes it reaches quite deeply 
into the structure of the mucous membrane. It is not possible to pull off this 
white matter, as one can loosen croupous membranes, although little bits may 
perhaps be scratched off with a spatula or a pair of forceps. These particles are 
found, on microscopic examination, to be made up merely of detritus, bacteria, epi- 
thelium, and pus-corpuscles. The necrosis is almost invariably confined to the 
tonsils, and a sharp boundary-line separates it from the reddened and inflamed 
pillars of the fauces. After a few days the slough may come away, leaving 
behind an ulcer, which, though usually shallow, has sometimes a considerable 
depth. This generally cleans up rapidly. In severe cases, however, the floor of 
the ulcer consists for a number of days of a dirty necrotic material, which comes 
away only gradually. The worst cases may be properly called " gangrenous ton- 
sillitis." 

Necrotic tonsillitis is almost always attended by considerable fever and marked 
constitutional disturbance. Children particularly seem very ill in the first days 
of the attack. The cervical glands are usually swollen, but seldom as much so as 
in genuine diphtheria. 

Despite the rather ominous commencement, the disease does not last much 
longer than the other forms of sore throat. It seldom continues more than five 
to eight days before a speedy convalescence begins. 

The necrotic tonsillitis is distinguished from the follicular form by the greater 
area of the white or grayish-white spots. Still it should be particularly noted 
that sometimes combinations of these two varieties, or transitional forms, occur. 

iETlOLOGY. — In our opinion, necrotic tonsillitis is in many instances an entirely 
different disease from genuine diphtheria. On the other hand, our experience in 
the last epidemic of diphtheria in this city taught us that in all probability mild 
cases of genuine diphtheria of the tonsils do occur, and that these objectively 
resemble necrotic tonsillitis. This is the only way to explain what other physi- 
cians as well as ourselves have often observed — namely, that necrotic tonsillitis 
appears not infrequently in families at the same time with severe cases of genuine 
diphtheria. Besides, these cases of necrotic tonsillitis are sometimes followed by 
the characteristic " diphtheritic " paralysis. 

5. Benign Croupous Sore Throat— This is probably in many cases, like necrotic 
tonsillitis, merely the mildest variety of specific diphtheria. Still it is possible 
that the inflammation may sometimes have a different aetiology. However this 
may be, the clinical fact is of great practical importance that there is a mild form 
of genuine croupous sore throat, which has a favorable prognosis and has no 
tendency to produce diphtheritic ulcers or to invade the larynx. 

The disease is frequent in children, but it also occurs in adults. It begins with 
fever, constitutional disturbance, and difficulty in swallowing. Inspection shows 
membranous deposits, which are usually at first of a brilliant white color. They 



332 



DISEASES OF THE DIGESTIVE OEGANS. 



generally begin on the tonsils, but spread to the pillars of the fauces, and less 
often to the uvula. Sometimes quite large strips of the membrane can be pulled 
off with forceps, particularly if the edges are already somewhat free. They are 
exactly similar to the croupous membranes of genuine diphtheria, and are shown 
by the microscope to consist of a fibrinous net- work holding in its meshes red 
blood-corpuscles and a still larger number of white blood-corpuscles. All the rest 
of the mucous membrane covering the soft palate is much reddened, and the ton- 
sils are usually considerably swollen. The cervical lymph-glands are also almost 
always swollen, though never to the degree seen in severe cases of genuine diph- 
theria. 

The prognosis is, as we have said, always favorable. The membranes come 
away after a few days ; the symptoms of inflammation and fever abate. We have 
never seen nephritis as a complication. On the other hand, the disease may now 
and then be followed by paralysis of the soft palate, and possibly of other parts. 

Combinations of croupous sore throat with follicular and parenchymatous 
tonsillitis occur. 

[The reader will observe that the author distinctly admits the frequent impos- 
sibility of distinguishing between his necrotic and croupous forms of sore throat 
and diphtheria. It is furthermore stated that the follicular form occurs in com- 
bination with either or both of the necrotic and croupous forms, the vague nature 
of which is thus apparent. 

A membrane or membraniform layer which is not confined to the tonsils, or 
which is seen on the soft palate or pillars of the fauces alone, should be regarded 
with great suspicion. A few days' isolation can do no harm in such a case, and 
may save bitter regrets. 

Similar deposits limited to the tonsils consist not infrequently of follicular 
secretion which has coalesced ; careful examination will show the follicular 
origin in these cases. 

A protest should be entered against the use of the term "diphtheritic sore 
throat," so often applied to severe simple inflammations as well as to mild or 
doubtful cases of diphtheria. A case is either one of diphtheria or it is not. It 
is our duty neither to excite needless alarm nor to encourage a false security. In 
doubtful cases the only safe way is frankly to express the doubt and prepare for 
the worse alternative.] 

Diagnosis. — It is never very difficult to recognize a sore throat, and a little 
practice makes it easy in most cases to decide what particular variety is present, if 
we examine the objective changes carefully. It is very important in practice to 
distinguish diphtheria from the benign forms of inflammation. Follicular and 
necrotic tonsillitis are very frequently mistaken for diphtheria — an error which 
explains the success of a large number of remedies said to cure diphtheria. Many 
physicians call every case of sore throat, where there is anything white to be seen, 
" diphtheria." Certainty in diagnosis of genuine diphtheria can only be gained by 
practice ; no description, however complete, can take the place of personal observa- 
tion. It may be a help to remember that in both follicular and necrotic tonsillitis 
the white spots are usually limited to the tonsils, while in croupous sore throat 
the deposits are generally from the very first also situated upon the pillars of the 
fauces and the uvula. The white spots of the follicular variety can generally be 
recognized by their arrangement. The plugs are seen projecting from the folli- 
cles. In necrotic sore throat there is never a separable croupous membrane with 
its characteristic histological structure, but there is simply a superficial necrosis of 
the mucous membrane and parenchyma. In doubtful cases the condition of the 
cervical lymph-glands is not unimportant ; as a rule, they are much more affected 
in diphtheria than in the benign cases. It is impossible to distinguish with 



CHRONIC HYPERTROPHY OF THE TONSILS. 333 



certainty between simple (non-specific ?) croupous sore throat and diphtheria, 
although here too the local limits of the process often make the diagnosis proba- 
ble from the start. As a rule, however, further observation of the case will alone 
decide which we have. We should therefore give a guarded prognosis in doubt- 
ful cases, particularly with children. 

Treatment. — These troubles run so favorable a course that active treatment is 
very seldom needed. The gargle usually prescribed generally gives the patient 
more discomfort than relief. The most common prescriptions are : Solutions of 
potassic chlorate (5-10:300), of alum (5-10:500), or of borax (10:300) ; salt 
and water ; and weak solutions of carbolic acid or of permanganate of potash. To 
paint the parts is a useless and now almost obsolete proceeding. Inhalations of 
spray are better, with alum, tannin, or carbolized water. It is beneficial to put a 
cold wet compress around the throat. Children must be kept in bed, and adults 
are generally forced to go to bed, if the constitutional symptoms are well marked. 

In parenchymatous tonsillitis, ice will sometimes alleviate the pain. Often, 
however, the patient can not bear it. If there is evident fluctuation, we can make 
an incision with a spear-pointed bistoury, after guarding a portion of the blade 
with sticking plaster. Great relief follows ; and, even if there is no abscess, scari- 
fication of the tonsils, if they are excessively swollen, usually lessens the pain. 
The operation causes little discomfort. 

As to prophylaxis, it should be borne in mind that, in case of necrotic or croup- 
ous tonsillitis, the possibility of diphtheritic trouble demands consideration ; chil- 
dren in particular should not come near the patient. We may add that if a person 
is subject to sore throat, he can lessen his liability to attacks by hardening his skin 
through the use of cold baths. 



CHAPTER II. 
CHRONIC HYPERTROPHY OF THE TONSILS. 

Chronic hypertrophy of the tonsils occurs not only in those who have had 
repeated attacks of tonsillitis, but also in cases where no occasion for it can be 
found. Even in childhood there may be well-marked hypertrophy, which must 
be due to a congenital predisposition. 

The condition is at once revealed by inspection. There may be no signs what- 
ever of any acute or chronic inflammation, or there may be an accompanying 
chronic pharyngitis. The tonsils bulge out in two great lumps. They may be so 
large as to touch the uvula on each side. Histologically, there is a genuine 
hypertrophy of the organ — that is, an increase of all its component tissues. 

In many cases, where the swelling is moderate, there is no discomfort. The 
possessor of the tonsils is not aware that they are enlarged. In other cases the 
hypertrophy proves of clinical importance, inasmuch as all forms of sore throat 
are found to occur more frequently if the tonsils are enlarged, and to cause more 
trouble when they do appear. The hypertrophied organs may also be the seat of 
a chronic catarrh, which by extension gives rise to chronic nasal catarrh, catarrh 
of the Eustachian tubes, or hoarseness. 

If the hypertrophy is considerable, the local discomfort may be quite marked. 
Swallowing is rendered difficult, if not painful. Frequently there is evident 
dyspnoea. The patient has to breathe through his mouth, and sometimes when 
asleep snores and snorts in a way to frighten one. Children are particularly apt 
to suffer in this way. Many instances of pavor nocturnus, or " night terrors," 



334 



DISEASES OF THE DIGESTIVE ORGANS. 



in children are referable to this cause. We have already mentioned that cases of 
bronchial asthma sometimes seem to be connected with hypertrophy of the tonsils 
(see page 157). 

Treatment. — The attempt to reduce the enlargement by applying lunar caustic, 
tincture of iodine, etc., usually fails. If there is much distress, if the patient is 
subject to frequent sore throats, or if the hypertrophy of the tonsils keeps up a 
chronic nasal or pharyngeal catarrh, then the simplest remedy is to remove the 
tonsils. The operation is free from any danger. The extirpation can be accom- 
plished either with the tonsillotome or with scissors and forceps. The latter way 
is the simpler, and is almost equally easy. 



CHAPTER III. 
CHRONIC PHARYNGITIS. 

iEtiology. — It is not practicable to distinguish between chronic catarrh of the 
soft palate and of the pharynx, for, as a rule, the two are combined. Sometimes 
the condition is the result of repeated acute attacks ; sometimes — and probably 
oftenest — it is due to persistent, injurious, local influences. A large number 
of cases originate in bad habits, or in abuse incident to certain vocations. Exam- 
ples are seen in smokers, drunkards, singers, preachers, teachers, and men who 
work out-doors. In talking and singing, the soft palate is strained ; or the dis- 
ease is excited by breathing cold or impure air, or by such chemical irritants as 
alcohol or tobacco. The general passive congestion due to cardiac disease or pul- 
monary emphysema may sometimes promote the development, or prolong the 
existence, of a chronic pharyngitis. 

Symptoms. — The local discomfort is often slight. The patient gets used to it, 
and does not mind it, except when there is some exacerbation. It becomes a more 
important matter if the calling of the patient is interfered with, as in a preacher, 
singer, or teacher. 

Deglutition is seldom impaired. There is often, however, a constant feeling of 
dryness, or burning, or scratching in the throat. The patient has to clear his 
throat frequently, and often acquires a short, sudden cough, which may be dry. 
The uvula becomes so long that its tip rests on the tongue or the posterior wall 
of the pharynx ; and this gives rise to a peculiar and disagreeable sensation of 
tickling. All these uncomfortable feelings are temporarily increased if anything 
affects the throat unfavorably ; and they are generally at their worst on rising in 
the morning, apparently because the mucous membrane has become dry, or a col- 
lection of tough mucus has formed during the night. Every one knows how 
drunkards have to hem and cough mornings, so that often they almost strangle or 
vomit. 

On inspection, we generally find the mucous membrane reddened. Very 
often a number of dilated and tortuous veins are visible both on the soft palate 
and in the back of the throat. Of equal frequency is the appearance of numerous 
small gray projections, corresponding to swollen follicles or hypertrophied mucous 
glands. This is called granular pharyngitis. Small follicular ulcers are not 
infrequent. Exceptionally there are more extensive catarrhal ulcers. The 
mucous membrane of the posterior wall of the pharynx may present patches of 
opaque or thickened epithelium, giving the surface a grayish-white appearance. 

Frequently chronic pharyngitis is combined with chronic laryngitis, evidenced 



CHRONIC PHARYNGITIS. 



335 



by hoarseness ; or with posterior nasal catarrh, or catarrh of the Eustachian tube, 
producing deafness and ringing in the ears. 

Varieties of Chronic Pharyngitis. 

1. Chronic Catarrh of the Naso-pharynx, or Chronic Posterior Nasal Catarrh.— 

This has the same aetiology as the ordinary form. It is practically important 
because the nose and ear are frequently involved. 

The anatomical changes are essentially those already depicted under chronic 
pharyngitis. The region involved can not be seen by direct inspection, so that 
accuracy in diagnosis requires the use of a nasal speculum (see particulars in the 
works mentioned on page 113). The ordinary examination of the throat may reveal 
a condition which is quite characteristic of posterior nasal catarrh : a collection 
of muco-pus, or of firmly adherent dry crusts, rests upon the posterior wall of the 
pharynx, and can be seen to extend upward toward the naso-pharynx. 

The local discomfort is somewhat similar to that experienced in chronic 
pharyngitis. There is a scratchy feeling, or a feeling as if there were a foreign 
body in the back of the throat, accompanied by a constant desire to blow the nose, 
hawk or cough. Dried and decomposing secretion often causes extremely foul 
breath. There is often also vertigo, and occipital headache. 

In many cases the nostrils are stopped up. The posterior opening of the nos- 
trils is closed in part by the swelling and hypertrophy of the mucous membrane, 
and in part by the accumulated secretions. The patient, therefore, usually has to 
breathe through the mouth. The ear is frequently involved. The catarrh 
extends into the Eustachian tubes and the tympanic cavity, or the opening of the 
tubes is occluded with the secretions. For a detailed consideration of the deaf- 
ness, tinnitus, etc., thus produced, consult works on otology. 

2. Pharyngitis Sicca, or "Dry, Atrophic Catarrh of the Throat and Naso- 
pharynx." — This name is applied to an atrophy of the mucous membrane, which 
sometimes is apparently spontaneous and sometimes is a sequel of chronic pharyn- 
gitis. The whole mucous membrane of the pharynx and the naso-pharynx (seen 
with the rhinoscope) seems pale, smooth, and perfectly dry, and has a peculiar 
luster, as if varnished. Here and there tortuous veins project from the general 
anaemic surface. 

This condition may not cause any symptoms, but, in many cases, the patient 
suffers constantly and considerably. The chief trouble is a feeling of dryness in 
the throat, rendering deglutition difficult or even painful. 

If an opportunity is afforded to examine the mucous membrane microscopic- 
ally, it will be found that the atrophy involves all the elements of the tissue, 
though the follicles and mucous glands suffer most. 

The disease is most frequent in the elderly. It may be associated with a uni- 
versal cachexia. 

3. Hypertrophic Catarrh of the Pharynx and Naso-pharynx.— An opposite 
condition to atrophy may be developed in the mucous membrane, as a sequel to 
chronic catarrh. The membrane becomes thickened, swollen, and sometimes is 
actually beset with polypoid elevations. This condition is particularly frequent 
in the naso-pharynx. Here Kolliker's pharyngeal tonsil takes a chief share in the 
hypertrophy. 

The symptoms are analogous to those of the simple chronic catarrh. Of course, 
the sensations due to obstruction of the choanae and of the Eustachian tubes are 
often very strongly pronounced. 

An accurate diagnosis requires rhinoscopy. Positive results are also often ob- 
tained by palpation. The index-finger, being passed backward and bent upward, can 
touch the protuberances and the enlarged pharyngeal tonsil in the naso-pharynx. 



336 



DISEASES OF THE DIGESTIVE ORGANS. 



Prognosis. — The prognosis in all forms of chronic pharyngeal catarrh should 
be somewhat guarded, for all severe cases are very obstinate and can seldom be 
permanently cured. Success may be depended upon only in cases where all unfa- 
vorable influences can be completely removed. We may afford great relief ; but 
there is a persistent tendency to acute exacerbations and to relapses long after- 
ward. 

Treatment. — Many of the milder cases never apply to a physician. The patient 
uses some domestic remedy or gargle, or becomes so accustomed to the disagree- 
able sensations that he does not consider it necessary to do anything in particular 
about it. 

The treatment of a well-developed case requires great patience and persistence 
on the part of all concerned. If there is some underlying disease, such as pulmo- 
nary or cardiac disease, that must be treated. All exciting causes must be avoided. 
Energetic local treatment is also indispensable. This has been greatly elaborated 
by specialists, and for the many details we must refer to their writings ; but the 
following remarks will meet the requirements of ordinary practice : 

Gargles are seldom satisfactory, for they never reach farther than the soft 
palate. Inhalations are better ; we can use solutions of alum or tannin, or, in 
mild cases, of common salt. Still more efficient is the painting of the entire sur- 
face of the pharynx with some concentrated solution. The physician usually has 
to perform this, although some patients learn to do it for themselves. Proper 
solutions are : Argentic nitrate, five or ten per cent. ; tannin, eight to twenty per 
cent. ; tincture of iodine, either pure or diluted ; or iodized glycerine, composed of 
pure iodine, parts 15 ; iodide of potassium, 5 ; glycerine, 500. These applications 
must reach all the diseased surface. If the naso-pharynx is involved, the brush 
must therefore be bent upward, to reach that region. For this a mirror may be 
needed. It is very important to make the applications to the mucous membrane 
itself, freed from any interposing secretions. 

In the treatment of chronic posterior nasal catarrh the nasal douche (vide Dis- 
eases of the Nose) plays an important part. It should be used two or three times 
a day. It not only removes the collected secretions, but is a means of making 
local applications. The instrument is merely a fountain-syringe. The nozzle 
must be of a size to fill the nostril completely. The force of the current should 
always be moderate, and the patient's head should be sharply flexed forward. 
The fluid used — the best is a one-per-cent. solution of sodic chloride or bicarbonate 
— must have about the temperature of the body. Other medicated solutions must 
be very weak, such as sulphate of zinc, 1 to 1000. 

The insufflation of powders into the throat can be made through any small 
glass tube, three to six times a week. Alum or tannin may be used, either pure 
or mixed with equal parts of pulvis gummosus [P. G. , made of gum-arabic, three 
parts ; licorice-root, two parts ; and sugar, one part]. For the naso-pharynx, a 
bent tube of glass or hard rubber is to be introduced through the mouth. There 
are numerous " insufflators " to be had at the instrument-makers. 

Many baths enjoy a great reputation for the cure of chronic pharyngitis. 
Beside Ems, there are Reichenhall, Kreuznach, Salzungen, the cold sulphur 
springs, such as Weilbach, and many others. Good results are also achieved in 
Kissingen and Marienbad, if these places are favorable to the patient's general 
constitution. 

In pharyngitis sicca, the nasal douche with a one-per-cent. salt solution is to 
be recommended. It is sometimes also beneficial to paint the parts with solution 
of argentic nitrate, iodized glycerine, etc. Many irritating influences which do 
harm in common pharyngitis seem sometimes actually to benefit this form — such 
as smoking and taking snuff. 



RETROPHARYNGEAL ABSCESS. 



337 



The treatment of the hypertrophic forms of pharyngitis is the same as of the 
ordinary chronic form. The repeated application of lunar caustic is of impor- 
tance, either in solution or solid. Lately, Voltolini, Michel, and other specialists 
have had very good results from destroying or removing the hypertrophied 
portions by the galvano-cautery. 



CHAPTER IV. 

RETROPHARYNGEAL ABSCESS. 

Retropharyngeal abscess is formed by a suppurative inflammation of the 
connective tissue lying between the posterior wall of the pharynx and the spinal 
column. It is a serious event, although a rare one. If unrecognized, it proves 
fatal in many instances, while, if a correct and timely diagnosis is made, the 
patient can usually be easily cured. It is commonest in childhood, and before 
the second year. It almost always appears as a primary, acute disease, without 
any special cause being evident. Probably the agents which excite the inflamma- 
tion penetrate into the tissue from the pharynx. The idea that the inflammation 
originates in the small lymphatic glands which lie in front of the vertebras lacks 
proof as yet. 

The disease attacks not only weakly children, but those who have been per- 
fectly healthy and vigorous. The child grows restless and fretful, and does not 
nurse well. Apparently, deglutition soon becomes painful, but one can not be 
certain about this except in older children. Generally, the respiration quickly 
takes on a peculiar stertorous character, particularly during sleep. Mucus 
collects in the mouth and throat. Upon swallowing, there is often regurgitation 
through the mouth or nose, or some of the food gets into the windpipe and causes 
violent coughing. The lymph-glands of the jaws are usually somewhat swollen, 
and the neighboring parts may seem slightly oedematous. After a week or two 
the dyspnoea gradually increases. Respiration becomes more and more laborious, 
with loud rattling, and the signs of stenosis. The jugular veins become distended, 
the lips cyanotic, and portions of the thorax are retracted during inspiration. 
The voice is feeble, and may be hoarse and indistinct. 

The correct interpretation of these symptoms, which are common to various 
disorders, requires a careful examination of the throat. It must be confessed that 
this has its difficulties in an infant. Still, we can sometimes see distinctly a swell- 
ing in the posterior wall of the pharynx. This may be either in the median line 
or on one side. All doubt is removed by digital examination, in making which, 
however, we must insert a wedge between the teeth, to avoid being bitten. The 
finger detects fluctuation. 

The diagnosis once established, the abscess must be opened at once. We 
should not delay, even if the dyspnoea has not yet become extreme. To use the 
finger-nail for the purpose, as has been recommended, is permissible only in an 
emergency. As a rule, incision is made with a bistoury, of which all but the 
point is guarded with sticking-plaster. The left index-finger is placed upon the 
abscess, and used as a guide. Meanwhile, the child's head is kept upright, and, as 
soon as the cut is made, bent over forward. The pus pours out in abundance. It 
is advisable to syringe out the mouth repeatedly with lukewarm water. The 
threatening symptoms vanish almost instantly upon the escape of the pus. 
Exceptionally, the abscess refills and requires a second incision. 

If the trouble is not correctly diagnosticated, or if the abscess is not opened 
22 



338 



DISEASES OF THE DIGESTIVE ORGANS. 



promptly, the patient may suffocate. Or the abscess may burst spontaneously ; 
then there is either speedy recovery, or asphyxia from the pus filling the larynx. 
In some instances, where a retropharyngeal abscess has not been properly treated, 
the pus has gravitated far down into the neck and posterior mediastinum. The 
recognition and incision of the abscess may prove very difficult if from the start 
it is situated lower down in the throat than usual. 

Analogous to this acute idiopathic abscess of which we have been speaking is 
the chronic abscess due to caries of the cervical vertebrae. This should not be 
opened unless there is danger of asphyxia. 

Retropharyngeal abscesses sometimes occur in pyaemia or other severe acute 
infectious diseases, but have hardly any interest except to the pathologist.* 



SECTION III. 
Diseases of the (Esophagus. 
CHAPTER I. 

INFLAMMATION AND ULCER OF THE (ESOPHAGUS. 

^Etiology and Pathology. — The various forms of oesophageal inflammation and 
ulceration are not of very great clinical importance. The processes are seldom of 
a severe grade, or, if so, they are generally a part of some complicated disease, to 
which they seldom contribute prominent symptoms. Very likely the milder forms 
of inflammation occur frequently ; but the symptoms are hardly ever character- 
istic. 

A simple catarrhal inflammation of the oesophageal mucous membrane may 
be caused by swallowing substances which are injurious mechanically, chemi- 
cally, or from their temperature. It may also occur in the general infectious 
diseases, such as typhoid and typhus fevers, and the acute exanthemata. Any 
inflammation of neighboring tissues may extend into the oesophagus. Chronic 
catarrh is seen in heart disease, from the passive congestion. It is also found in 
the vicinity of other chronic oesophageal diseases, particularly cancers and diver- 
ticula (vide infra). 

The acute catarrh is distinguished by not having the usual increase of secre- 
tion. The epithelium grows spongy, as a rule, and is cast off more rapidly than 
usual, so as to suggest the name of a desquamative catarrh. It is in only a few 
cases that the scanty mucous glands become swollen and look like papules upon 
the surface of the membrane ; this form is called follicular catarrh. In limited 
areas the desquamation may be complete, giving rise to small catarrhal erosions. 
Likewise, the swollen follicles may break down into small follicular ulcers. 

In chronic catarrh there is a moderate increase in the secretion of mucus, and 
a marked thickening of the epithelium. In very protracted cases actual papillo- 
mata may finally be formed. In some cases ulcers are seen. 

Croupous and diphtheritic inflammations of the oesophagus are very rare. We 
have already said that the specific pharyngeal diphtheria frequently extends into 
the larynx, but only exceptionally into the gullet. Still, we have ourselves seen 
in a child a stricture in the upper third of the oesophagus, which was said to have 



* Tuberculosis of the pharynx is spoken of in the chapter on pulmonary tuberculosis, page 210, 
New growths in the mouth or pharynx belong to the domain of surgery. 



DILATATION OF THE OESOPHAGUS. 



339 



been a result of a severe attack of diphtheria. Isolated cases of diphtheritic oeso- 
phagitis have also been seen in connection with severe infectious diseases, such as 
typhus, typhoid, small-pox, cholera, pyaemia, and pulmonary tuberculosis, as well 
as in the course of Bright's disease and cancer. In variola it is not rare for 
pocks to appear upon the oesophageal mucous membrane. 

A purulent, phlegmonous oesophagitis now and then attacks the submucous 
layer. It may be either diffuse or circumscribed. The mucous membrane is dis- 
sected up from the muscular layer by the pus, and pushed inward, so as to dimin- 
ish the lumen of the oesophagus more or less. Most of the cases end by the dis- 
charge of matter into the tube, when complete recovery may ensue. If the mucous 
membrane, however, has been extensively undermined, Zenker states that a Assure- 
like cavity may be left, even after healing has taken place. Its walls grow smooth, 
and finally acquire a layer of fresh epithelium. 

Purulent oesophagitis is caused either by the presence of foreign bodies in the 
oesophagus, or by purulent inflammation in neighboring parts, as in glandular 
abscess, vertebral abscess, or laryngeal perichondritis. It has now and then 
resulted from the action of concentrated acids and the like upon the mucous 
membrane. 

The action of corrosive poisons (corrosive oesophagitis) is to cause necrosis 
and destruction of the tissues, which in its turn produces the inflammation. 
The inner surface of the oesophagus is converted into a rotten, hemorrhagic, 
sloughing mass, of a dirty gray or almost black color. The muscular layer itself 
may be partly destroyed. If death does not occur speedily, the necrosed portions 
come away, leaving extensive purulent ulcers behind. These, if they heal at all, 
cause large cicatrices and stenosis. 

Symptoms. — The milder cases, as we have stated, produce almost no distinctive 
symptoms. Possibly there may be pain along the oesophagus, or at some one point 
in it, during deglutition. In a more severe case the pain may be great ; but the 
other symptoms are usually too grave for this to excite special attention. Labo- 
rious deglutition, and the feeling as if the food were inclined to stick in the throat, 
result from implication of the muscular layer. A diagnosis of the particular form 
of oesophagitis is attainable only when the aetiology guides us to it. 

Treatment must be purely symptomatic. No solid food should be taken. The 
pain is to be allayed by bits of ice, or by morphine. 



CHAPTER II. 
DILATATION OF THE CESOPHAGUS. 

1. Diffuse Dilatation. 

Diffuse, spindle-shaped dilatation of the oesophagus is observed as a result of 
stricture of the cardiac orifice. At first the muscular coat hypertrophies as the 
orifice contracts, and is able to overcome the obstruction, so that there is no dila- 
tation ; but as soon as the muscles are paralyzed, and food collects behind the 
stricture, the dilatation begins and keeps on increasing. The ectasis is greatest at 
the lower end of the tube, as is natural from its mode of origin, and gradually 
diminishes upward. 

There have been a very few well-substantiated instances of this diffuse spindle- 
shaped dilatation, without any demonstrable stenosis of the cardiac orifice. Their 
cause is unknown. Sometimes the walls of the oesophagus may have been ren- 



34:0 



DISEASES OF THE DIGESTIVE ORGANS. 



dered more yielding and less contractile by a precedent inflammation or other 
disorder. In other cases, some chance bend or distortion of the lower end of the 
oesophagus may have produced a mechanical obstruction. In some cases the excit- 
ing cause is said to be a blow on the chest, or the lifting of a heavy weight. 

The symptom of this condition, when well developed, is a chronic difficulty in 
deglutition, lasting perhaps for years. The patient himself feels that most of the 
food he eats does not reach the stomach, but lodges higher up. Usually the food 
is soon afterward vomited, or rather gulped up. When there is stenosis of the 
cardiac orifice, the explanation of these symptoms is easy. It is much harder 
to explain the almost equal dysphagia where there is dilatation without stenosis. 
Probably its chief factor is muscular paralysis. Sometimes a localized bulging of 
the wall causes the food to collect in that spot, and thus to obstruct the lumen. 
As is to be expected, the partial or complete hindrance to the ingestion of food 
results in marasmus. 

If there is stenosis, it can easily be detected with the oesophageal sound, and 
all the symptoms thus explained. In the rare cases, however, of diffuse dilata- 
tion without stenosis, the use of the sound does not give us so much information. 
If the instrument passes readily into the stomach, we may safely exclude strict- 
ure ; but, in one case of our own, we made an erroneous diagnosis of a diverticu- 
lum, because the sound sometimes glided readily into the stomach, and sometimes 
could not be passed. A pocket must have been formed at the lower end of the 
dilated tube, in which the sound caught. 

The treatment is directed chiefly to the satisfactory nourishment of the patient ; 
for the oesophageal trouble itself is dangerous only as it prevents the taking of 
food and leads to starvation. We do not speak of the initial lesion, if there be 
one, which causes the dilatation. If nourishment can be given through a stomach- 
tube, the patient almost invariably shows a rapid improvement, which lasts as 
long as the artificial feeding can be kept up. If, however, any cause prevents the 
introduction of the tube, we must resort either to nutrient enemata (vide infra) — 
and these will not support the system indefinitely — or we must make a gastric 
fistula. In the latter case the prognosis depends on the success of the operation 
and the nature of the original lesion. 

2. Diverticula. 

iEtiology and Pathology. — Circumscribed pouches in the wall of the oesopha- 
gus are termed diverticula. They are divided into two essentially distinct varie- 
ties, according to their mode of origin. Zenker has given them the names of 
pressure and traction diverticula. 

The diverticulum due to pressure is extremely rare. It is caused by pressure 
upon the mucous membrane from within, by which some abnormally weak spot 
is forced outward. All cases that have been carefully examined thus far have 
shown that, histologically, the wall of the diverticulum is not the distended, but 
otherwise unchanged wall of the oesophagus, but is composed exclusively of the 
mucous membrane and the thickened submucous coat. We are therefore obliged 
to suppose that the mucous membrane is pushed out like a hernia through some 
gap in the muscular coat. It is only about the neck of the diverticulum that any 
muscular fibers are found. 

The original factor, therefore, in the occurrence of a pressure diverticulum is 
apparently to be sought in some circumscribed lesion of the muscular coat. As a 
result of several observations, it is established that a foreign body, sticking in the 
throat, may separate some of the muscular fibers and push the mucous membrane 
through the gap thus formed. Or a severe injury leads to a trifling rupture of 
the muscular coat, and then the food, as it is being swallowed, presses out the 



DILATATION OF THE (ESOPHAGUS. 



341 



mucous membrane at this weakened spot. There are still many other cases where 
the true origin of the diverticulum remains obscure. 

As soon, however, as the formation of the pouch has once begun, there are 
plenty of influences to make it grow larger. Each successive bit of food, as it 
glides by, presses upon this yielding and inelastic spot. Gradually a little sac is 
formed, in which bits of food lodge. These exercise a constant pressure upon the 
walls of the pouch, and by their weight drag it bodily downward. The larger the 
pouch, the more it holds, and consequently the more it grows. Thus a pressure 
diverticulum of the smallest size originally may gradually attain to a diameter of 
four inches or more. The general shape of the diverticulum may approach the 
hemispherical, or it may be more cylindrical or pear-shaped. 

It is remarkable that, with very rare exceptions, these pressure diverticula are 
always situated at the beginning of the oesophagus, or rather between it and 
the pharynx, and almost invariably affect the posterior wall. The pouch hangs, 
therefore, in front of the spinal column. It pushes out through the lowest fibers 
of the inferior constrictor of the pharynx ; and the feebleness of this muscle is 
apparently a potent factor in determining the precise point of origin. 

The cases thus far seen have been almost all in men, and at a rather advanced 
age. A few cases have occurred in children. 

Traction diverticula are much more common, but in most instances have little 
interest except for the pathologist. They are not infrequently found unexpectedly 
at the autopsy. Rokitansky and later Zenker have given explanations of their 
occurrence : some tissue, which has formed adhesions to the oesophagus, contracts 
and gradually pulls out the oesophageal wall in the shape of a funnel. Bronchial 
glands are apt to be the seat of the contractile change. These glands are situated 
near the bifurcation of the trachea, and accordingly the traction diverticula occur 
oftenest at this level. There may be two or three in one subject. They are rarely 
over a third of an inch in depth. From within, the mucous membrane, much 
wrinkled transversely, is seen to be drawn toward the apex of the diverticulum. 
The wall of the latter consists either of the mucous membrane alone, bulging out 
like a hernia, or of the mucous membrane covered by the muscular layer. Inas- 
much as children quite often suffer from suppuration and caseation of bronchial 
glands, with subsequent shrinkage, we see why traction diverticula are frequent 
in children. 

Clinical History. — The large pressure diverticula always cause grave symptoms, 
for they obstruct more and more each day the passage of food. At first there is 
scarcely any disturbance. Gradually, however, deglutition is impeded. A por- 
tion of the food lodges in the pouch and is either wholly or in part regurgitated, 
though perhaps not immediately. Decomposition is apt to take place in the con- 
tents of the diverticulum, giving rise to f oulness of the breath and to nausea. The 
danger reaches its climax when the distended sac presses sidewise upon the 
oesophagus and closes its lumen, so that no food reaches the stomach. After 
protracted strangling and vomiting, the material may be in part ejected, and the 
patient enabled once more to swallow something. 

Of course the symptoms in individual cases depend upon the mechanical con- 
ditions present, and may vary greatly. Patients contrive all sorts of manipula- 
tions, by which they manage to get at least some portion of their food down. Such 
individuals may maintain a tolerable degree of nutrition for years, although they 
scarcely ever are in a normal condition. But at last some cause or other renders 
the amount of food ingested inadequate ; whereupon a rapidly progressive maras- 
mus sets in, and the patient will inevitably starve to death, unless some relief is 
afforded. 

The most valuable objective evidence in these cases is gained by the use of the 



342 



DISEASES OF THE DIGESTIVE ORGANS. 



oesophageal sound. If the sound enters the sac, its passage is impeded. If it 
happens to slip by the mouth of the diverticulum, it glides readily into the 
stomach. This varying result may sometimes be obtained at one sitting by 
repeated trials, and is of the greatest importance in making the diagnosis. 

In some instances where the sac was large, a tumor in the neck has been 
observed at one side of the trachea, appearing after eating and disappearing when 
the sac emptied itself. Symptoms due to compression of the recurrent and 
phrenic nerves and of the blood-vessels have been noticed in some cases. 

Auscultation of the oesophagus during the act of swallowing has been practiced ; 
and of late, attempts have been made to examine it with a speculum. "Whether 
these methods of investigation will prove valuable for diagnosticating diverticula, 
experience must determine. 

The traction diverticula are usually of no clinical importance. They do not 
affect deglutition at all, and their size is too limited to permit any great accumu- 
lation of food in them. There is but one way in which they are dangerous : the 
apex of the funnel may undergo ulceration and perforation. A foreign body, like 
some bit of food, produces necrosis of the wall, by what is probably at first a purely 
mechanical irritation. The tissue ulcerates ; and then the inflammation may 
gradually progress till it causes a severe and usually fatal illness. The most fre- 
quent event is perforation into a bronchus, followed by the aspiration of food and 
pulmonary gangrene. Or the perforation takes place into the pleural cavity, 
exciting an ichorous empyema. In other cases the pericardium or a large vein 
has been perforated. Many a case of apparently spontaneous pulmonary gan- 
grene or of purulent inflammation of the anterior mediastinum or of empyema has 
been found at the autopsy to have been brought about in the way above indicated. 
These cases are fortunately, however, exceptional. 

Treatment. — The only possible way of treating the large pressure diverticula 
successfully would be by operation. Perhaps surgery will some day win victories 
in this domain. In the meanwhile our efforts are confined to sustaining the 
patient. If he can not swallow, we must try to feed him through a tube. As 
long as this is possible, starvation is averted. The best way is to have the patient 
pass the tube himself. He will find out how best to avoid the sac and reach the 
stomach. If food can no longer be given in this way, there remain two alterna- 
tives : rectal feeding (vide infra), or making a gastric fistula. As to the latter, 
there has been thus far very little practical experience, because cases are so rare. 

The traction diverticula admit of no special treatment. If the events above 
mentioned occur, we must endeavor to meet the indications of the individual case. 



CHAPTER III. 
STENOSIS OF THE CESOPHAGUS. 

iEtiology and Pathology.— Contractions of the oesophagus occur with such 
relatively great frequency that they are the most important of all its disorders. 
They originate in various ways. By far the commonest cause is ring-shaped car- 
cinoma of the tube. The new growth in the mucous membrane encroaches more 
and more upon the lumen of the oesophagus, until finally it fills it. Carcinoma will 
be discussed at length in the next chapter. We shall here confine our attention to 
its purely mechanical action in causing stenosis. 

(Esophageal tumors other than cancer are very rare. Fibrous pedunculated 



STENOSIS OF THE (ESOPHAGUS. 



343 



polypi have been observed a few times. They usually originate in the lowest 
portion of the anterior wall of the pharynx, hanging down into the oesophagus, 
which they may thus obstruct. 

A second cause of stenosis is the contraction of cicatrices of the oesophageal 
wall. The most frequent occasion for this is the extensive ulceration caused by 
caustic poisons, such as concentrated acids or alkalies. If the victim escapes a 
speedy death, he is almost certain to have extensive scars formed in the wall of 
the oesophagus. These scars radiate irregularly in all directions, and, contracting, 
may almost completely close the tube. 

Ulcers from other causes, resulting in stenosis due to the scars they leave, are 
among the greatest rarities. Syphilis has been the well-established cause in some 
instances, and Quincke has described a few cases where there were ulcers at the 
lower end of the oesophagus analogous to the round ulcer of the stomach, or 
"ulcer due to digestion" {vide infra). These ulcers also may eventually produce 
cicatricial stenosis. 

A third and rare cause of stenosis of the oesophagus is compression from 
tumors external to it. Such swellings may originate in the thyroid gland, or in 
the lymph-glands of the neck or the anterior mediastinum ; or the swelling may 
be due to a vertebral abscess or an aortic aneurism. This form of stenosis is sel- 
dom extreme, for the portion of the tube pressed upon is usually limited. 

Next on the list after stenosis due to compression, is usually placed what is 
called intermittent dysphagia {dysphagia lusoria). This term is applied to the 
difficulty in swallowing which is said to be caused by an anomaly in the course of 
the subclavian artery. The artery is given off as the last branch from the arch of 
the aorta, and runs toward the right side just behind or just in front of the oesoph- 
agus. It seems, however, a priori improbable that the feeble pressure of this 
vessel as it pulsates should impede deglutition ; nor has it yet been proved to do 
so. It would be more natural to believe, what was indeed the original explana- 
tion of the phenomenon, that a large morsel of food passing down the oesophagus 
compresses the vessel and thus excites uneasiness and palpitation. 

Stenosis due to foreign bodies belongs to surgery. It need not be said that 
the clinical symptoms differ greatly in different cases. Not only the obstruction, 
but also a possible laceration and consequent inflammation are to be considered. 
Occasionally thrush has been abundant enough to cause pronounced symptoms of 
stenosis. 

Above the point of stenosis, no matter how the condition arose, if only it is 
well developed and has lasted a certain length of time, the circular fibers of the 
muscular coat are more or less hypertrophied. This hypertrophy is due to the 
increased force required to propel the ingesta downward. In many cases the tube 
is also diffusely dilated above the stenosis. 

Symptoms. — The effect of every oesophageal stenosis is to render deglutition 
difficult. If the case is a mild one, the patient experiences nothing more than a 
moderate pressure in the oesophagus upon swallowing. He feels that the morsel 
is longer than usual in reaching the stomach. Very soon he notices that solid 
food and large morsels can be swallowed only with difficulty. Accordingly, he 
is gradually led to confine himself to a liquid diet, takes only small mouthfuls, 
and always washes down any solid food with a swallow or two of liquid. The 
narrower the stenosis, the more he is troubled. Finally, even liquids can be 
taken only slowly and in sips. 

It must not be thought that the dysphagia just described is due exclusively to 
the mechanical obstruction of the lumen. Sometimes a patient is almost entirely 
unable to take nourishment, and yet at the autopsy no adequate mechanical 
obstruction is found. The dysphagia must therefore be due to some lesion of the 



DISEASES OF THE DIGESTIVE ORGANS. 



muscular coat of the oesophagus. The impaired contractility of the muscular coat 
at the affected spot is always a potent factor in impeding deglutition. 

As soon as the dysphagia has become considerable there is usually regurgita- 
tion of food. At first only a portion of the food comes up, but at last all of it. If 
the tube has become dilated above the stenosis, food may collect for some hours, 
and then be regurgitated, mixed with an abundance of very tenacious mucus. 
We saw a case of this kind where the patient could fill the sac above the stricture 
with quite a large amount of fluid without a drop reaching the stomach. If he 
bent his head sharply forward, the collected fluid would run out again through 
his mouth. It was not until the pouch was completely filled that a small amount 
of liquid would trickle through the stenosis into the stomach. 

Although the dysphagic symptoms above described generally imply oesopha- 
geal stenosis, the diagnosis can not be really established without using a sound. 
Upon introducing this, it is usually easy to detect the obstacle, which may either 
allow the instrument to pass, with a noticeable jerk, or else prevents its further 
progress. By measuring the length of the portion introduced before the stenosis 
is reached we can learn its position. On the average, the entire distance from the 
teeth to the cardiac sphincter is in adults sixteen inches (40 cm.) ; from the teeth 
to the beginning of the oesophagus, six inches (15 cm.); and consequently the 
length of the latter is about ten inches (25 cm.). If we succeed in passing a 
smaller sound through the stricture, the feeling as we move it back and forth will 
give us some idea of the length of the stenosis, or will detect the existence of several 
lying one below the other, etc. If the end of the sound can be moved about very 
freely above the stenosis, we may conclude that the tube is dilated there. 

Hamburger has employed auscultation of the oesophagus for diagnostic pur- 
poses. If we listen behind, to the left of the upper dorsal vertebrae during deglu- 
tition, we hear a gurgling sound, due to the act of swallowing, extending down 
the tube to the stenosis, but no farther. Then come all sorts of sounds, some of 
them caused by the fluid trickling slowly through the narrow part, and some 
caused by regurgitation. In general, the results obtained by auscultation are 
rather variable and uncertain. 

Having established the fact of the existence of a stenosis, we have next to deter- 
mine its nature, which is our chief guide to prognosis and treatment. In certain 
instances the history of the case gives us the needed information. The diagnosis 
of cicatricial stricture can hardly be made unless the patient himself tells us of 
being burned or injured by caustic poisons. The previous history is likewise of 
great importance if the stenosis be due to foreign bodies or to syphilis. If no deci- 
sive setiological factor can be elicited, we must carefully examine the neck and 
thorax, with regard to the possible existence of a swelling, compressing the 
oesophagus. In cases where an aortic aneurism has acted in this way, a rhythmic- 
al movement has sometimes been communicated to the free end of a sound intro- 
duced as far as the stenosis. If the physical examination does not reveal a com- 
pressing tumor, and particularly if the stenosis has developed gradually and in an 
elderly person, we are almost compelled to assume that there is cancer of the 
oesophagus. This is, after all, by far the most frequent cause of oesophageal strict- 
ure. If the new growth has ulcerated, a little portion of it may adhere to the 
end of the probe, and, on microscopic examination, render our diagnosis of carci- 
noma certain. 

The prevailing characteristic in stenosis of the oesophagus is inanition, iu creas- 
ing as the dysphagia increases. The patient gets to be very much emaciated and 
so feeble that he can not leave his bed. The temperature is subnormal ; for 
weeks it keeps at 95° to 97° (35°-36° C). The pulse grows very small and slow, 
being 40 to 60 per minute. The heart-sounds are soft. Respiration is superficial 



STENOSIS OF THE (ESOPHAGUS. 



345 



and slow ; and toward the close of life short pauses occur after expiration, before 
inspiration begins. The stomach and intestines are so empty that the abdomen 
is very concave, while the abdominal walls usually feel tense and resistant. In 
all cases where the nature of the stenosis precludes the possibility of cure or 
improvement, death results from increasing exhaustion, the lamp of life gradu- 
ally nickering out. 

Prognosis and Treatment. — In prognosis the main factor is of course the 
nature of the stenosis. If it is due to foreign bodies or to cicatrices, it may be 
completely cured. In stenosis from other causes it is often possible to produce 
considerable improvement, at least temporarily. The final result must be con- 
fessed to be usually unfavorable, as we should expect from the nature of the origi- 
nal trouble. 

The treatment is chiefly mechanical. We shall not speak of operations for 
the removal of new growths, etc. What we do refer to is a methodical and grad- 
ual dilatation of the stricture. Its results are sometimes brilliant, particularly in 
cicatricial stenosis. Other varieties, like the stenosis from cancer, may sometimes 
undergo considerable though but temporary improvement with this treatment. 

The best instrument to employ is the flexible, so-called English, oesophageal 
bougie. It is made in all sizes. If the stenosis is very narrow indeed, we may 
have to resort to catgut at first. Whalebone bougies, with olive-shaped ivory tips 
of various sizes to screw on the end, are also good, except that, being stiff er, there 
is more danger in using them. For introduction of the bougie, the patient should 
be seated, with the head slightly extended backward. The first two fingers of the 
left hand are introduced into the throat and guide the instrument, previously 
well oiled, over the back of the tongue and the epiglottis into the oesophagus. Of 
course, no violence must be used. Otherwise a perforation might occur if there 
were a soft, broken-down cancer, or an aortic aneurism. However, such a mis- 
fortune is very exceptional. 

The use of the bougie is almost invariably beneficial if the stricture can be 
passed. The patient generally finds that he can swallow easier than before, and 
will himself request a repetition of the performance. If the patient is an intelli- 
gent person, it is advisable to have him introduce the bougie himself. Patients 
often acquire even greater skill at it than the physician has. The bougie should 
be passed regularly once a day, or, at most, twice daily ; and in favorable cases we 
shall be able gradually to increase the size. If so, the symptoms speedily abate, 
and, with the increased ingestion of food, the patient gains flesh very fast. 

If the stenosis is extreme, and, although it admits the bougie, does not allow 
of sufficient nourishment, we must pass a tube into the stomach, through which 
to introduce liquid food. Milk is the best food to choose. Raw eggs, sugar, wine, 
etc., may be mixed with it. The various infant's foods and Hartenstein's "legu- 
minose " are also excellent. Their consistence is favorable for the purpose, and 
they supply a considerable amount of nourishment in a small bulk. 

If this means also fails us, two alternatives are left, unless we are to resign our 
patient to a death by starvation : (1) cesophagotomy if the stenosis is high up, 
otherwise gastrostomy ; (2) rectal feeding. 

For information about the operations we must refer to surgical literature. 
As to feeding per rectum, its results are never brilliant. It is indeed probable 
that life may be by this means somewhat prolonged, but not indefinitely. But 
the moral effect is very valuable, when the patient could otherwise receive no 
nourishment whatever. The sufferer feels that something is being done to avert 
absolute starvation. 

The simplest materials for the nutrient enemata are milk, eggs, and wine ; to 
which we may add prepared pepsine and pancreatine in the hope of promoting 



DISEASES OF THE DIGESTIVE OKGANS. 



absorption. Leube's pancreatic meat emulsion is still better, although more trouble- 
some in its preparation. Leube's directions are as follows : About five ounces 
(150 grm.) of meat, cut very thin and then minced finely, and about two ounces 
(50 grm.) of minced pancreas (from the calf) free from fat, are to be stirred with 
about three ounces (100 grm.) of lukewarm water until the mixture has the con- 
sistence of gruel. Before it is injected, the rectum should be cleansed by an enema 
of plain water. One such enema is to be given daily. 



CHAPTER IV. 
CANCER OF THE (ESOPHAGUS. 

JEtiology and Pathology. — Cancer is the most important and most frequent 
affection of the oesophagus. We have already mentioned in the preceding chap- 
ter how often stenosis is the result of carcinoma in the oesophageal walls. 

Little is known about the aetiology. It has been often maintained that 
mechanical, chemical, or thermic irritation of the mucous membrane may result 
in the development of cancer ; but this is not certain. It receives some support 
from the remarkably frequent occurrence of oesophageal cancer in hard drinkers. 
Now and then the patient himself will allege a perfectly definite cause for his 
disease, such as the lodging of a foreign body, or the swallowing of a very large 
or very hot morsel. Still it is hardly possible in any particular case to decide 
how much value such statements have. It has been maintained that the carci- 
noma sometimes develops in the scars of old ulcers. This is of interest when we 
recall the similar fact in regard to gastric carcinoma {vide infra). 

(Esophageal cancer follows the general rule in being most frequent in elderly 
people — somewhere between forty and sixty years of age. The male sex is decid- 
edly more often attacked than the female. 

As we might expect from the histological character of the epithelium lining 
the oesophagus, primary cancer here is invariably composed of pavement cells. 
The new growth may be either hard, firm, and fibrous, or it may be soft, succulent, 
and but scantily supplied with connective tissue. The first variety corresponds to 
the " scirrhus " of older writers, and the second to " medullary " cancer. Usually 
the new formation encircles the entire tube like a ring, extending three to ten 
centimetres longitudinally. Exceptionally a still larger portion of the oesophagus 
is involved, sometimes almost all the mucous membrane. The tumor is usually 
seated in the lower and middle thirds of the oesophagus, being much rarer above. 

Symptoms and Complications. — In the great majority of cases the symptoms 
are those of a gradually increasing stenosis, with its results. We may therefore 
refer to the preceding chapter for most of the particulars. There are, however, 
exceptional cases where the carcinoma is flat and entails no dysphagia, or so little 
that oesophageal trouble may not be suspected. We have repeatedly seen cases of 
extensive secondary hepatic cancer, or of pulmonary gangrene {vide infra), where 
the real primary disease was a flat cancer of the oesophagus which gave no clin- 
ical signs of its existence, and was therefore not diagnosticated. 

• It is characteristic of the stenotic symptoms produced by oesophageal cancer 
that sometimes a considerable and apparently spontaneous amelioration occurs. 
This is the result of an ulceration of the new growth. It crumbles away, as the 
result of superficial disintegration. The tumor is transformed into an ulcer, and 
one can easily understand how this may result in a temporary improvement in 
deglutition. 



RUPTURE OF THE OESOPHAGUS. 



347 



Important clinical symptoms may result from conditions secondary to the new 
growth. The cancer may extend to neighboring organs. Not infrequently the 
cardiac extremity of the stomach is thus involved. Sometimes such a tumor may 
be felt in the epigastrium ; but in most cases there is nothing to indicate that the 
stomach is attacked. 

The neighboring parts of the trachea or bronchi are sometimes involved, and 
important symptoms result from such a complication. If perforation occurs, an 
almost certain result is the inhalation of food or of decaying bits of the tumor, with 
consequent pulmonary gangrene, and, as a rule, speedy death. The disease has 
also been observed to attack the pleura, and end in perforation. The same is true 
of the pericardium and the aorta. A few instances are known where the vertebrae 
have been involved, the spinal cord compressed, and paraplegia thus induced. We 
have ourselves seen one such case. 

Quite frequently the recurrent nerve is affected, and a paralysis of the vocal 
cords is produced, which can be detected by the laryngoscope. This nerve lies 
so close to the oesophagus that it is peculiarly exposed to injury from the new 
growth itself, or from any inflammatory process which may be set up around it. 

Metastatic cancer in distant organs is not infrequent, and may give rise to 
important symptoms. It attacks most frequently the liver and the lungs. The 
kidneys, pancreas, bones, and brain are also liable to it. 

Pulmonary gangrene must be mentioned as a relatively frequent complication, 
and one which has serious consequences. We have already stated that it may 
result from perforation. A still more frequent cause is the inspiration of decaying 
masses vomited or regurgitated by the patient. 

Clinical History, Termination, Prognosis, and Treatment. — The disease is 
incurable. Operative removal has never been successful. The entire duration of 
the disease seldom exceeds a year, or a year and a half. At the end of this period 
the patient dies either from lack of nourishment or as a result of some one of the 
complications above enumerated. Treatment is purely symptomatic. Temporary 
improvement may be obtained by mechanical treatment of the stenosis. The par- 
ticulars about this may be found in the preceding chapter. 



CHAPTER V. 
RUPTURE OF THE OESOPHAGUS. 

Medical literature records a small number of cases which prove that the sud- 
den rupture of the oesophagus in persons previously perfectly well is possible, 
although of course very rare. The first and most famous instance was described 
by Boerhaave in 1724. 

The symptoms, according to the observations thus far reported, usually com- 
mence with sudden nausea and vomiting, during or shortly after a hearty meal. 
There is simultaneously an extreme, general collapse. There is pallor of the face 
and extremities, cold perspiration, and an extremely feeble pulse. Sometimes the 
patient feels a sudden darting pain in the chest. Almost invariably an extensive 
emphysema overspreads the neck and thorax. Death results in a few hours, or 
at latest in a few days. 

The autopsy reveals a tear in the oesophagus, invariably situated in its lower 
half. It may be five centimetres long, and is almost always longitudinal. Food 
has usually escaped into the surrounding tissues, in which case a secondary puru- 
lent inflammation exists, if death was not immediate. 



348 



DISEASES OF THE DIGESTIVE ORGANS. 



Zenker has attempted to explain this remarkable phenomenon by a supposition 
which is really very plausible, namely, that cesophagomalacia always precedes 
these so-called spontaneous ruptures. The cause of this softening of the oesopha- 
geal walls is probably the action of gastric juice escaping into the tube and attack- 
ing a surface which, through some temporary disturbance in the circulation, has 
lost its normal powers of resistance. 



CHAPTER VI. 
NEUROSES OF THE CESOFHAGUS. 

1. Spasm of the (Esophagus. — In rare instances oesophageal disturbances are 
observed, which appear to result from spasmodic contraction of its muscular coat. 
Nervous and hysterical subjects are particularly apt to present temporarily the 
symptoms of extreme stenosis, for which there can be no anatomical basis. Such 
cases are termed " spastic stenosis" of the oesophagus, or " cesophagismus. " It is, 
of course, possible that there may exceptionally be some real lesion at the founda- 
tion of the trouble, and that the spasm is the reflex result of an ulcer or inflamma- 
tion affecting the oesophagus. It is even affirmed that the reflex influence may 
sometimes originate in distant organs, such as the uterus. The dysphagia is usu- 
ally attended by a painful sense of constriction in the throat and chest. The 
bougie comes upon an obstruction, which usually soon yields. The diagnosis is 
confirmed by the easy passage of the bougie after the spasm is over. Other impor- 
tant factors are, the character of the symptoms as a whole and the other attendant 
nervous and hysterical disturbances. Some authors also explain the " globus 
hystericus " — that feeling as if a lump were passing up or down in the throat and 
chest — as a spasm of the oesophagus. 

2. Paralysis of the (Esophagus.— Of this subject we have little accurate knowl- 
edge. It is not improbable that an extensive bulbar paralysis, affecting the mus- 
cles of the pharynx and larynx, may sometimes involve the oesophagus ; although 
such a disturbance hardly ever gives rise to prominent symptoms in this disease. 
Ziemssen asserts that sometimes the oesophagus seems to participate in post-diph- 
theritic paralysis, when extensive. 



SECTION IV. 
Diseases of the Stomach:. 
CHAPTER I. 

ACUTE GASTRIC CATARRH. 

{Acute Gastritis.) 

iEtiology. — As the gastric mucous membrane is not open to direct inspection, we 
usually have to base our conclusion that an acute gastric catarrh exists, upon the 
analogy of the symptoms with those which we have seen in other mucous mem- 
branes. The pathology of gastric catarrh has thus far been very little studied, for 
the disease almost always ends in recovery ; and in those cases which, on account 
of some other disease, do terminate fatally, the signs of catarrh become very indis- 



ACUTE GASTRIC CATARRH. 



349 



tinct. Nevertheless, we are fully justified in assuming" that a catarrh of the gas- 
tric mucous membrane is the cause of most of the brief gastric disturbances which 
occur. That there may be other acute disorders of the stomach, in which there is 
no anatomical change whatever, but merely some functional anomaly, is possible, 
but has not yet been proven. 

The most frequent cause of acute gastric catarrh is some direct injury of the 
mucous membrane ; the injury may be thermic, as by taking food too hot or too 
cold, or mechanical, or chemical. The last is the most important. It is irritation 
that produces the frequent cases of catarrh which follow over-eating or the inges- 
tion of improper, indigestible, highly spiced, or very sour articles. In the same 
way arise the disorders caused by excess in alcohol, or by taking certain medi- 
cines, as well as a large portion of the milder cases of poisoning from all sorts of 
injurious substances. 

A special importance attaches to the ingestion of decaying substances. The 
incautious use of tainted meat or fish may be followed by relatively severe forms 
of acute gastric catarrh. The products of decomposition act as chemical irritants 
upon the mucous membrane ; and the ferments and putrefactive agents likewise 
continue in activity after reaching the stomach, and thus contribute to produce 
the inflammation. 

It is universally assumed that catching cold may excite gastric catarrh ; but 
the importance of this factor can seldom be demonstrated. 

Individual predisposition to the disease varies greatly. Weakly children are 
peculiarly liable to it ; also anaemic persons, fever patients, convalescents from 
severe diseases, and chronic invalids whose general nutrition and vigor are 
impaired. Such persons may be affected by things which the strong and healthy 
would not feel at all. The probable explanation of this especial liability to the 
disease is that, under the circumstances enumerated, the physiological functions of 
the stomach are not a little restricted. It has been experimentally proven that in 
fever, and in most anaemic or weakly persons, the secretion of the gastric acids is 
subnormal in amount. Digestion is thus considerably protracted. The contrac- 
tions of the muscular coat of the stomach, which are set up by the normal gastric 
secretions, are also rendered less vigorous. And, further, it is probable that the 
muscular fibers themselves may participate in the general debility. Thus it 
happens that the food is not carried on into the duodenum, but remains undi- 
gested in the stomach. It undergoes abnormal decomposition to a certain extent, 
and acts both as a mechanical and as a chemical irritant upon the gastric mucous 
membrane. 

Symptoms. — The most constant subjective symptom is anorexia. In many 
cases the very thought of food excites disgust. What the patient does eat tastes 
flat, and he is therefore very eager for piquant dishes, highly spiced or very sour. 
Thirst is often present, and a feeling of dryness in the mouth. 

The subjective gastric sensations are seldom those of marked pain. The usual 
complaint is of constant pressure and fullness. Sometimes the patient is conscious 
of the peristaltic movements of the stomach. He has " rumbling " of the bowels. 

There is nausea, and often even vomiting. The vomitus consists for the most 
part of undigested food, with which mucus, and sometimes bile, is mingled. Eruc- 
tations of gas or liquid are frequent. 

Physical examination reveals little. The epigastrium may be somewhat promi- 
nent as a whole, and may be tender on pressure. The tongue is almost always 
thickly coated and dry. The breath ig usually disagreeable, and there is a persist- 
ent flat or bitter taste in the mouth. 

In all well-marked cases of acute gastric catarrh the general health is consider- 
ably impaired. The patient is languid, and disinclined to exertion. Moderate 



350 



DISEASES OF THE DIGESTIVE ORGANS. 



elevations of temperature, with chilliness and feverishness, are not infrequent. 
Now and then there is a decidedly typhoidal condition, with marked nervous 
symptoms, such as intense headache, vertigo, and dullness. The term "gastric 
fever " is applied to such cases, and it is possible that they may sometimes be the 
result of a constitutional infection. It is also probable that toxic influences are 
exerted by the abnormal products of the fermentation which takes place in the 
stomach. For example, Senator mentions sulphuretted hydrogen as thus gen- 
erated. A short time ago Litten described a few cases in which at first there were 
such dyspeptic symptoms as nausea, vomiting, flatulence, and a coated tongue, but 
which soon gave evidence, by restlessness, headache, great muscular weakness, and 
somnolence, of rather severe nervous disturbance in addition. The breath had a 
marked "fruity" odor; and, on adding chloride of iron to the urine, a strong 
reddish color was developed, as in the so-called acetone-reaction. So that it seems 
probable that an auto-intoxication had occurred, somewhat resembling diabetic 
coma. 

Chief among complications are the intestinal symptoms, which are frequently 
coincident with the gastric disorder. Constipation is the rule. There may be 
diarrhoea. The gastric catarrh may by extension involve the duodenum, and give 
rise to jaundice. Sometimes herpes appears upon the skin. This fact argues for 
the infectious nature of many cases of gastric catarrh. 

The course of the disease is invariably brief. If we infer that the stomach is 
still loaded with undigested food, an emetic is indicated, and often proves bene- 
ficial. To avoid any local irritant action, we may resort to the subcutaneous injec- 
tion of apomorphia, in the dose of a sixth of a grain (0*01 grm.), to produce vom- 
iting. 

In most cases of acute gastritis, however, we may dispense with emetics. "We 
restrict the diet to milk porridge and the like, and prescribe small doses of dilute 
hydrochloric acid, five or ten drops in a half tumblerful of water, or some of the 
various stomachic tonics or bitters like tincture of rhubarb, tinctura amara (P. G.), 
or compound tincture of gentian. If there is obstinate vomiting, the greatest 
benefit may be derived from bits of ice, or small swallows of cold Seltzer water, or 
small doses of opium. For repeated acid regurgitations, as much magnesia or 
bicarbonate of soda should be prescribed as can be taken up on the point of a 
knife, to be repeated at intervals. If the constipation persists, some mineral- 
water or a dose of rhubarb should be administered. 



CHAPTER II. 

CHRONIC GASTRIC CATARRH. 

{Chronic Gastritis. Chronic Dyspepsia.) 

iEtiology.— The same injurious influences which produce acute gastric catarrh, 
if frequently recurring, excite the chronic form of the disease. The most potent 
causes are improper diet and the improper use of alcohol. Individual predisposi- 
tion is important in this as well as in the acute disease. Sometimes it even seems 
to be a matter of inheritance. It is not a rare thing to find that a large number 
of the members of a family have a "weak stomach." 

Chronic gastric catarrh is not always a primary affection. It may be secondary 
to some other disease. All diseases which result in passive hypersemia of the 
portal system, such as cirrhosis of the liver or thrombosis of the portal vein, are 
not infrequently followed by gastric catarrh ; and when the disease occurs in per- 



CHRONIC GASTRIC CATARRH. 



351 



sons afflicted with chronic cardiac or pulmonary disease, it is to be regarded as in 
part due to stasis. 

Pathology. — The macroscopic changes in the gastric mucous membrane are in 
most cases very slight. Usually it is coated with a layer of tough, grayish-white 
mucus, in which is suspended a greater or less amount of detached epithelium. 
The membrane is red, unless rendered gray by excessive pigmentation. The 
changes are almost always most extensive in the pyloric region. 

If the catarrh is of long duration, there may be still further changes. The 
mucous membrane often seems smooth and atrophied. The glands are narrower 
and shorter than normal, and the connective tissue between them is increased in 
amount. Other cases present hyperplasia of the mucous membrane. The internal 
surface of the stomach is thickened and mammillated. The hyperplasia in these 
cases affects chiefly the tubes of the glands in the mucous membrane, although 
the submucous layer may also be considerably thickened. 

Symptoms. — The symptoms of disturbed gastric digestion, or dyspepsia, to be 
observed in all sufferers from chronic gastric catarrh, are referable to the follow- 
ing functional anomalies : 

The secretion of the gastric juice depends upon the integrity of the circulation of 
the blood in the gastric mucous membrane. This is merely in accordance with a 
general rule. It is easy, therefore, to comprehend that any inflammation, disturb- 
ing as it does the circulation of the blood, must modify the gastric secretions. We 
may also assume that a deficiency in the secretion of the gastric juice is the chief 
factor in producing the dyspepsia which accompanies either the primary and inflam- 
matory catarrh or that resulting from venous stasis. The possible diminution in 
the production of pepsine is probably not of great importance in this connection ; 
for, like any other ferment, a very small amount of it would prove efficient under 
favorable circumstances. What seems of more importance is the diminished 
proportion of hydrochloric acid in the gastric juice of patients with chronic gas- 
tric catarrh— a condition which has been repeatedly proven to exist. The pro- 
cesses of digestion are thereby not a little lowered and impeded. It is self-evident 
that in cases where there is actual atrophy of the mucous membrane and of the 
glands in particular, the normal processes of gastric secretion may be still more 
seriously impaired. 

A further bad result of the imperfect digestion dependent on the lack of hydro- 
chloric acid is that the undigested food is very apt to undergo abnormal fermenta- 
tion and decomposition. These fermentative processes give rise to lactic, butyric, 
and acetic acids, and to alcohol. The direct cause of their production is that the 
ferment-producing spores are not destroyed by the gastric juice, as they would be 
under normal conditions. On the contrary, they find in the food stagnating 
within the stomach the most favorable conditions for the development of their 
activity. These products of abnormal fermentation in their turn irritate the 
gastric mucous membrane and prolong the catarrh. 

Another factor contributes to the disturbance of the normal digestive processes, 
namely, the excessive secretion of mucus. As mucus has an alkaline reaction, its 
presence neutralizes a portion of the acid in the gastric juice and lessens the 
potency of the latter. The mucus also does harm in a purely mechanical way. 
It envelops all the ingesta, and thus to no small degree prevents the gastric juice 
from reaching them. Morsels completely covered with mucus can remain for 
quite a long time in the stomach without being digested. 

A very great importance attaches to the motor disturbances which the stomach 
suffers in chronic catarrh. The normal peristalsis is of course an essential factor 
in the process of digestion. It is its function to bring all portions of the contents 
of the stomach successively into adequate contact with the mucous membrane. 



352 



DISEASES OF THE DIGESTIVE OKGANS. 



Thus alone is the uniform digestion of the entire mass rendered possible ; and, as 
physiology has taught us, the gastric secretions are continually being stimulated 
by the contact of the still undigested food with the lining membrane. Lastly, it 
is the peristalsis again which pushes on the already digested food into the duode- 
num, and thereby prevents the useless accumulation of matter within the stomach. 

Now, gastric peristalsis is undoubtedly much impaired in catarrh. One reason 
for this is the actual harm done the muscular coat. Every decided inflammation 
renders the muscular layer cedematous, and thus impedes its activity. In all 
cases where food accumulates in undue amount in the stomach, the muscular coat 
is gradually so stretched as to become still more incapacitated for its proper func- 
tions. A factor which is perhaps of still greater importance than these lesions is 
the diminished vigor of the normal excitants of these peristaltic movements. 
We learn from physiology that the chief part in arousing peristalsis is played by 
the normally constituted gastric juice, and more especially by the acid therein 
contained. It follows that all influences which modify the amount or composi- 
tion of the gastric juice must have the remote effect of diminishing the gastric 
peristalsis. The resulting evils can be inferred from what has been already 
stated. Digestion is impaired, and abnormal decomposition promoted ; and each 
effect becomes in turn a cause of further derangement — a condition of things 
which we are constantly meeting in the pathology of digestion. 

It remains to be stated that absorption is impeded in chronic gastric catarrh. 
It has been recently shown in Ludwig's physiological laboratory, here in Leipsic, 
that no inconsiderable portion of the peptones manufactured in the stomach are 
absorbed by the blood-vessels, in its walls. Now, as the circulation is disturbed by 
the inflammation, we should expect the absorption of peptones to be thereby 
diminished. The peptones remaining in solution within the stomach and not 
absorbed have been shown by experiment to disturb and delay the transformation of 
fresh albuminous substances into peptones. The diminished peristaltic action also 
tends to prolong the time during which the peptones remain in the stomach ; and 
numerous observations teach that normal peristalsis has a direct influence in pro- 
moting absorption, so that, if it be diminished, absorption is checked. 

We have therefore a whole series of factors, all of which contribute to disturb 
the normal processes of digestion. We have discussed them at some length, 
because they serve to explain not only the digestive symptoms of chronic gastric 
catarrh, but those of almost all the other gastric diseases. 

If we now proceed to the symptoms which lead us to a diagnosis of dyspepsia 
or chronic gastric catarrh, we find first anorexia. This symptom is common to all 
gastric disorders. There is sometimes a moderate appetite, but it is soon changed 
to a feeling of repletion upon the ingestion of even a slight amount of food. In 
other cases there is actual dislike for any form of nourishment ; the patient eats 
little, and prefers highly spiced, piquant dishes. There is often a persistent bitter, 
flat, or otherwise abnormal and disagreeable taste in the mouth. 

Subjective sensations in the region of the stomach are rarely entirely absent. 
As a rule, there is a feeling of fullness or pressure and of dull pain. These troubles 
may either be constant, or occur after meals. 

The eructation of gas is a very frequent and annoying symptom. Often a sour 
liquid comes up with the gas ("sour stomach"). The gas is a mixture of atmos- 
pheric air and the abnormal gaseous products of the decomposition which takes 
place in the stomach. Hydrogen, carbonic dioxide, and occasionally inflammable 
gases, such as marsh gas, have been detected. The sour masses regurgitated irri- 
tate the oesophagus, and give rise to a sharp, burning sensation, known as "heart- 
burn." 

In many instances the feeling of nausea is superseded by actual vomiting. 



CHRONIC GASTRIC CATARRH. 



353 




This almost always takes place either directly after eating or an hour or two later. 
The vomitus consists mainly of undigested food, usually mixed with a large 
amount of mucus. The chemical reaction may be either neutral or strongly acid. 
If acid, however, it is often not made so by hydrochloric acid, but by the acetic, 
lactic, or fatty acids generated by the abnormal fermentation going on within 
the stomach. That the contents of the stomach have an acid reaction is no proof 
that the gastric juice has peptonizing properties, for none of these other acids have 
nearly as much efficiency in promoting digestion as has hydrochloric acid. They 
may even at times check the process. A small amount of blood may be mixed 
with the matter vomited, but need not excite apprehension. Microscopic examina- 
tion reveals little that is characteristic. The cells of the yeast fungus are fre- 
quently found, and also the sarcina ventriculi (see Fig. 32). We may add that 
this latter has apparently no connection with the abnormal processes of fermen- 
tation. 

A peculiar kind of vomiting is extremely frequent in the chronic gastric catarrh 
of drunkards. We refer to the well-known morning vomiting of a watery fluid, 
which is usually alkaline in reaction and apparently consists 
at least in part of saliva that has been swallowed. (Vide 
also page 334.) 

The physical examination shows malnutrition (vide 
infra), but not much that is distinctive of the disease. The 
center of the tongue is often coated, while its point and 
edges are red. Considerable salivation not infrequently 
exists. 

. . . . i t o Fig. 32. — a, Sarcina ven- 

The epigastrium seems m many cases unchanged. Some- tricuii. 6, Yeast-ceils, 
times the stomach is distended, and somewhat tender on 

pressure. On palpation, a splashing can sometimes be both heard and felt. Its 
presence usually indicates dilatation of the stomach (q. v.). 

Leube and others have introduced the practice of examining the contents of the 
stomach with a view to diagnosis ; and valuable information can be obtained in 
this way. In the first place, we can learn how much time is occupied in digestion. 
The patient is given a definite amount of food upon an empty stomach. The 
meal usually consists of soup, a piece of steak, and some bread. Seven hours later 
the stomach is washed out (see the chapter on dilatation of the stomach) with a 
stomach-pump. If digestion is normal, nearly everything will by this time have 
been absorbed or passed on into the duodenum, so that the water will come back 
almost clear. Indeed, the process is often complete at the end of three or four 
hours. If, on the other hand, the returning current brings portions of food with 
it, we know that digestion is disturbed, and that the ingesta are detained longer 
than normal in the stomach. Still more important information is obtained by 
examining the gastric juice. In order to get this in a pure state, Leube excited 
secretion by pouring three ounces (100 c. c.) of iced water into the perfectly empty 
stomach, and then tested the fluid which he removed as to the amount of hydro- 
chloric acid it contained, and as to its digestive properties. Under normal condi- 
tions, the diluted gastric juice thus obtained, at the natural temperature of the 
body, will completely dissolve a thin slice of coagulated egg albumen in an hour 
or an hour and a half. But in gastric disease the process takes much longer, or 
may require the addition of hydrochloric acid. 

Occasionally the iced water does not stimulate secretion sufficiently, and Riegel 
has therefore resorted lately to the examination of the contents of the stomach 
some hours after eating. This material he obtains by means of sponges in as pure 
a state as possible, and then filters. His method has the advantage of affording 
information as to the presence or absence not only of free hydrochloric acid, but 
23 



354 



DISEASES OF THE DIGESTIVE ORGANS. 



also of the organic acids produced by fermentation, such as lactic, butyric, and 
acetic acids. We can not here describe the minutiae of the analysis, but will just 
mention that formerly tropseoline was employed, its yellow color being changed 
to red by the presence of free acids. If the acid be organic, the tropseoline will 
re-assume its yellow color on shaking with ether, while if hydrochloric acid be 
present the red persists. This test, however, has many sources of error. At pres- 
ent, methyl violet is more employed, which is colored blue by hydrochloric acid 
(and also by the other acids mentioned, only to a much less degree). Uffelmann 
recommends a test which is said to be still more trustworthy^ in which the color- 
ing matter of bilberries is used. This is turned rose-red by free hydrochloric acid. 
Uffelmann's favorite test for lactic acid is carbolized chloride of iron. To 10 c. c. 
of a four-per-cent. solution of carbolic acid and 20 c. c. of distilled water one drop 
of liquor ferri sesquichlorati, P. G. [nearly equivalent to liquor ferri chloridi, 
U. S.], is added. The blue color of this mixture at once changes to yellow on add- 
ing lactic acid. In ordinary cases of chronic gastric catarrh, free hydrochloric 
acid is present, only in diminished amount. The above-mentioned organic acids 
are always proof that abnormal fermentation exists ; and in such cases we natu- 
rally find yeast-cells and bacteria upon microscopic examination of the contents 
of the stomach. 

Of the other organs, the intestine most frequently suffers in chronic gastric 
catarrh. The combination of gastric disease and intestinal disease is not infre- 
quent. In almost all cases of chronic gastric catarrh the bowels are irregular. 
Habitual constipation is the rule. If much gas is generated in the stomach, the 
intestinal canal often becomes implicated, and tympanites and flatulence develop. 
There may be catarrh of the duodenum leading to jaundice. 

The urine is often only feebly acid in reaction, and therefore frequently deposits 
a large amount of phosphates. The diminished acidity is probably in part a result 
of the deficient secretion of acid by the stomach, though excessive vomiting (com- 
pare the chapter on dilatation) may also have some influence, because of the acid 
thus lost. 

It has been often maintained that eczema and other chronic cutaneous diseases 
are sometimes referable to gastric catarrh, but the fact has not yet been definitely 
established. 

There is a more evident relation between chronic gastric catarrh and certain 
nervous derangements. The disease has a notable influence on the spirits. In 
numerous instances it is accompanied by decided hypochondriasis. There may be 
other nervous symptoms, such as headache, vertigo, and dullness or listlessness. 
Vertigo in particular is a familiar concomitant of the disease (" vertigo e stomacho 
Zceso"). It is possible that in many cases these symptoms are toxic, resulting 
from the absorption of the abnormal matters generated within the stomach (vide 
supra, page 350). In the majority of instances, however, they are due to the 
neurasthenic and hypochondriacal condition of the patient (see the chapter on 
nervous dyspepsia). 

Whenever the catarrh is of any duration and severity, the general nutrition is 
seriously impaired. The diminished appetite and the imperfect digestion and 
absorption of what is eaten contribute to produce a gradual and considerable loss 
of weight. The fatty and muscular tissues atrophy. The skin grows dry and 
harsh, and usually has a dirty-pale color. 

Individual cases differ greatly in the combination of symptoms they present 
and in their course. The anorexia, gastric oppression, eructations, vomiting, and 
other important disturbances already mentioned, exhibit the greatest diversity in 
their intensity and their grouping. In the milder cases loss of appetite and mod- 
erate local uneasiness may be the only symptoms. Frequent vomiting is seen 



CHRONIC GASTRIC CATARRH. 



355 



only in the severer cases. The disease often lasts for years, especially if the 
patient neglects himself. In most cases there are frequent remissions and exacer- 
bations, usually dependent upon external causes. 

The disease is not intrinsically fatal, but the general debility consequent upon 
it may indirectly shorten life. 

Diagnosis. — The diagnosis is based upon the existence of chronic gastric symp- 
toms unattended by evidence of any more serious lesion, whether of the stomach 
itself or of some other organ. For example, the possibility of gastric ulcer, can- 
cer, or dilatation is to be considered. This elimination of other diseases is very 
important. It is not at all exceptional to meet in practice cases that have been 
carelessly diagnosticated as chronic gastric catarrh where a more thorough exami- 
nation or the further progress of the case leads to an entirely different conclusion 
— chronic pulmonary or cardiac disease, chronic nephritis, or one of the other 
gastric affections above mentioned. It should, therefore, be our invariable rule 
to reach the diagnosis by exclusion, after making a careful and complete physical 
examination, in order to detect any other possible disease to which the gastric 
symptoms might be referred. The differential diagnosis between chronic gastric 
catarrh and so-called nervous dyspepsia will be discussed hereafter. 

Treatment.— If the disease seems to be merely symptomatic— the result, for 
example, of venous stasis due to chronic cardiac, pulmonary, or hepatic disease — 
our efforts must, of course, be chiefly directed to the relief of the original trouble. 

Treatment of the primary form, on the other hand, must always begin with 
regulation of the diet. Such vague injunctions as " to be cautious " or " to avoid 
indigestible articles of food" are useless. The patient must have a perfectly 
definite bill of fare prescribed for him ; nor can any universal one, suitable for 
all cases, be drawn up. In each individual instance the individual circumstances 
must be considered. The personal experiences of the patient himself are by no 
means to be disregarded. One man may be quite unable to digest what is well 
borne by others, and vice versa. 

In the first place, certain foods must be utterly forbidden to such patients as do 
not themselves avoid whatever disagrees with them. All articles must be pro- 
hibited which may irritate the mucous membrane, either mechanically or chemi- 
cally. This includes all the coarser sorts of vegetables or fruits containing a large 
proportion of indigestible cellulose; and all dishes that are very sour, strongly 
salted, or highly spiced. Potatoes, farinaceous food, and all substances mainly 
composed of hydrocarbons, must also be interdicted ; because almost all the abnor- 
mal fermentative processes, the evil consequences of which have already been 
considered, are promoted by the hydrocarbons. Fat is also harmful. It impedes 
digestion by protecting the contents of the stomach from the action of the 
gastric juice, in a purely mechanical way ; and then, being changed into the fat 
acids, it causes sour eructations and pyrosis. It is important that all forms of 
alcohol should be forbidden. Fleischer and others have proved by actual experi- 
ment that even small amounts of alcohol prolong and hinder the digestive process. 
An injunction to abstain totally is usually better obeyed in a severe case than the 
advice to be very moderate in the use of liquors. The food should neither be very 
hot nor ice-cold. 

In determining what the patient may be allowed to eat, we are to consider, as 
already mentioned, his own personal experience as well as our more general 
knowledge. An intelligent patient will often be himself the best judge of what 
agrees or disagrees with him. The following foods are very easy to digest : Milk, 
soft-boiled or raw eggs, broths, and certain artificial preparations, chief among 
which stand the Leube-Rosenthal meat solution and the meat peptones which 
have been lately put upon the market. The brain and sweetbread of calves are 



356 



DISEASES OF THE DIGESTIVE ORGANS. 



easily digestible ; also birds, such as pigeons, chickens, and partridges, and thin 
shavings of raw meat or raw ham. Gradually we may proceed to somewhat 
heartier food — veal, game, roast beef, and light farinaceous dishes. The worse the 
symptoms are in any case, the more strict must we be in regard to diet. For drink, 
besides water or Seltzer water, very weak tea and non-oleaginous cocoa are good. — 
Shall we permit coffee ? This is often a question of great interest to the patient. 
It must be answered according to his individual experience. Coarse bread is to 
be forbidden. Ordinary white bread, toasted if it seems desirable, may be allowed 
in moderate amount. 

Solid articles of diet must be finely cut up and well chewed before being 
swallowed. It is sometimes advantageous to take more than three meals a day, 
each one being proportionally smaller. . Other patients relish their food better if 
the intervals between eating are prolonged. 

There are other special indications to be met. As we have already seen, one of 
the chief factors in maintaining digestive disturbance is the abnormal detention 
of undigested food in the stomach. If we can only empty the viscus properly, we 
thereby relieve it of the abnormal processes of decomposition and fermentation, as 
well as of mucus which may have collected in injurious amount. This indication 
is best fulfilled by the mechanical treatment of chronic gastric catarrh by means 
of the stomach-pump. Its results are often brilliant ; but rinsing out the stomach 
is never agreeable to the patient ; and the method should not be resorted to except 
in severe and inveterate cases. The most suitable are those where an examination 
of the contents of the stomach, made as above described, shows that abnormal fer- 
mentative processes are going on, or that the ingesta stagnate in the organ. For 
further particulars we refer to the chapter on dilatation. 

With the same object, of relieving the stomach of its unnatural contents, mild 
laxatives are frequently prescribed. The alkaline mineral waters, containing 
sulphate of soda, are very often chosen for the purpose. These waters fulfill other 
indications at the same time. Being alkaline, they tend to neutralize the excessive 
acidity of the stomach. And it has been proved by experiments that sodic carbon- 
ate, sodic chloride, and carbonic dioxide promote the secretion of gastric juice. 
Carlsbad enjoys the highest reputation for all chronic diseases. Ems, Kissingen, 
Tarasp, and Vichy should also be mentioned as favorable resorts. Of course a 
large part of the success in these places is due to the fact that the patients in them 
obey dietetic injunctions much more conscientiously than they would at home. 

The attempt has been made to check the abnormal decomposition of food by 
administering substances which check fermentation. The best remedies of this 
class are salicylic acid, ten or fifteen grains (grm. O'5-l'O) a day, in divided doses ; 
two or three half -grain (grm. 0*03) pills of creasote daily ; or twenty drops of 
benzine in water or milk several times a day. 

Another indication is to supply an artificial substitute for the deficient gastric 
juice. We have seen that in many cases of gastric disease the proportion of 
hydrochloric acid has been proved to be subnormal. We have, therefore, both 
theoretical and practical reasons for prescribing hydrochloric acid. We may give 
five to ten drops of the dilute acid in half a glass of water fifteen or thirty minutes 
after meals. An excess of acid impedes digestion, so that we should always begin 
with small doses. If the acid by itself seems ineffectual, we must try the effect of 
combining pepsine with it. We have never used any but the plain pepsine, in 
eight-grain (grm. 0'50) powders or capsules after meals. The wine of pepsine 
which is so much in vogue is ineligible because of the alcohol it contains. The 
administration of hydrochloric acid and pepsine is sometimes very beneficial ; but 
in many cases we meet with disappointment. 

The best drugs to stimulate the secretion of gastric juice are the bitters. It is 



PHLEGMONOUS GASTEITIS. 



357 



this property which, has earned them the name of stomachic tonics. Compound 
tincture of gentian, tincture of nux vomica, tinctura amara, and tinctura calami, 
P. G. , quassia and columbo — these are the most employed. In general, however, 
they are not very efficient. An excellent tonic in many of these cases is cundu- 
rango bark. A decoction may be made (15 parts to 200 of water ) ; or we may 
write for powders of seventy-five grains (grm. 5) each, one powder being made 
into one or two cups of infusion by the patient himself. 

A few remedies remain to be mentioned, which are said to exert a direct bene- 
ficial influence upon the catarrh, and which many physicians extol highly. Their 
efficacy, however, is somewhat problematical. We refer chiefly to subnitrate of 
bismuth, sulphate of zinc, and nitrate of silver. 

Certain symptoms may demand especial treatment, such as vomiting. It will 
usually yield to regular and persistent washing out of the stomach. Other reme- 
dies are small bits of ice, and minute doses of opium or chloral. Potassic bromide 
may also be tried. 

Violent gastralgia requires narcotics, such as hydrocyanic acid and morphine. 
" Sour stomach " may be relieved by a pinch of bicarbonate of soda or calcined 
magnesia. Persistent anorexia may yield to the bitters mentioned above, or to 
small doses of quinine. If the bad taste in the mouth is annoying, the mouth 
should he frequently rinsed out with Seltzer water, a one-per-cent. solution of 
carbolic acid, or five drops of tincture of myrrh to a glass of water. For habitual 
constipation, enemata, or the various mineral waters, are good ; also Carlsbad salts. 
In obstinate cases pills of rhubarb or aloes may be employed. Still, we ought 
never to forget that the infrequency of the stools is often merely a natural con- 
sequence of the scanty diet, and that it is therefore possible to do harm with our 
purgatives. Iron is often prescribed for the concomitant anaemia ; but it should 
be employed cautiously, for it is often ill borne in gastric disease. 

We see, then, how many remedies are at our disposal in the treatment of 
chronic gastric catarrh. But success in any case depends most of all upon the 
perseverance and fidelity with which the patient follows directions and avoids 
harmful influences. Our first aim in every instance should be to obtain the 
benefits of a well-regulated diet. We usually add a prescription for hydrochloric 
acid, or such other medicine as the special indications call for. In summer, the 
patient should go to Carlsbad, or Ems, or Tarasp, if his circumstances allow it. 
Mountain air or the sea-shore are often very advantageous, by way of toning up 
the entire system. In severe cases the greatest relief is to be obtained by mechan- 
ical treatment, in combination with a restricted diet. We can best measure our 
success by the increase of weight, and also by the improvement in the patient's 
own feelings as well as the diminution of the gastric disturbances. 



CHAPTER III. 

PHLEGMONOUS GASTRITIS. 

{Purulent Inflammation of the Stomach.) 

PURULENT inflammation of the stomach is very rare, and little is yet known 
about it. In most cases, no special causes for it were ascertainable. It is occa- 
sionally one of the symptoms of grave pyaemic or puerperal inflammation. 

Two forms are distinguished— a diffuse and a limited variety. The latter is 
equivalent to gastric abscess. The submucous layer is almost invariably the chief 



358 



DISEASES OF THE DIGESTIVE OKGANS. 



seat of suppuration. From this starting-point the process invades the muscular 
and serous coats on the one hand, and the mucous membrane itself on the other. 

The usual symptoms are violent gastric derangement, with pain and vomiting, 
high fever, and the indications of constitutional infection, namely, headache, 
delirium, and general prostration. Sometimes the disease is quickly fatal, some- 
times it runs a more chronic course. The few cases in which recovery has beeu 
reported are somewhat obscure. 

The disease can never be diagnosticated with absolute certainty. Treatment 
must be purely symptomatic. Ice, both internally and externally, and the nar- 
cotics, are chiefly employed. 



CHAPTER IV. 

GASTRIC ULCER. 

(Simple or Hound Ulcer of the Stomach.) 

iEtiology. — Since Cruveilhier gave the first accurate description of gastric 
ulcer, numerous explanations of its occurrence have been propounded. Even yet 
there is no universally accepted view. There is, however, one point about which 
most authors are agreed — namely, that the u leer is due to a self-digestion of the 
stomach at one limited spot. Hence it is frequently termed " peptic ulcer of the 
stomach." 

The reason that the stomach is not continually being digested by its own juices 
is, as we all know, chiefly the alkalinity of the blood, which is constantly coursing 
through the mucous membrane. Wherever the circulation is in any way inter- 
fered with, we should therefore expect to find, and we do find, that the mucous 
membrane begins to be digested.* If, as a result of inflammation, a minute 
haemorrhage occurs at any point, the little area thus deprived of its blood-supply 
is at once digested. This is what is called a " hemorrhagic erosion." The experi- 
ment of occluding the arterioles of the gastric mucous membrane with emboli has 
been tried by Panum and Cohnheim. The resulting hemorrhagic infarctions 
were transformed into ulcers. Just what the essential conditions are, in man, 
under which a local disturbance of the circulation and a consequent round ulcer 
of the stomach are produced, we are thus far confined to conjecture. Virchow 
assumed that most cases were the result of thrombosis or embolism of the minute 
blood-vessels, caused by various diseases. Klebs suggested the possibility of a 
local spasm in the vessel. Bottcher has succeeded in detecting numerous colonies 
of micrococci in the margins of gastric ulcers, and regards them as the cause. 
As we have already said, however, no one of these views has been universally 
accepted. 

It may be that in many cases some local injury of the mucous membrane is the 
original cause of the ulceration. Such possible causes are burns or mechanical 
lesions. But, even then, we are unable to explain why the ulcers should spread 
laterally and downward. For all gastric ulcers experimentally produced, whether 
by embolism, contusion, burning, or even cauterization (as practiced by Quincke), 
exhibit a decided tendency to rapid healing. It has therefore been suggested that 

* After the circulation is terminated by death, this digestive process at once begins, producing the 
softening of the stomach, or gastromalacia, frequently found at autopsies. There has been much dis- 
cussion as to the origin of this condition, but it now seems indubitable that it is in every instance a 
post-mortem change. 



GASTRIC ULCER. 



359 



the further extension of the ulcers, in such cases, is due to an abnormally great 
acidity of the gastric juice. 

Ulcer of the stomach is commonest in young adults, between seventeen and 
twenty-five years of age. It is rare in children ; less so in older people. The 
disease is noticeably more frequent in females than in males. It is more prone 
to attack the weakly, anaemic, and chlorotic than the vigorous. 

Pathology. — The ulcer is usually of a circular shape. Its borders are sharp ; 
the walls often slope inward, giving the ulcer the form of a shallow funnel. Its 
base is almost always perfectly clean. If superficial, it does not extend farther 
than to the muscular coat, but it may be deep enough to expose the serous mem- 
brane, or even to perforate it (vide infra). The size varies greatly. Some are 
hardly as large as a pea ; others may measure ten to fifteen centimetres in their 
greatest diameter. As to position, most of them are found near the pylorus. 
They attack the posterior wall of the stomach, particularly the neighborhood of 
the lesser curvature, more frequently than the anterior wall. As a rule, we find 
but a single ulcer, although exceptions to this statement are not very rare. 

If an ulcer of any size heals, a scar is formed, with radiating lines and often of 
considerable size. Cicatricial contraction may alter the shape of the stomach 
considerably. Pyloric ulcers may leave scars which eventually produce stricture 
of the pylorus and consequent dilatation of the stomach. 

If the ulcer attacks the serous membrane, perforation may finally result, unless 
an adhesive peritonitis attaches the stomach, at the point threatened, to some neigh- 
boring organ. The ulcers being usually on the posterior wall of the stomach, it 
is oftenest the pancreas to which the stomach becomes adherent. In other 
instances it is the liver, transverse colon, diaphragm, or spleen. If the ulcer pene- 
trates organs to which the stomach has become attached in this way, the inflam- 
mation extends, so as to cause empyema, for example, or hepatic abscess ; or the 
pleura, lungs, pericardium, or transverse colon may be perforated. We shall 
revert to this subject under the symptomatology of gastric ulcer. 

The ulcer may cause erosion of a blood-vessel, and thus give rise to one of the 
most important symptoms of the disease, namely, gastric haemorrhage. 

Clinical History. — There may be absolutely no symptoms. It is not a rare 
thing to find at autopsies a still active ulcer of the stomach, or the cicatrix left by 
one, in subjects who never had during life any gastric disturbances whatever. 
Nor is it exceptional for a person to exhibit suddenly grave symptoms, like gastric 
haemorrhage, or peritonitis due to perforation, where there has been no reason 
previously to apprehend the existence of an ulcer. 

In other instances the ulcer does, indeed, give rise to symptoms, but they are 
not sufficiently characteristic to point to the correct diagnosis. There are anorexia, 
occasional gastralgia, vomiting, and eructations — symptoms which might, with 
equal probability, be referred to a simple chronic catarrh. In fact, it seems likely 
that the ulcer has little share in their production, and that they are mainly due to 
a co-existing catarrh. In these cases, also, grave symptoms, consequent upon the 
ulceration, may suddenly arise. 

In a third class of cases there are symptoms which are, to a certain extent, 
characteristic, and lead with more or less definiteness to the true diagnosis. These 
" symptoms of ulcer " are chiefly a peculiar epigastric pain, which is usually inter- 
mittent, and vomiting, or, what is yet more distinctive, the vomiting of blood, or 
hsematemesis. These symptoms and their diagnostic value we must now consider 
in detail. 

Pain in the stomach is one of the most frequent symptoms of round ulcer. Its 
forms are very diverse. Often the patient complains only of a diffuse, painful 
sensation of pressure referred to the entire region of the stomach. This may be 



360 



DISEASES OF THE DIGESTIVE ORGANS. 



uninterrupted, or it may occur only after meals, or after excessive exertion, or as 
the result of some other special cause. This sort of pain is the least diagnostic of 
any, inasmuch as exactly similar sensations may be caused by a simple chronic 
catarrh. More characteristic of ulcer is a decided cardialgia — that is, a very vio- 
lent pain, coming on at intervals like neuralgia. It is described as " cutting," 
" tearing," " boring," and the like. The pain may come on irregularly at any 
hour ; or it may occur with considerable regularity at the end of a definite time 
after eating, say, half an hour or an hour. It, too, is felt chiefly in the epigas- 
trium, but not infrequently extends toward the umbilicus, backward toward the 
vertebrae, into the thorax, or even into the upper extremities. In many instances 
a marked sensation of thoracic oppression accompanies it. Another characteristic 
point is that a change of position may sometimes affect the severity of the pain. 
An attack of cardialgia may last for a few minutes or for several hours. It is 
commonly thought to be due to the direct irritation of the ends of nerves lying 
exposed at the base of the ulcer. As an isolated symptom, this cardialgia can not 
be distinguished from the purely nervous variety, but, taken in connection with 
other symptoms, it is often a great aid to diagnosis. We should add that precisely 
similar attacks of cardialgia may be produced by the scars of ulcers which have 
already entirely healed. 

A third variety of pain may be observed in gastric ulcer. The suffering may 
be localized in a very limited area. Such pain is thought to be due to irritation of 
the floor of the ulcer by food, or to its edges being pulled upon during the move- 
ments of the organ. It generally comes on after eating, and ceases if the stomach 
is perfectly quiet. In position, this pain is generally epigastric, but sometimes it 
is umbilical, or even, now and then, more toward the back. In many cases of 
gastric ulcer there is also tenderness on pressure in a quite sharply defined area 
and at one particular spot. Most authors regard the accurately localized pain as 
the most nearly pathognomonic ; but it must be said that it is decidedly the least 
frequently exhibited of any. Transitional forms and combinations of the various 
kinds of pain are often observed. 

Vomiting is a very frequent symptom of gastric ulcer, but if the vomitus is 
composed of nothing except food, or food mixed with mucus or bile, the symptom 
is not at all characteristic. In quite a large proportion of cases, however (about 
one third), "haeraatemesis occurs either once or repeatedly. The vomiting of a con- 
siderable amount of blood is beyond doubt the most important factor in diagnosti- 
cating gastric ulcer. Very often it alone suffices to render us pretty certain of 
our diagnosis. 

Haematemesis is frequently the symptom which first leads the patient to apply 
to a physician. Up to this time he may have felt perfectly well, or, although there 
may have been some gastric derangement, he has not thought anything of it. 
The patient suddenly becomes faint, perhaps while he is pursuing his regular 
occupation, or it may be at night. He feels dizzy, and it looks black before his 
eyes. Then he has nausea, and finally has to vomit. The vomitus is either pure 
blood, or a mixture of blood and food. It is partly coagulated, and often has a 
rather dark or blackish color. This change in color, as well as the coagulation, is 
due to the action of the gastric juice. The amount varies greatly in different cases : 
there may be a quart or more. Not infrequently blood is repeatedly vomited 
either at short intervals or on successive days. Part of the blood escapes through 
the pylorus, so that, after a profuse gastric haemorrhage, blood is sure to be found 
in the stools. In them it is black and tarry. Exceptionally it happens that all 
the blood, beyond what is absorbed from the intestinal canal, passes off per anum, 
so that none whatever is vomited. In such cases it is often a difficult matter to 
locate the haemorrhage. 



GASTEIC ULCER. 



361 



The consequences of gastric haemorrhage depend, of course, chiefly on the 
amount of blood lost. Sometimes, although fortunately rarely, a large blood- 
vessel is eroded and the patient dies. This event may be sudden, or it may occur 
more gradually under the influence of repeated haemorrhages and after a few 
days, during which all the symptoms of acute anaemia are exhibited. On the 
other hand, the loss of blood may be so insignificant as to produce no especial 
symptoms. In most instances life is not actually threatened, but yet the signs 
and results of a more or less marked general anaemia are clearly visible. 

In such cases the patient feels extremely exhausted, and at once takes to his 
bed. He has also all the subjective symptoms of cerebral anaemia. There are 
vertigo, tinnitus aurium, specks before the eyes, frequent gaping, and sometimes 
headache. To assume an erect posture aggravates the disturbance. There is usu- 
ally excessive thirst. Now and then a temporary amaurosis has followed an 
excessive haemorrhage. 

Objectively, we notice at once the excessive pallor of the skin, particularly of 
the face. The lips and conjunctivae are also blanched. The pulse is rapid, and 
often ill sustained. For some days there may be anaemic murmurs over the heart, 
and there is a distinct sound to be heard in the femoral arteries. A moderate rise 
of temperature is very common. This is known as the anaemic fever. The urine 
is pale, and usually rather abundant. Its specific gravity is not infrequently rela- 
tively high, namely, 1015 to 1020. All these symptoms are directly referable to 
the loss of blood, and will be discussed with greater detail in the section on 
anaemia. 

If the haemorrhage is not repeated, the patient gradually regains his strength. 
To be sure, the pallor usually persists for a long while, but the disagreeable symp- 
toms gradually abate. Where gastric discomfort has existed previously to the 
haemorrhage, it often disappears entirely after it — a circumstance which is probably 
in part due to the excessive caution of the patient thereafter. At the end of a few 
weeks the patient often feels perfectly well again ; and, indeed, recovery is not 
infrequently complete and permanent. In other cases, however, the symptoms of 
ulcer return, sooner or later. 

Other symptoms than those already discussed are more uncertain. Anorexia, 
eructations, and obstinate constipation may be present, or may be wholly wanting. 
In cases of suspected ulcer, it is usually inadvisable to introduce a stomach-tube 
for diagnostic purposes, because bleeding or perforation might result. The digest- 
ive symptoms are also probably less the effect of the ulcer than of a coincident 
catarrh. The general nutrition often suffers comparatively little, unless there are 
persistent anorexia and vomiting. 

An event which has been already mentioned under pathology — namely, perfo- 
ration of the ulcer— is of great clinical importance. It would be impossible to par- 
ticularize here all the possibilities incident to it. We shall confine ourselves to the 
two most important, because most frequent varieties of perforation : (1) into the 
peritoneal cavity, causing peritonitis, and (2) into the left pleura, or left lung. 

Perforation into the peritoneal cavity leads almost invariably to a quickly fatal 
peritonitis. When the ulcer has previously caused few symptoms, if any, the 
excruciating abdominal pain, tympanites, vomiting, collapse, and sudden death of 
peritonitis may abruptly supervene upon a state of apparently perfect health. It 
is the exception to have the peritonitis limited. This is more apt to occur if adhe- 
sions have been formed previously. An encapsulated abscess then results, which 
points either into the intestine or externally, and may rarely terminate in com- 
plete recovery. 

Perforation into the left pleural cavity we have observed repeatedly. It causes 
a purulent or septic pleurisy on that side, and pulmonary gangrene may develop 



362 



DISEASES OF THE DIGESTIVE ORGANS. 



at the same time or later, as a result of perforation into the lung. Whenever we 
meet a case of apparently spontaneous, left-sided empyema, we should at any rate 
always think of the possibility of gastric ulcer. 

The general course of round ulcer of the stomach varies, as we can see, so 
greatly in different cases that it can not be depicted simply. Complete recovery 
is by no means rare. In other cases the symptoms persist for years with varying 
intensity. We have already sx>oken of the haemorrhage and perforation which 
may suddenly intervene, and of their significance. Relapses are not infrequent, 
even after apparent recovery. If the ulcer cicatrizes, the scar itself may give rise 
to persistent disturbances ; there may be obstinate cardialgia, or, if the scar is at 
the pylorus, dilatation of the stomach {vide infra) may gradually be developed. 

Diagnosis. — The diagnosis can be made only when the above-mentioned char- 
acteristic symptoms are present. Of these, haematemesis is by far the most signifi- 
cant, for it is with very few exceptions the result of gastric ulcer. Particularly is 
this true of individuals under middle age. — But how shall we determine whether 
the blood ejected did not come from the nose or the lungs, rather than the stom- 
ach ? The answer is not always easy. If an epistaxis occurs at night, a part of 
the blood often flows back into the naso-pharynx, and, being swallowed, excites 
vomiting, so that a gastric haemorrhage is suggested. In such cases a careful 
inspection of the nostrils and naso-pharynx will almost always remove our doubts. 
We may find that the patient has been subject to nose-bleed ; and there will be 
no history of gastric disturbance previously. 

The diagnosis between gastric and pulmonary haemorrhage in doubtful cases 
depends on the following factors : 1. The previous condition of the patient — whether 
he has had cough, expectoration, and other pulmonary symptoms, or, on the other 
hand, gastric pain and vomiting. 2. On the character of the haemorrhage, whether 
accompanied by vomiting or by cough. But there may have been both. Violent 
vomiting may excite a cough ; and, on the other hand, blood which has been 
coughed up may be in part swallowed and induce vomiting. 3. On the character 
of the blood : if from the lungs, it is usually bright-red and frothy, containing 
bubbles of air, with few clots, and of alkaline reaction. In gastric haemorrhage it 
is usually dark, mixed with food, partly clotted, and acid in reaction. 4. On the 
results of physical examination. In this, of course, we must be extremely cautious 
after a haemorrhage, lest the movements of the patient excite fresh bleeding ; and 
yet we may be able, from the general condition of the patient, or from dullness at 
the apices, or moist rales, to demonstrate pulmonary disease. If the blood came 
from the stomach, we usually detect nothing but the signs of anaemia. 5. The 
subsequent symptoms. In cases of pulmonary haemorrhage there is almost sure 
to be an expectoration for the next few days, either of pure blood or of matter 
stained with blood ; and, in gastric haemorrhage, the next dejection will almost 
certainly be black, from the presence of decomposed blood. In doubtful cases, the 
appearance of blood in the stools almost invariably settles the question in favor of 
gastric haemorrhage. 

In cases of gastric ulcer, unaccompanied by haematemesis, the diagnosis is only 
more or less probable, not certain. The existence of cardialgia and localized pain 
in the stomach must always make us consider the possibility of an ulcer, but we 
can not be positive about it. 

The differential diagnosis between gastric ulcer and purely nervous cardialgia, 
and between ulcer and cancer, will be discussed later in the appropriate chapters. 

Prognosis. — The dangers in ulcer of the stomach, particularly haemorrhage 
and perforation, have already been spoken of. Whether these misfortunes will 
actually occur in any individual case, and when, we can not determine. 

There can be no doubt that a large number of ulcers heal perfectly ; but, as we 



GASTRIC ULCER. 



363 



have already said, even the resulting scar may cause trouble. This possibility 
must be borne in mind. Of these persistent symptoms, cardial gia is the most fre- 
quent. Dilatation is also possible. And, finally, it is probably not a very rare 
event that cancer eventually develops in the floor of the old ulcer. We shall 
revert to this matter under cancer of the stomach. 

Treatment. — The plan of treatment which we are about to describe should be 
rigidly followed, not only where we are almost certain of our diagnosis, but also 
in doubtful cases, where there is merely a possibility that ulcer exists. 

As we have no means of directly promoting the cicatrization of a gastric ulcer, 
our chief efforts must be directed to the removal of all injurious influences which 
may in any way delay or impede the natural process of healing. We must 
endeavor, in the first place, to allay any mechanical or chemical irritation of 
the ulcerated surface. We must therefore regulate the diet carefully. The best 
way would be to afford the organ a period of absolute rest ; but we can not let our 
patient starve to death, nor does rectal feeding sustain the system indefinitely. We 
must then have recourse to foods which are as little objectionable as possible, and 
they must be exclusively liquid. In many cases good results are obtained by a 
simple milk diet, to which may perhaps be added a raw or soft-boiled egg, or thor- 
oughly soaked bread. The pain and vomiting will be sensibly abated. A particu- 
larly appropriate preparation, which is at once nutritious and unirritating, is the 
meat solution of Leube-Rosenthal. About a box of it may be given in a day. It 
is best administered mixed with broth. Lately the artificially prepared meat pep- 
tones of Kochs and Kemmerich have been highly praised ; but we have not yet 
had much personal experience with them. The various infants' foods may also 
be sometimes employed with advantage in gastric derangements. This strict regu- 
lation of the diet must be kept up at least three or four weeks. As soon thereafter 
as gastric symptoms have wholly disappeared, we may allow a cautious change to 
heartier food, such as fowl, shavings of raw meat, potato-soup of homogeneous 
consistency, etc. 

The use of Carlsbad salts has become very general, particularly since Von 
Ziemssen's recommendation of it ; and it is really beneficial in many cases. A 
tablespoonful of the salts is dissolved in a half -pint of water at about 111° (44° C), 
and this solution is to be drunk, in the morning, fasting, in three portions at inter- 
vals of ten or fifteen minutes. Probably its beneficial influence is twofold : it 
modifies the acidity of the gastric juice ; and, through the sulphate of soda it con- 
tains, it acts as a laxative, and empties the stomach. 

Leube insists that in any severe case the patient should keep his bed. Thus 
any violent bodily exertion is avoided. Hot poultices or cold wet compresses 
should also be applied to the abdomen. 

The above methods will usually accomplish all that we can hope to do, and it 
is not till they prove unavailing that, while persisting in our dietetic treatment, we 
should try the other remedies, whose efficiency is often extolled, but has never been 
demonstrated. Among these, the favorite is subnitrate of bismuth in powders of 
five to fifteen grains (grm. 0'30-l*00) each, mixed with sugar. To this we may 
add a sixth of a grain (grm. 0 - 01) of morphine, if there is cardialgia. One powder 
is to be given three times a day, fifteen minutes before meals. Nitrate of silver is 
also frequently administered in pills of one sixth of a grain (grm. 0-01) thrice 
daily ; or in a solution of 1 to 400, of which the dose is one or two teaspoonfuls. 

Finally, there are special symptoms which may need to be relieved. Violent 
pain, when not yielding to regulation of the diet, demands morphine. We may 
also try warm or cold applications, or chloroform, externally. Gerhardt recom- 
mends three or four drops of liquor ferri chloridi in a wineglass of water, for the 
relief of pain. 



364: 



DISEASES OF THE DIGESTIVE OEGANS. 



Excessive vomiting is likewise to be combated by the narcotics, such as opium, 
morphine, chloral, or bromide of potassium. If it prove very obstinate, we may 
try creasote, or three or four drops of tincture of iodine. At the first appear- 
ance of blood in the vomitus the greatest bodily quiet and most careful dieting is 
absolutely indispensable. For the first day or two it is best to allow nothing 
except ice-cold milk and bits of ice in the mouth to appease the burning thirst. 
The patient must lie as quietly as possible in bed. A flat ice-bag, not too heavy, 
should be placed on the epigastrium. In case of persistent nausea or eructations, 
small doses of morphine are to be prescribed. We must wait till four or five days 
after the haemorrhage before we cautiously increase the amount of nourishment, 
which must still be liquid. 

If peritonitis appears as the result of perforation, the best means to try are the 
outward application of ice on the epigastrium and the internal use of opium in 
large amounts — that is, half a grain to a grain (grm. 0*03-0 "05) every one or two 
hours. Unfortunately, however, the cases are exceptional in which the perito- 
nitis does not become general. Then, possibly, operative interference might be 
of some avail. Other measures are almost hopeless. We may try to alleviate the 
pain by narcotics, but it is very rarely that we can prevent a fatal issue. 

[In the treatment of gastric ulcer the leading indication is to promote cicatri- 
zation, and the most powerful agent whose aid we can invoke is rest. The wants 
of the system must be reduced by keeping the patient in bed, and exclusive rectal 
alimentation, with fully peptonized milk, beef peptonoids, etc., should be tried at 
first. In some cases the rectum does not become irritable and the strength is well 
maintained for three weeks or more, no nourishment whatever being given by 
the stomach. In other cases it is necessary, sometimes earlier, sometimes later, 
to give food by the stomach ; but the constant aim should be to demand the mini- 
mum amount of work from that organ until the rest treatment has been given a 
thorough trial.] 



CHAPTER V. 
CANCER OF THE STOMACH. 

^Etiology. — We can not here discuss the astiology of carcinoma in general, 
and we shall therefore merely enumerate the factors which experience has shown 
to favor the development of cancer in the stomach. 

Age has a remarkable influence. Gastric cancer is decidedly most frequent 
late in life, between the fortieth and sixtieth year. Still it is occasionally seen in 
younger persons. We have ourselves seen several cases in persons between 
twenty-two and twenty-five years of age. 

Sex is of no importance. 

Heredity has a slight but undeniable influence. The most famous example of 
the transmission of cancer is presented by the family of Napoleon. 

The relation of gastric cancer to other antecedent diseases of the stomach is 
very interesting. Whether frequent errors in diet or the use of alcohol increase 
the liability to this disease is uncertain. On various sides attention has been 
called to a possible, and as it seems to us very probable, connection of gastric can- 
cer with antecedent ulcer. Not only at the bedside, but at the post-mortem table, 
a relatively large number of cases have been observed where cancer had developed 
on the floor of an old (and usually cicatrized) ulcer. Hauser made the interesting 
discovery a short time ago of a-typical growths of epithelium in the scars of gastric 
ulcers, a phenomenon which points strongly toward the relation suggested. 



CANCER OF THE STOMACH. 



365 



Pathology. — The stomach is a favorite seat for cancer. About a third of all 
cases of cancer are gastric. The parts of the organ most often attacked are the 
pyloric end and the lesser curvature. Less frequently the cardiac end and the 
fundus suffer. 

The new growth takes the form either of a circumscribed tumor or of a diffuse 
infiltration, thickening the walls. The disease invariably originates in the 
mucous layer, extending thence into the submucous and muscular coats. The 
connective and muscular tissues in the neighborhood of the cancer are quite 
often considerably hypertrophied and thickened. 

Histologically, gastric cancer is of the cylindrical-cell variety, starting from the 
glandular epithelium. The soft tumors are termed medullary ; the firm and hard, 
scirrhus or fibroid. The medullary cancers are particularly apt to be quite exten- 
sively broken down on their exposed surface, thus forming what are known as 
cancerous ulcers. This seems to be mainly the result of the gastric juice acting 
on the superficial and insufficiently vascularized portion of the tumor. The base 
of these ulcers is usually clean, as we should expect from the mode of their pro- 
duction. In many cases of rather young subjects, and also in others, we find 
colloid cancer. This form also may appear either in nodules or as a diffuse 
growth, infiltrating the tissues. As to metastasis of gastric cancer, vide infra. 

Clinical History. — Most cases of gastric cancer exhibit a combination of grave 
digestive disturbances with a relatively rapid loss of flesh and strength. Now 
and then the gastric symptoms assume less prominence. The chief sign of dis- 
ease is a constantly progressive marasmus or anaemia, the true cause of which is 
either entirely latent or not unmistakably recognizable till late in the illness. 

Some of the gastric symptoms are not very characteristic. They merely show 
that digestion is disordered. There is loss of appetite and distress after meals. 
The patient complains of a disagreeable sensation of pressure in the epigastrium, 
increased by food. Sometimes this amounts to actual cardialgia. Many patients 
are annoyed by frequent eructations. Occasionally vomiting is frequent ; in 
other instances it is exceptional. The vomitus may contain nothing but mucus 
and the ingesta ; or it may assume, from the admixture of blood, a very charac- 
teristic and somewhat pathognomonic appearance. 

Free gastric haemorrhage and consequent haematemesis is exceptional, or at 
least much less frequent than in ulcer of the stomach ; but the vomitus often 
contains decomposed blood, and in many cases this will be for a time almost a 
constant appearance. Most of the ulcerated cancers bleed frequently, a little at a 
time. The escaping blood is broken up by the action of the gastric juice, its red 
haemoglobine being transformed to the black haematine, which produces that 
" coffee-ground " or u chocolate-colored " appearance of the vomitus so significant 
of the disease. In such cases the presence of blood can be demonstrated conclu- 
sively by the spectroscope, or by means of the so-called haemine reaction. To 
perform this a small portion of the vomitus is heated to boiling in a watch-glass, 
having first been mixed with a little glacial acetic acid and a few crystals of com- 
mon salt. A drop of this is then allowed to dry upon an object-glass, when the 
rhombic crystals of haemine are quickly formed. These crystals have a dark- 
brown color, and are easily recognized {vide Fig. 33, page 366). We should men- 
tion that in the case of ulcerating carcinoma ventriculi the vomitus may have so 
foul an odor that it may even be regarded as stercoraceous. 

Immediate microscopic examination of the vomitus may reveal red blood- 
globules. Other characteristic constituents are rare. It is only rarely that bits 
of cancer can be demonstrated. Of course, if seen, they end all doubt. Sarcinae 
are often seen, just as in other gastric diseases. 

Now and then the chemical examination of the contents of the stomach, or of 



366 



DISEASES OF THE DIGESTIVE OKGANS, 



the gastric juice (vide supra, page 353), may aid in diagnosis. Von den Velden 
Was the first to note that in most cases of cancer the gastric juice contains no free 
hydrochloric acid. Why this should be so is not yet ascertained. Kiegel has dis- 
covered that even normal gastric juice has its digestive power weakened, if the 
secretion of a cancerous stomach be added to it. This makes it seem probable that 
the normally constituted hydrochloric acid is in some way altered by the car- 
cinoma. 

Physical examination of the stomach, and palpation in particular, are of the 
greatest value. In a large number of cases the new growth can be more or less 
plainly felt through the abdominal walls, as a hard, 
. nodular tumor. The tumor is situated in the epigastrium, 

^ in a majority of cases, but it may be lower down or more 
to one side, according to the region attacked. It should 
t\ ^ ^ 0 he remembered always that a permanent tumor may 

Ik # ^1 ^ essentially alter the position of the stomach to which it 
J f ^ ^ is attached. As an illustration, a case of pyloric cancer, 

lj* \ ^ ^ which we saw, with secondary dilatation of the stomach, 
JL> ||^ had resulted in such a displacement of the pylorus that 

™ the tumor was to be felt through the abdominal walls, 

Fig. 33.— Haemine crystals. about a hand's breadth above the symphysis pubis. Some- 
times the tumor varies in position according to the full- 
ness of the stomach. The effect of the respiratory movements upon the tumor 
varies. In some cases, particularly if the tumor is adherent to the liver, it can 
be plainly felt to move downward with each inspiration, while in other cases it 
remains perfectly stationary. 

In a minority of the cases no tumor can be felt at any time. Under such cir- 
cumstances the diagnosis can not often be definitely established. The tumor is 
undiscoverable, first, in most cases of diffuse cancerous infiltration of the stomach- 
walls. We may, indeed, notice an increased sense of resistance and hardness in 
the epigastrium, but can not refer this condition with certainty to a new growth. 
Secondly, the new growth may extend chiefly inward, toward the cavity of the 
organ, and may thus escape detection. And, finally, the tumor may be so concealed 
by the liver or the edge of the ribs that it is inaccessible to the touch . Such 
cancers as attack the cardiac extremity, the posterior wall, or the lesser curvature 
of the stomach, are particularly apt to be out of reach of palpation. 

Percussion of the cancer rarely gives flatness, but instead a muffled tympanitic 
resonance. This is sometimes an influential factor in the differential diagnosis 
from cancer of the liver. 

The physical examination sometimes yields secondary evidences of cancer, in 
addition to those which are due directly to the new growth. In most cases of 
pyloric cancer a resultant dilatation of the stomach can be demonstrated. 

Next in importance to the gastric symptoms is the disturbance of general 
nutrition. Loss of flesh is not rarely the very first symptom which calls the 
patient's attention to his disease. This wasting is observed earliest in cases which 
are attended with anorexia and vomiting. The patient also gradually takes on 
that familiar cachectic look which is characteristic of most cases of cancer. Some 
patients become excessively anaemic. The skin acquires a waxy pallor, and there 
are all the symptoms which result from great anaemia, such as cerebral symptoms 
and functional cardiac murmurs. Sometimes the blood itself presents decided 
peculiarities in such cases. Thus we may find microcytes and poikilocytes in it. 
Gastric cancer and pernicious anaemia (q. v.) have been repeatedly confounded. 
The cause of this excessive anaemia is not always perfectly clear. In one such 
case we made the interesting discovery of extremely abundant metastatic cancer 



CANCER OF THE STOMACH. 



367 



in the bones. As the bone marrow is known to have something to do with the 
production of the blood, it may be that the ansemia was due to this abnormal con- 
dition. At any' rate, the grave anaemia which results from caucer, and sometimes 
also from other chronic diseases of the stomach, particularly gastric ulcer, can 
not be regarded in just the same light as are the loss of flesh and the cachexia. 
Often the anaemia is very great before the general nutrition has suffered much 
impairment. 

When the disease is pretty well advanced there may be moderate oedema of the 
ankles and the back of the hands. This is to be explained, as in other cachectic 
and anaemic conditions, by the impaired nutrition of the vascular walls, the 
hyclraemia, and he cardiac weakness. 

Special derangements of other organs are relatively infrequent. Metastatic 
cancer is of importance. It attacks the liver chiefly. If the hepatic new growth is 
considerable it may quite overshadow the primary cancer. Secondary carcinosis of 
the peritoneum is also apt to cause marked symptoms, such as ascites and abdomi- 
nal pain. Secondary cancer may also involve the mesenteric and retro-peritoneal 
lymph-glands, the lungs, and other organs, but does not usually give rise to strik- 
ing symptoms when so situated. It may be added that patients with cancer of 
the stomach sometimes present a swelling of the lymphatic glands above the clavi- 
cles, especially on the left side, and that many authors regard this fact as of some 
value in making a diagnosis. 

Direct extension of the new growth into neighboring organs is not very fre- 
quent. "We will venture to mention one case which we saw, on account of its 
great rarity. The new growth caused adhesion of the anterior wall of the stomach 
to the abdominal walls, and then, penetrating through them and the skin of the 
epigastrium, finally appeared as a tumor, of about the size of one's fist, projecting 
outward. If a cancer ulcerates, it may destroy all the layers of the stomach, and 
result in perforation and secondary peritonitis ; or, if previous adhesions have 
been formed, the perforation may open up an abnormal communication between 
the stomach and some neighboring part of the intestine. The transverse colon is 
the part usually perforated ; less often the small intestine. 

As to the bowels, constipation is the rule. Diarrhoea is rare. The urine is 
usually pale and but slightly acid. Its amount is diminished, as we should expect 
from the slight amount of nourishment taken, and from the vomiting. Over the 
heart we may sometimes hear soft anaemic murmurs. The pulse is usually accel- 
erated, although, if there be extreme marasmus, it may be slow. The tempera- 
ture is normal, or even subnormal. If there is some inflammatory complication, 
or if the anaemia is extreme, fever may occur. 

The entire duration of the disease may occupy one or two years. It is excep- 
tional for it to last longer, except where the cancer develops in the floor of a 
pre-existing ulcer. In this event, the symptoms of ulcer gradually give place to 
those of cancer. In individual cases the disease, of course, exhibits many varia- 
tions and departures from the typical course. Sometimes the constitutional 
symptoms of weakness and emaciation are more prominent, and sometimes the 
distinctively gastric disorders. 

The fatal termination is usually preceded by the symptoms of constantly in- 
creasing weakness. It may be hastened by complications. Now and then grave 
nervous symptoms appear, often quite suddenly. The patient falls into a condition 
resembling that of diabetic coma (q. v.), he is somnolent, and has a peculiar 
dyspnoea, with deep and labored respirations, and such an attack almost always 
ends fatally. Recovery from cancer of the stomach is unknown. 

Diagnosis. — In addition to the ordinary symptoms common to most gastric 
disorders, such as pain, eructations, and vomiting, the distinctive factor in diag- 



368 



DISEASES OF THE DIGESTIVE OKGANS. 



nosis is the discovery of a tumor connected with the stomach. The demonstration 
of this is almost conclusive. Other subsidiary evidence can be obtained in most 
instances. The patient is wasted, has a cachectic look, and is somewhat advanced 
in years. The most characteristic gastric symptom, a» we have already said, is 
coffee-ground vomitus, containing blood. 

It is not always easy, nor even possible, to make sure that a tumor in this 
region is really of gastric origin. The chief characteristics of the tumor of gastric 
cancer have already been mentioned. The chief thing to exclude is cancer of the 
left lobe of the liver, or of the pancreas, omentum, or transverse colon. No general 
scheme for the differential diagnosis between these and the gastric disease can be 
given, for the circumstances and difficulties vary with almost every case. A careful 
consideration of all the facts, and wide personal experience at the bedside and the 
post-mortem table, are requisite here ; and yet the most practiced diagnostician 
may be misled. 

We may be able, however, to feel a tumor plainly, and to be sure that it is 
gastric, and still find it difficult, or even impossible, to determine whether it is 
cancerous, or whether it is not a circumscribed induration and thickening result- 
ing from an ulcer of the stomach. This is particularly true of small tumors near 
the pylorus, attended with secondary dilatation. The clinical symptoms are usu- 
ally valueless here, for stenosis of the pylorus must produce identically the same 
symptoms in either case. The age of the patient, the duration of the disease, and 
possibly the history of characteristic symptoms earlier in the illness, may enable 
us to reach a probable diagnosis. In such cases, and indeed in any doubtful ones, 
we may test the contents of the stomach for free hydrochloric acid, and, if this is 
invariably absent, cancer may be inferred. We should add that there are cases, 
as we know from our own personal experience, of simple, non-cancerous, pyloric 
hypertrophy, with stenosis. These may yield no evidence of previous ulceration, 
and can not be clinically differentiated from cancer. Nor is it at all exceptional 
to meet with difficulty, even at the autopsy, in diagnosticating between cancer, 
cicatrized ulcer, and hypertrophy. We are then obliged to resort to the micro- 
scope, unless we find metastatic cancerous nodules. 

In the cases of cancer where no tumor can be made out, a probable diagnosis 
may be made, if there is clear evidence of grave gastric disturbance, with excessive 
emaciation, in an elderly person. The characteristic, dark-colored vomitus would 
strengthen our diagnosis if it occurred. The chief points in the differential diag- 
nosis bet ween cancer and ulcer are the duration of the disease, and the presence or 
absence of the hsematemesis, cardialgia, and other symptoms characteristic of 
ulcer. Still, it may be no easy matter to decide, particularly in rather young 
patients. 

Treatment. — As to treatment, we must be content if we relieve the patient's 
suffering. We possess no means of antagonizing the new growth. The bark of 
cundurango, which Friedreich recommended a few years ago, has not proved 
efficient. It may, however, be given with some advantage, as it seems to be a 
good stomachic tonic. A decoction may be made of 15 parts of the bark to 150 of 
water, and 10 parts of syrup of orange-peel may be added to improve the taste. 

Great interest has been evinced in the attempts lately made by Billroth and 
others to remove gastric cancer by operation. Certainly some of the cases have 
been very encouraging, although many, of course, have been unsuccessful. Beside 
the technical difficulties of the operation, it is often very hard to determine the site 
and extent of the new growth, or whether there are secondary deposits. We have 
reason, however, to hope that operative treatment will prove valuable in simple 
hypertrophy and cicatricial stenosis of the pylorus, with secondary dilatation 
(see the following chapter). 



DILATATION OF THE STOMACH. 



369 



The symptomatic treatment of gastric carcinoma does not differ greatly from 
that repeatedly described in the preceding chapters. The diet must be regulated, 
and the administration of hydrochloric acid is important, inasmuch as we know it 
to be absent from the gastric juice in this disease. Otherwise we merely fulfill 
such indications as arise. For pain we use the narcotics, and warm or cold appli- 
cations. If there is persistent vomiting, we give small doses of opium or mor- 
phine, chloral, bits of ice, creasote, or tincture of iodine. For acid eructations, we 
prescribe bicarbonate of soda or magnesia. Very considerable, although unfor- 
tunately only temporary, benefit is derived from washing out the stomach. The 
most suitable cases for this are those of pyloric cancer with consequent dilatation. 
The various stomachic tonics and bitters must not be forgotten. Our chief aim 
must be to maintain the patient's strength as long as possible, and to do what we 
can, morally as well as physically, to alleviate his unhappy fate. 



CHAPTER VI. 
DILATATION OF THE STOMACH. 

iEtiology and Pathology. — Dilatation of the stomach is, in a majority of 
instances, a secondary condition, the result of pyloric constriction. As we have 
already seen in the preceding chapters, this constriction is usually due either to 
cancer or some other new growth, or to the scars of ulcers. Narrowing produced 
by pressure from without is relatively infrequent. Tumors in the neighborhood 
may, however, thus cause dilatation ; and, if Bartels be correct, a movable right 
kidney may also compress the pylorus or the beginning of the duodenum suffi- 
ciently to produce the same result. 

The manner in which the stenosis leads to dilatation is perfectly analogous 
with that in which stenosis of the aorta causes dilatation of the left ventricle. The 
propulsion of food out of the stomach into the duodenum becomes more difficult, 
and consequently the muscular fibers of the stomach are aroused to abnormal 
activity that this hindrance may be at least in part if not wholly overcome. As 
a physiological sequence, we find in most cases of pyloric stenosis the muscular 
coat hypertrophied, and particularly so in the neighborhood of the pylorus. It 
is not till the muscle proves inadequate to overcome the obstruction that the 
dilatation begins. A portion of the ingesta remain in the stomach, and the bulk 
of this stagnating mass gradually increases. Its weight and pressure have a 
direct mechanical influence in promoting the gradual expansion of the organ. In 
addition, the processes of decomposition usually attack the contents of the stom- 
ach, and the gases thus generated contribute largely to the mechanical dilatation. 
Speedily these abnormal chemical and other irritants excite catarrh. The catarrh 
lessens the resisting powers of the tissues, interferes with the absorption of the 
contents of the stomach, and in both ways tends to increase the dilatation. The 
united effect of all these pernicious influences may finally be to produce a dilata- 
tion up to three or four times the normal volume of the organ, the flabby fundus 
hanging down like a great bag into the hypogastrium. 

In a smaller number of cases of dilatation we find no stenosis of the pylorus. 
A large dilatation of this sort is very rare. Smaller degrees of enlargement may 
frequently exist; but still they are so difficult to diagnosticate with certainty that 
we can not really say just how frequent they are. The cause of such dilatations 
is in many instances an impaired power of resistance, affecting chiefly the muscu- 
24 



370 DISEASES OF THE DIGESTIVE OKGANS. 



lar layer. This condition may sometimes be due to congenital weakness of the 
muscular fibers, which not only makes them more yielding, but also favors the 
retention and stagnation of food in the stomach. In other cases the walls are 
weakened by disease. Thus, a persistent chronic catarrh may lead to moderate 
dilatation ; or constitutional weakness resulting from anaemia or severe illness 
sometimes renders the gastric muscular fibers so weak as to permit dilatation. In 
all such cases muscular insufficiency is the chief factor, because it favors the 
accumulation of ingesta within the stomach. In chronic gastric catarrh, it is 
probable that the muscular fibers become not merely weak but paretic, just as the 
muscles of the larynx frequently do in laryngeal catarrh. 

One factor of gastric dilatation remains to be mentioned. It is the habitual 
overloading of the stomach with ingesta. That gluttons and drunkards are liable 
to dilatation of the stomach has long been a familiar fact. Such a condition may 
well be compared to cardiac dilatation from excessive tension, and may be termed 
"overstraining of the stomach." The condition does not become strictly patho- 
logical till compensation begins to be insufficient, so that even the hypertrophied 
muscles are no longer equal to the task of propelling the food properly into the 
duodenum. In diabetes excessive ingestion and deficient nutrition combine to 
produce dilatation, and it has been repeatedly observed in this disease. 

Symptoms and Diagnosis. — The gastric symptoms are only in part due to the 
dilatation, being also due to the original lesion or to other attendant circumstances. 
Most patients complain of loss of appetite, frequent or constant pressure in the 
region of the stomach, heartburn, eructations,* and vomiting. The vomiting is 
frequently to a certain extent characteristic. It occurs at rather long intervals, 
and then a very considerable amount is vomited at once. There may be several 
quarts ejected. The vomitus not infrequently contains bits of food eaten several 
days previously. Usually vomiting affords the patient temporary relief. 

We must have recourse, however, to physical examination in order to be cer- 
tain about our diagnosis. In many cases, although by no means in all, inspection 
reveals the contours of a distended stomach through the abdominal walls. The 
fundus and the greater curvature are most prominent. Sometimes we can observe 
the peristaltic movements of the stomach, which if not present may perhaps be 
started up by the mechanical irritation of sudden and repeated palpation. If we 
administer to the patient a half -drachm each of so die bicarbonate and tartaric acid, 
one after the other, as suggested by Frerichs, the consequent distention of the 
stomach with carbonic-dioxide gas will often render its dimensions much more 
evident, and we shall also be able to ascertain if the prominence already noticed 
is really gastric. 

By palpation it is often possible to make out the greater curvature and the 
fundus still better than by inspection, particularly if the muscular coat happens 
to be contracted. A splashing sound may sometimes be evoked by giving quick, 
short blows with either hand alternately upon the walls of the stomach. We can 
hear and feel the contents of the stomach rushing to and fro with great distinct- 
ness. This is very characteristic, though not pathognomonic. 

To determine the size of the stomach by percussion is so difficult that percus- 
sion is seldom as reliable as inspection and palpation, but now and then it does 
aid us. The patient must be examined in both the erect and the recumbent pos- 
ture, and both when the stomach is full and when it is empty. If we introduce 
about a quart of water into the empty stomach and then find a line of dullness 
below the navel which was not there before, we have good reason to believe that 
the organ is dilated. This is Penzoldt's test. Sometimes we are unable to define 



* In some instances the regurgitated gases have proved inflammable. 



DILATATION OF THE STOMACH. 



371 



the limits of the stomach, by percussion until we have dilated it with carbonic 
dioxide ; but of course we are to bear in mind that the stomach is thus expanded 
beyond its usual limits. 

The use of the bougie is valuable. In health the instrument will only pene- 
trate about sixty centimetres, measured from the mouth, while in dilatation it can 
often be introduced as far as seventy centimetres. Occasionally we may be able 
to feel the end of the bougie through the lax abdominal walls, as Leube first 
remarked. In such a case the nearer the point is to a horizontal line joining 
the two anterior superior spinous processes of the ilium, the greater is the cer- 
tainty that dilatation exists. Under ordinary conditions the bougie does not prob- 
ably extend any lower than the level of the umbilicus, if as far as that. 

A consideration of the symptoms already enumerated, combined with the 
above methods of physical examination, will in many cases enable us to diagnos- 
ticate with certainty any considerable dilatation of the stomach ; and yet it must 
be confessed that sometimes quite extensive dilatation may escape observation. 
In such instances there may be either a partial or complete absence of symptoms 
suggestive of any serious gastric derangement, so that no careful examination of 
the organ is made, or the methods of physical examination already mentioned, 
when employed, yield a negative or ambiguous result. It is true that other 
methods have been suggested by various authorities to determine the size of the 
stomach and test the functional capacity of its muscular tissue ; but none of these 
have as yet been generally adopted. Thus Schreiber introduced an India-rubber 
bag on the end of a catheter, and tried by blowing it up to gain information as to 
the size and position of the organ. With the same end in view, Eosenbach prac- 
ticed auscultation of the rales caused by blowing into a catheter, the opening of 
which was placed at the level of the fluid contained in the stomach. 

Other symptoms are mostly analogous to those seen in other severe gastric dis- 
orders. The general nutrition becomes gradually so impaired, particularly if 
there is much vomiting, that the patient may seem like a skeleton. Kussmaul 
has sometimes observed painful cramps in the flexors of the arms, the calves, and 
the muscles of the abdomen. These he refers to the abnormal dryness of the 
muscular tissue. The bowels are almost always very much constipated, mainly as 
a result of the diminished amount of ingesta which reaches the intestine. The 
urine is small in amount, and often neutral or alkaline in reaction. The alkaline 
reaction Quincke believes is more apt to be present while the stomach is being 
washed out, because in this way the system is deprived of a relatively large 
amount of acid. 

Course of the Disease and Prognosis— The course and duration of the disease 
are chiefly dependent upon the nature of the original lesion from which the dila- 
tation proceeds. If there is cancerous stenosis of the pylorus, of course the case 
is hopeless. Cicatricial stenosis with secondary dilatation allows a more favorable 
prognosis. With proper treatment and a sensible mode of life, the patient may 
be tolerably comfortable for years ; but finally nutrition becomes more and more 
impaired and death ensues. 

The general course of the disease presents all sorts of vicissitudes. As long as 
the hypertrophied muscles are able to overcome the abnormal obstruction, there 
may be no symptoms of importance. Just as in cardiac cases, it is only when 
compensation becomes disturbed that the results of dilatation are observable. If 
we can tone up the muscles again, or reduce the work they are called upon to per- 
form to an amount which they are capable of accomplishing, marked relief fol- 
lows. 

Those cases of dilatation which are not due to pyloric stricture have, on the 
whole, the best prognosis. In milder cases of this kind there may be permanent 



372 



DISEASES OF THE DIGESTIVE OEGANS. 



ally at its lower end. 



recovery, provided proper mechanical and dietetic treatment be promptly and per- 
sistently employed. 

Treatment. — Our first aim in treatment should be to relieve the dilated organ 
of the great amount of material it contains and to avoid new accumulations. If 
this double effort is successful, we have removed the injurious influences, both 
mechanical and chemical, which we have seen to maintain and persistently to 
aggravate the dilatation. 

The indication is best met by the " mechanical treatment of dilatation," for 
which we are so deeply indebted to Kussmaul. This method is beneficial to the 
chronic catarrh which accompanies the dilatation, or which may even have pro- 
duced it. We have no direct means of treating stenosis of the pylorus, if it exists, 
unless possibly by surgical operation (vide supra). 

The most thorough way to empty the stomach is by means of the stomach- 
pump — that is, a piston-syringe with two tubes attached to it. One is connected 
with a stomach-tube, and through it the contents of the stomach are drawn into 
the barrel of the syringe, to be forced out through the other tube into a suitable 
receptacle. In this manner the contents of the stomach are gradually removed. 
It is important to have the stomach-tube long enough. It should measure at least 
seventy centimetres ; and it should have a sufficiently large opening placed later- 
The soft Nelaton catheter is now made in appropriate sizes, 
and is the best instrument to use, as its introduction can 
not result in mechanical injury. 

If the opening of the stomach-tube gets stopped up, we 
must not make violent efforts to overcome the obstruction 
by suction, but should wash the tube clear by injecting 
a little water. When the stomach has been pretty well 
emptied, we have next to rinse out the organ. In this 
way the last remnants of food and, what is still more im- 
portant, the tenacious coating of mucus, are removed. 
One or two pints of fluid are slowly injected and then 
pumped out ; and this process is repeated till the fluid 
comes away almost perfectly clear. Pure water may be 
used, or, still better, a one- or two-per-cent. solution of 
bicarbonate of soda or Carlsbad salts. If there is reason 
to suppose that the processes of decomposition are espe- 
cially active, we may employ a one-per-cent. solution of 
salicylic acid, or a two-per-cent. solution of resorcine. The 
stomach should be washed out once a day, half an hour 
before the heartiest meal. 
1 , 1 Of late, a siphon apparatus has largely taken the place 

I ^^^F of the stomach-pump. The credit of it belongs chiefly to 

I Ploss and Jiirgensen. It is much simpler and cheaper, 

II and in many cases answers every requirement for the 
% mechanical treatment of the stomach. Still, the stomach 

can not be so completely emptied by siphonage as by the 
pump. On the other hand, it has repeatedly happened that 
a person using the stomach-pump has drawn a bit of 
mucous membrane into the fenestrum of the tube, and 
actually torn it off, while the use of siphonage never 
entails this misfortune. 

The apparatus is made by connecting a rubber tube, 
one metre long, with a stomach-tube at one end, and at the other with a medium- 
sized glass funnel (vide Fig. 34). The stomach-tube being introduced and the 




X 



Fig. 34. —Stomach tube, 
with Hegar's funnel. 



DILATATION OF THE STOMACH. 



373 



funnel raised, the external tube is entirely filled with, water and then lowered 
to the floor, whereupon a siphon is formed and the contents of the stomach are 
drawn off. By alternately pouring water or solution of soda into the stomach 
and emptying the organ, we can usually get it quite thoroughly rinsed out. It 
is still more convenient to connect the upper end of the stomach-tube with a 
Y-shaped glass tube (vide Fig. 35, c), one branch of which has a rubber tube 
attached to it and leading to an irrigator, while the other branch has a tube lead- 




FiG. 35. 



ing to a receptacle upon the floor. This arrangement renders it possible, by 
alternate opening and closure of the two external tubes d and e, to introduce fluid 
into or allow it to flow from the stomach at will. 

The siphoning apparatus and the manipulations required are so simple that we 
have repeatedly treated patients with dilatation who washed out their own stom- 
achs every day. 

The patient's diet should be carefully regulated. The food should be nourish- 
ing, easily digestible, and of the least possible bulk. We should therefore try 
Leube's meat solution, fine shavings of raw beef or ham, soft-boiled eggs, and milk 
in small amounts, but should avoid vegetables, coarse bread, and the like. In this 
way we can usually succeed in improving the patient's nutrition decidedly, and 
the vomiting and sense of gastric oppression as well as other disagreeable symp- 



374 



DISEASES OF THE DIGESTIVE ORGANS. 



toms will cease. Whether the improvement will be permanent depends, as has 
been said, upon the nature of the dilatation and the causal lesion. 

In case the persistent objection of the patient or outward circumstances renders 
the mechanical treatment impracticable, we may seek to empty the stomach gradu- 
ally by regulating the diet and administering Carlsbad salts or some other mild 
laxative. We may also have recourse to the various remedies proposed for chronic 
gastric catarrh. It is advantageous to have the patient wear an elastic bandage 
firmly applied around the abdomen. 

In conclusion, we should mention that the attempt has been made to tone up 
the muscular fibers of the stomach and stimulate them to more vigorous contrac- 
tion. Energetic faradization and galvanization of the stomach have been recom- 
mended. The application may be made through the abdominal walls, or by 
means of an electrode introduced through a stomach-tube. Nux vomica has also 
been employed to meet the same indication. 



CHAPTER VII. 
GASTRIC HEMORRHAGE. 

The most important and frequent forms of gastric haemorrhage have been 
already fully discussed under ulcer and cancer of the stomach. We have there- 
fore merely to point out briefly some other circumstances under which such a 
haemorrhage may arise. 

First comes haemorrhage as a result of venous stasis in the blood-vessels of the 
stomach. The chief diseases in which this occurs are cirrhosis of the liver and 
thrombosis of the portal vein. It is much less frequent in other hepatic disorders 
and in pulmonary or cardiac diseases. The consequent loss of blood may be con- 
siderable and may occur repeatedly. 

Gastric haemorrhage may also take place where there is a general haemor- 
rhagic diathesis, as in scurvy or purpura haemorrhagica. The gastric haemor- 
rhages of leukaemia come under the same head. Haemorrhage from the stomach 
has also been observed in yellow fever, acute yellow atrophy of the liver, and 
other severe acute diseases which have a tendency to cause haemorrhage. 

Finally, there is one peculiar disease to be mentioned — namely, the so-called 
melasma neonatorum. Children in the first week of life may in rare instances 
suffer from gastric and intestinal haemorrhage, with haematemesis and bloody 
stools. The cause has not yet been definitely made out. In a certain proportion 
of cases there are gastric or duodenal ulcers. In others the haemorrhage is said 
to result from a disturbance in the circulation due to insufficient respiration. 
The condition is rather dangerous, for most of the children die, although recovery 
may ensue in what seem to be the most hopeless cases. 

For particulars as to symptomatology, diagnosis, and treatment, we may refer 
to the chapter on gastric ulcer. 



NERVOUS AFFECTIONS OF THE STOMACH. 



375 



CHAPTER VIII. 

NERVOUS AFFECTIONS OF THE STOMACH. 

{Nervous Dyspepsia.) 

The frequent experiences of daily life show how largely the functions of the 
stomach are subject to nervous influences. Great emotional excitement, in par- 
ticular, affects the stomach in a way which we can not fail to recognize. Prob- 
ably every one has experienced the complete loss of appetite attendant upon either 
violent anger, deep anxiety, lively expectation, or any sudden excitement, 
whether sad or joyful. In emotional persons the disturbance is greater ; so that 
in them it is by no means exceptional, under such circumstances, to observe nau- 
sea, vomiting, and pain in the epigastrium. The pain may even assume the violent 
neuralgic character of cardialgia. If such occasions recur frequently, or if the 
symptoms evoked by a single period of violent excitement do not immediately 
vanish, a diseased condition is gradually developed. Such a state is appropriately 
termed a nervous gastric disorder, or nervous dyspepsia. The disease is also very 
often occasioned by hypochondriasis, the attention of the patient being abnor- 
mally directed to the processes of digestion. 

Men and women are attacked with equal frequency. In most cases there is a 
pronounced " neurotic constitution " — that is, an excessive sensitiveness to physical 
influences, a predisposition to those innumerable nervous derangements which are 
classed as " hysterical " or " neurasthenic " in order to mask the inaccuracy of our 
knowledge under a term which is universally accepted. The different gastric 
symptoms are the same as in other diseases of the stomach, only they have no dis- 
coverable anatomical basis. The patient complains of anorexia, but is liable, to 
temporary attacks of ravenous hunger. Quite often the stomach is excessively 
sensitive, so that the ingestion of a small amount of food excites a marked feeling 
of oppression. External pressure upon the stomach may likewise cause pain, or 
it may, on the other hand, relieve the disagreeable sensations already present. 
Vomiting is frequent, and it differs from the vomiting which occurs in the gastric 
diseases where there is an anatomical lesion, in that it is not wholly, if at all, 
dependent upon the ingestion of food. It often takes place when the stomach is 
entirely empty — the vomitus consisting of nothing but mucus, bile, and the like. 
Occasionally there may be very violent attacks of vomiting, persisting for hours 
or even for some days, and attended with violent cardialgia and a wretched gen- 
eral condition. Leyden terms this " periodical vomiting with cardialgic attacks." 
If the matter vomited in such attacks is excessively acid, we have the condition 
described by Rossbach as " nervous gastroxynsis " (ogvs, sharp or acid). Eructa- 
tions are still more frequent than vomiting. As a rule it is only common air that 
is thus emitted, and very seldom any abnormal or offensive gas. If a portion of 
the contents of the stomach is actually regurgitated, there is sometimes acute 
heart-burn. In many instances gastric peristalsis is observed to be exaggerated, 
so that it can be both seen and felt through the abdominal walls. The move- 
ments may occasion all sorts of abnormal cooing sounds, and may often prove a 
source of annoyance to the patient. Kussmaul has made a special study of this 
phenomenon, and given it the name of nervous " peristaltic restlessness." 

Almost invariably there are also other nervous symptoms than those referable 
to the stomach. Very great light will be thrown upon the diagnosis by careful 
attention to the mental condition and the influence of the latter upon the gastric 
symptoms. Many patients display great mental irritation in their behavior, and 
are extremely sensitive and easily thrown out of equilibrium. Others develop 



376 



DISEASES OF THE DIGESTIVE ORGANS. 



pronounced hypochondriasis. Very frequently a headache comes and goes simul- 
taneously with the gastric disturbance, or there is a sense of pressure in the head, 
or vertigo. Many cases of " gastric vertigo " certainly belong, as we have said, 
under this category. Abnormal sensations in the extremities are also not very 
infrequently observed, such as pain or numbness or a sense of coldness. Very 
often intestinal symptoms accompany the gastric troubles. The patient complains 
of persistent abdominal distention, and of difficulty and irregularity in the move- 
ments of the bowels. 

The general nutrition sometimes remains unimpaired. The healthy appear- 
ance and ruddy cheeks of the patient offer a striking contrast to his complaints of 
a " severe disease of the stomach," and of inability to take proper nourishment ; 
but in many cases there is decided malnutrition. If the patient really takes very 
little food for a long period, and suffers from frequent vomiting, he becomes 
greatly emaciated, so that a severe disease may well be suspected. 

In such instances, the diagnosis is not always obvious. We should consider 
the serological factors first of all, and in particular the relation of the symptoms 
to mental disturbances. Influences which experience has shown to be capable of 
disordering the nervous system should also be regarded, such as undue mental 
exertion, hereditary predisposition to nervous diseases, and in women sexual 
disorders and menstrual derangements. The coincidence of the gastric symptoms 
with other constitutional, nervous, or " neurasthenic " symptoms (vide supra) is 
also significant. The result of the physical examination of the stomach in 
nervous dyspepsia must of course be negative in every case. Possibly there may 
be tenderness on pressure — that is, hyperesthesia of the region of the stomach. 
This is sometimes quite acute ; but, as we have said, it is characteristic of many 
cases of purely nervous cardialgia, that the pain is diminished by firm pressure 
over the stomach. Other injurious influences, which would aggravate a gastric 
disease due to any pathological lesion, such as errors in diet, are not at all certain 
in these nervous troubles to work any great harm. If it is practicable to examine 
the contents of the stomach by means of the stomach-tube (vide supra), it will be 
found that digestion pursues a perfectly normal course, a discovery which is of 
course of value in diagnosis. 

The prognosis depends mainly upon the outward circumstances of the patient. 
If the harmful mental influences or other etiological factors are persistently 
active, actual and permanent recovery is hardly to be expected ; but if the cause 
can be removed, complete recovery is not rare, even in what seem to be grave 
cases. A liability to relapses is, of course, almost always left behind. 

Treatment. — If nervous dyspepsia has once been diagnosticated, the proper aim 
of our therapeutic efforts becomes perfectly definite. We must, in the first place, 
convince the patient that he has no incurable nor even dangerous gastric disease, 
but that, on the contrary, his stomach is perfectly capable of performing its 
functions in a normal manner. Nothing could be more harmful to a sufferer 
from nervous dyspepsia than to have his physician manifest great anxiety about 
treatment, and prescribe a very strict diet. The patient must rather be gradually 
led to use an abundance of nutritious food. It is in this way alone that he 
regains a confidence in himself, when he sees that the hearty food does him no 
harm, that he is gaining flesh, and that the bowels are becoming regular. 

Internal remedies are best omitted altogether if the patient has already taken 
a good deal of medicine. We should particularly warn him against the abuse of 
purgatives. If we must prescribe something, a bitter tonic is very good, such as 
tincture of nux vomica. Anemic patients may also take iron. 

On the other hand, those methods of treatment are of great value which are 
directed to the toning up of the body in general and the nervous system in par- 



INTESTINAL CATAERH. 



377 



ticular. The patient may go into the country or to the mountains or the sea- 
shore. Methodical treatment with cold water is good ; in particular, sponging, 
combined with rubbing of the trunk and the whole body, almost always gives 
good results. We have repeatedly found electricity valuable, although we are 
not prepared to deny that its subjective effect may be of chief importance. Gal- 
vanism is applied along the spinal column, and through the stomach horizontally, 
one large electrode being placed upon the epigastrium and the other on the back. 
It is well to reverse the current frequently. Faradization of the abdominal walls 
is indicated, especially when there is constipation. 

We need hardly add that the serological factors must not be overlooked. The 
patient must be warned against useless over-exertion, emotional excitement, etc. 
(Compare the chapter on neurasthenia.) 



SECTION V. 
Diseases of the Intestines, 
CHAPTER I. 

INTESTINAL CATARRH. 

{Catarrhal Enteritis.) 

JEtiology. — The majority of cases of intestinal catarrh, like gastric catarrh, are 
due to an abnormal irritation of the mucous membrane of the intestine by its 
contents. In most cases the irritants are of a mechanical or a chemical nature 
and depend upon the quantity and quality of the food taken, which explains why 
catarrh of the stomach and of the intestine are so often combined with each other. 
Noxious substances, taken into the intestine by the ingestion of spoiled food, like 
spoiled meat, fish, beer, etc. , very often play a part in the origin of intestinal catarrh. 

To the intestinal catarrhs caused by improper food we may add the toxic 
catarrhs which are produced by the direct ingestion of poisonous substances into 
the digestive tract. Severe inflammations of the intestinal mucous membrane 
arise from poisoning by mineral acids and corrosive alkalies, arsenic, corrosive 
sublimate, etc. Intestinal catarrh may also arise from the imprudent use of 
certain drugs, especially active cathartics. 

A great many mild and severe cases of intestinal catarrh are due to infectious 
influences, including most of the apparently spontaneous catarrhs, and also many, 
if not all, the catarrhs attributed to taking cold or getting wet, and, finally, those 
affections which often develop epidemically or endemically in hot weather, and 
which we term summer complaint, cholera morbus, etc. Cholera morbus is an 
especially severe form, and will be described more fully later on. We must also 
mention here that intestinal catarrh is very often one symptom of other general 
infectious diseases, like typhoid, dysentery, septic diseases, or severe malaria. 

In a final class of cases intestinal catarrh develops from disturbances of the 
circulation, which cause a passive hypersemia of the intestinal mucous membrane. 
Diseases of the liver and portal vein, and also chronic diseases of the heart and 
lungs, are the chief affections which produce a stasis in the portal system, and 
thus an intestinal catarrh ; but here the stasis is probably, in most cases, only a 
predisposing factor in the development of the catarrh, since the action of all other 
irritants is made easier by the disturbance of the circulation. 

The great frequency of intestinal catarrh in both sexes, and at every age, is 



378 



DISEASES OF THE DIGESTIVE ORGANS. 



well known. Children, above all, have a pronounced tendency to diseases of 
the intestine, so that, by a probable estimate, almost one third of the illnesses 
of children are to be referred to the intestinal canal. We will give a special 
description of intestinal catarrh in children on account of the importance of this 
fact. 

Pathological Anatomy. — The pathological changes in catarrhal inflammation 
of the intestines are essentially the same as are met with in the inflammation of 
any other mucous membrane. Redness and swelling of the mucous coat, increased 
secretion of mucus, and in severe cases purulent products on the surface of the 
membrane, and a cellular in fi ltration of the tissue itself, are the well-known pro- 
cesses characteristic of all catarrhal inflammations. The solitary and agminated 
follicles often swell in follicular catarrh, and may finally become the seat of 
superficial follicular ulcers. We often find superficial erosions on the rest of the 
mucous membrane, and in severe cases the so-called catarrhal ulcers. 

If the catarrh has lasted a long time, we sometimes find quite a considerable 
thickening of the mucous membrane, which is due to a hyperplasia of the connect- 
ive tissue, and which gives an uneven, puffy appearance to the internal surface 
of the intestine. Circumscribed hyperplasia of the connective tissue may actually 
lead to the formation of polypi. If the orifices of Lieberkiihn's follicles are 
stopped, we have a cystic degeneration of the follicles from the retention of the 
intestinal juice. 

We very often find, however, a considerable atrophy of the mucous membrane, 
especially in the chronic intestinal catarrh of children. This atrophy, which has 
lately been carefully investigated, especially by Nothnagel, affects chiefly the 
glandular layer of the mucous coat. In place of the glands, which in many parts 
may wholly disappear, we find connective tissue more or less rich in cells. The 
atrophy is usually most pronounced in the colon and the lower part of the ileum. 
The muscular coat may also take part in the atrophy. 

Certain peculiarities of catarrh affecting single portions of the intestine will be 
mentioned later on. 

Symptomatology. — The symptom by which we chiefly determine an affection 
of the intestinal canal, and which in the milder cases is often almost the only sign 
of an intestinal catarrh, is diarrhoea — that is, abnormally frequent stools of a looser 
consistency than usual ; yet, strictly speaking, we should not attribute every 
diarrhoea to a catarrh of the intestinal mucous membrane, since a large number of 
influences may directly produce an increased peristalsis and a consequent diar- 
rhoea. Thus, for instance, it is a well-known fact that sudden terror or great 
anxiety may sometimes cause an obstinate diarrhoea in a very short time. In 
general nervous and neurasthenic conditions we sometimes have a chronic diar- 
rhoea which can be due only to abnormal processes of innervation — u nervous 
diarrhoea. " The diarrhoea which may arise immediately after taking cold is also 
merely the result of abnormally great peristaltic movements excited in a reflex 
manner. Probably a number of chemical and infectious irritants may also stimu- 
late the movements of the intestines, and thus set up a diarrhoea, without causing 
at the same time a catarrh of the mucous membrane. Practically, however, we can 
not make a sharp distinction between diarrhoea and intestinal catarrh, and, in most 
of the diarrhoeas which have lasted for some time, we are certainly right in suppos- 
ing that there are actual anatomical lesions of the intestine, as well as functional 
disturbances. 

There are two chief factors which cause diarrhoea in intestinal catarrh. In the 
first place, as has already been intimated, the same injurious substances which 
cause the catarrh also excite peristalsis. The many products of the abnormal pro- 
cesses of decomposition in the intestine also exert a like influence. Beside the 



INTESTINAL CATAKKE. 



379 



abnormal irritants, however, we must probably also consider an abnormally great 
irritability of the intestinal walls in catarrh. Thus it happens that the fluid con- 
tents of the intestine are expelled by the vigorous peristaltic movements, which 
the patient often feels himself as a " rumbling in the abdomen," before the normal 
consolidation of the faeces is completed by the absorption of water. The food, 
under normal conditions, passes through the small intestine in two or three hours, 
and thus the consolidation of the fasces takes place, as is well known, almost exclu- 
sively in the colon. We see, therefore, why the diarrhoea owes its origin chiefly 
to the increased peristalsis of the large intestine ; although in many cases the 
peristaltic action of the small intestine is also increased. 

In the intestinal catarrh from passive congestion we must probably consider 
still another factor beside increased peristalsis, to explain the thin and watery 
stools — namely, the diminished absorption of water by the intestine from disturb- 
ance of the circulation. In other catarrhs this factor is quite subordinate to 
increased peristalsis. 

The diarrhoeal dejections show a considerable difference in regard to their minor 
characteristics. Their number varies very much. There are sometimes two or 
three, and sometimes ten or more, evacuations in the twenty-four hours. The con- 
sistency of the stools is pap-like, or almost wholly watery. This is due to the 
abnormal amount of water in them, amounting to ninety or ninety-five per cent., 
while the amount in normal stools is about seventy-five per cent. The color of the 
thin stools in intestinal catarrh is usually bright yellow, but they are sometimes 
greenish from the admixture of bile pigment, and sometimes slimy (vide infra). 

In only a part of the cases does microscopic examination give us information 
as to the extent and intensity of the catarrh. We usually find the remains of the 
food, muscular fibers, starch-granules, and fat, and also countless bacteria, and 
often triple phosphates, occasional pus-corpuscles, and cylindrical epithelium — 
chiefly the constituents which are found in normal stools. Further peculiarities 
will be mentioned below. 

Beside the diarrhoea, there is often, but by no means always, abdominal pain in 
intestinal catarrh, either continuous, or having the character of the paroxysmal, 
so-called colicky pains. In catarrh of the rectum there is that constant painful 
desire to go to stool which we term tenesmus. 

Physical examination of the abdomen gives, on the whole, few important results. 
Sometimes the abdomen is flat, and sometimes there is meteorism. Marked peris- 
taltic action of the intestines often causes gurgling and rumbling noises — borbo- 
rygmi. On palpation, the abdomen is often somewhat sensitive. The peculiar 
colicky pains, however, are, as a rule, alleviated by external pressure. In rare 
cases we may detect a fluctuation on palpation, if the intestine contains much 
fluid. The results of percussion depend largely upon the fullness of the intes- 
tines. 

In many cases of simple diarrhoea the general health is practically unaffected, 
but in other cases of acute intestinal catarrh, especially in the severe infectious 
forms, the disturbance of the general health may be quite considerable. The 
patient feels so dull and weak that he stays in bed. We often see a moderate rise 
of temperature, between 100° and 102° (38°-39° C). There are very often gastric 
symptoms also, especially loss of appetite and vomiting. Other organs are quite 
rarely affected, except in duodenal catarrh, when the liver is involved {vide infra). 
In acute infectious intestinal catarrhs there is sometimes an eruption of herpes on 
the lips. We have repeatedly seen, in severe cases of acute enteritis, marked mus- 
cular and articular pains, and even slight but manifest swelling of the joints. 

Different Forms of Intestinal Catarrh.— Since the intestine is an organ which 
is only slightly accessible to physical examination during life, and since we can 



380 



DISEASES OF THE DIGESTIVE ORGANS. 



only rarely make a post-mortem examination in the mild diseases of the intes- 
tine, our knowledge as to the different forms of enteritis is defective in many 
respects. In practice we content ourselves in most cases with diagnosticating an 
intestinal catarrh simply from the existence of diarrhoea, without laying much 
stress upon the special variety ; but in many cases some points can be obtained 
which give information as to the more accurate seat of the catarrh. The distinc- 
tion between acute and chronic intestinal catarrh is also of practical significance. 

Duodenal catarrh can be diagnosticated only if it is combined with jaundice. 
The details regarding it may be found in the chapter on catarrhal jaundice. 

Isolated catarrh of the small intestines, of the jejunum and ileum, is probably 
only of rare occurrence, except when the upper portions of the colon are involved. 
We can very rarely diagnosticate it with certainty, but there are a number of fac- 
tors which permit us to decide that the small intestine is chiefly affected, or at least 
that it is involved in the disease. In the first place, we may assume an affection 
of the small intestine, from obvious reasons, in all those cases in which there are 
also gastric disturbances. It is evident that, in the frequent combination of gas- 
tric and intestinal catarrh, the portions of the intestine nearest the stomach will be 
chiefly affected. Physical examination of the abdomen also gives some indica- 
tions, since the slight sensitiveness and swelling of the abdomen, as well as the 
visible abnormal peristaltic action, chiefly affect the middle and lower portions of 
the abdomen in catarrh of the small intestines, while the analogous symptoms in 
catarrh of the large intestine affect the lateral and upper portions of the abdomen, 
corresponding to the anatomical course of the colon. We can not make a sharp 
distinction, however, in this respect. The results which auscultation and percus- 
sion over the abdomen give in regard to the point of origin of the gurgling sounds 
and the fullness of the loops of intestine are very rarely unequivocal, and hence 
are of little value in diagnosis. 

Careful examination of the stools gives us more information. As has already 
been said, we need have no diarrhoea in a catarrh confined to the small intestines, 
since diarrhoea is due only to the increased peristalsis of the large intestine ; hence 
diarrhoea is absent, for example, in most cases of duodenal catarrh (catarrhal jaun- 
dice). In extensive isolated catarrh of the small intestines the firm stools passed 
may, however, be regarded as pathological, because, on microscopic examination, 
they appear intimately mixed with little lumps of hyaline mucus (Nothnagel). As 
a rule, of course, catarrh of the small intestines is combined with a catarrh of the 
upper portion of the large intestine. Then we have a diarrhoea, but the thin stools 
show some peculiarities which point to an implication of the small intestines. As 
a result of the increased peristalsis of the small intestines, we find certain constitu- 
ents in the stools which are normally contained in the small intestines, but which 
under normal conditions are no longer to be met with in the faeces in the large 
intestine. We find here, in the first place, undigested constituents of the food, 
large masses of muscular fiber, or even fragments of meat which may be recog- 
nized by the naked eye, and also starch and fat. Of course the opposite hypothesis 
does not hold good, that, if we find a large amount of the undigested portions of the 
food in the stools, it must necessarily always point to a catarrh of the small intes- 
tines, since the digestion may be impaired by other circumstances, like fever or 
anaemia, and increased peristalsis of the intestines, from any cause, must result in 
the same symptoms. A diarrhoea, where the thin stools contain a very large 
amount of undigested particles of food which can be recognized by the naked eye, 
was formerly called lientery, and the term is still occasionally used. 

If the stools contain bile in addition to some portions of the food, it is to a cer- 
tain degree characteristic of catarrh of the small intestines. Under normal con- 
ditions the contents of the small intestines alone show Gmelin's test for bile-pig- 



INTESTINAL CATAEEH. 



381 



ment, but the contents of the large intestine, and also the normal stools, do not. 
In intestinal catarrh, with increased peristalsis of the small and large intestines, 
there is, however, often quite a large admixture of still undecomposed bile-pig- 
ment. The green stools which are so often seen in the diarrhoea of children, and 
more rarely in that of adults, are also well known. Such stools usually show a 
marked color-reaction with nitric acid. In other cases we find only certain con- 
stituents of the stools stained with bile, a fact to which Nothnagel has called spe- 
cial attention. Yellow pigmented bits of mucus and cylindrical epithelium, and 
round cells stained with bile, are especially characteristic of the diarrhoea of 
catarrh of the small intestines. 

Catarrh of the large intestine is probably present in every diarrhoea, as has 
been repeatedly stated, inasmuch as the thin stools can be explained only by an 
increased peristalsis of the large intestine; but in a number of cases we have 
symptoms which point especially to a disease of the large intestine, particularly of 
its lower portion. 

Physical examination of the abdomen should show changes, like swelling, 
sensitiveness to pressure, etc., chiefly in the lateral portions, corresponding to 
the course of the colon ; but this is rather a theoretical hypothesis than a sign of 
practical value. We can not definitely affirm, either, that " colicky pains " are 
characteristic of catarrh of the large intestine alone. The condition of the stools, 
however, is of importance. In the first place, we may note that, if the stools con- 
tain many masses of mucus which may be recognized by the naked eye, it is of 
diagnostic significance. As we have seen above, the stools in catarrh of the small 
intestines also contain mucus, but it is intimately mixed with the other constitu- 
ents of the faeces, and hence it can usually be recognized only by the microscope. 
In catarrh of the large intestine, however, the mucus rather adheres to the outside 
of the other constituents, and is often present in large masses visible to the naked 
eye. If the catarrh affects the lower part of the large intestine chiefly, it may be 
that the intestinal contents are already formed into firm lumps, which may some- 
times be wholly or partly inclosed in a layer of mucus. In acute catarrh of the 
lowest part of the large intestine the evacuations are sometimes composed chiefly 
of pure mucus, with a greater or less admixture of pus, as is seen chiefly in the 
" catarrhal flux " (see the chapter on dysentery). The more the rectum is involved 
in the inflammation, the worse is that painful feeling of tension and pressure at 
the anus during and after the evacuation, which we term tenesmus. 

Isolated inflammation of the rectum (proctitis) is, at least in part, directly 
accessible to examination by the finger or by the speculum. Painful tenesmus and 
an admixture of mucus, and especially of pus in the stools, are the chief symp- 
toms of the disease. In most cases, however, we have to do, not with a primary 
disease, but with a secondary catarrh of the rectal mucous membrane as a result 
of different morbid conditions in the vicinity of the rectum, or of new growths, 
syphilitic processes, etc., in the rectum itself. Periproctitis (ischio-rectal abscess) 
belongs to the domain of surgery, and can not be described here. 

Intestinal catarrh is divided into an acute and a chronic form. 

In the acute intestinal catarrhs, excluding the toxic inflammations, we class 
simple diarrhoea, which usually passes off in a few days, and the severe enteritis, 
which is probably usually infectious, and which is attended by a marked disturb- 
ance of the general health, by fever, and sometimes by gastric symptoms also; by 
herpes, by occasional slight albuminuria, by articular pains, etc. It lasts from 
three to ten days. Cholera morbus (vide infra) is also to be regarded as a special 
form of acute infectious inflammation of the gastric and intestinal mucous mem- 
branes. 

Chronic intestinal catarrh either comes from an acute disease of the intestinal 



3S2 



DISEASES OF THE DIGESTIVE ORGANS. 



mucous membrane, or it gradually develops independently. In adults it is by no 
means a frequent disease, at least as regards pronounced cases, and is much rarer, 
for example, than chronic gastric catarrh ; but we have already mentioned that it 
is very common in practice among children. 

[Chronic intestinal catarrh is much more common in the southern than in the 
northern portions of our country. It was the great scourge of camps during our 
late civil war, and there are many men alive to-day, pensioned and unpensioned, 
who have never recovered from the diarrhoea contracted during their army life.] 

In regard to the aetiology and symptomatology, much the same may be 
said of chronic catarrh which we have learned to recognize in considering 
acute catarrh. In regard to aetiology we must note, in adults, chiefly the intesti- 
nal affections remaining after an attack of an acute disease, like dysentery, severe 
malaria, or typhoid. Among the most prominent symptoms are the abnormal 
evacuations, usually alternating between diarrhoea and constipation, but some- 
times a persistent constipation, due chiefly to the atrophy of the muscular coat 
and the disturbance of the nervous apparatus. We must also mention, as a promi- 
nent symptom, the secondary disturbances of the general nutrition, like emacia- 
tion and anaemia. In regard to peculiarities in the character of the stools, we 
must refer to what has been said above. As chronic catarrh of the large intestine 
is far commoner than chronic catarrh of the small intestines, we very often find 
large amounts of mucus in the stools. Special mention must here be made of a 
particular form of chronic catarrh of the large intestine, in which large pieces of 
membrane and complete mucous casts of the intestinal canal are evacuated. 

This peculiar condition, of which we have seen several cases, affects women 
most frequently, but it is also met with in men. The disease is almost always 
associated with obstinate constipation. Either at the same time with hard scybala, 
or quite independently, large masses of this membrane are from time to time 
evacuated, and the passage of them is often associated with quite severe colic. 
These masses, as the microscope shows, consist of mucus, and often contain also 
much cylindrical epithelium, and more rarely a few round cells and occasional 
crystals of cholesterine and triple phosphate. The general nutrition sometimes 
suffers but little, but in other cases quite a good deal. We very often see in 
women, at the same time, all sorts of hysterical and nervous symptoms. The dis- 
ease, which is termed membranous enteritis, desquamative catarrh of the large 
intestine, or mucous colic (colica mucosa), may last for years. No thorough 
examination has yet been made into the aetiology and pathology of the disease, 
but it is most probable that the intestinal mucus collects into the membranous 
formations above described in the bottom of the longitudinal folds of the spas- 
modically contracted large intestine (Marchand). 

Treatment. — Most of the milder cases of acute intestinal catarrh need only a 
dietetic treatment. If the patient avoids all injurious substances for a few days, 
he recovers completely in a short time. The different gruels, like barley and oat- 
meal gruel, and also weak broths and rusks, are generally regarded as the most 
suitable food. The coarser vegetables and fruits, fat meat and brown bread, are 
to be avoided as much as possible with a severe diarrhoea. In other respects we 
may refer to the dietetic rules laid down under the treatment of chronic gastric 
catarrh. 

It is also an important rule, confirmed by much experience, to keep the abdo- 
men warm. Children should always stay in bed, and adults should do so, at 
least in all severe cases. It is also a good plan, particularly in children, to protect 
the abdomen from cold by a flannel band. 

In many of the mild cases it is scarcely necessary to use internal remedies. 
Gum mixture or almond mixture is a good prescription if there is no special indica- 



INTESTINAL CATAKKH. 



383 



tion, but in severe cases further medication may be proper. If we have reason to 
suspect some irritating ingesta or a collection of faeces as a cause of the intestinal 
catarrh, a cathartic acts favorably at the beginning of the treatment, in spite of 
the existence of diarrhoea. Our best cathartic in such cases is castor-oil or calo- 
mel. In all those cases where many thin dejections point to a greatly increased 
peristalsis of the intestine, we use astringents, especially opium, which we give in 
the form of the simple tincture or the wine in doses of ten or fifteen drops, once 
to three times a day ; or as a powder, half a grain to a grain (grm. 0*03 to 0*05) 
of opium with a grain (grm. 0*05) of sugar, two or three times a day. It is also 
recommended to combine the opium with some mucilaginous vehicle, as 2 parts 
of laudanum to 150 of gum mixture or decoction of salep, a teaspoonful every two 
or three hours. 

Beside opium, the different astringents are used in the treatment of intestinal 
catarrh, especially tannic acid, acetate of lead, logwood, columbo, catechu, and 
many others. These remedies are often given combined with opium, as in the 
following prescriptions : 



5 Opii . 

Acidi tannici 

Sacchari albi 

S. As a powder two or three times a day. 

5 Decoct, radicis calumbae ...... 

Extract, opii 

Syrup, aurantii 

S. Tablespoonf ul every two hours. 



gr. ss. (grm. 0*03) ; 

gr.j. ( " 0-05); 

...... gr. j. ( " 0-05). M. 

(1-15) 1 v. (grm. 150-0); 

gr. j. ( " 0-05); 

fss. ( " 15-0). M. 



If there is severe colic, opium, or, under some circumstances, an injection of 
morphine is the best remedy. In milder cases it is sufficient to apply warmth to 
the abdomen, by warm poultices or hot towels. The colic, however, often depends 
upon the presence of old faecal masses in the intestine, when it is necessary to 
prescribe a cathartic, like castor-oil. 

In all cases where the symptoms point to a more intense disease of the large 
intestine, local treatment may be employed. This is chiefly of importance in the 
treatment of chronic intestinal catarrh, which is situated mainly in the large 
intestine. We irrigate the large intestine daily with weak astringents, and some- 
times with disinfectants. The necessary apparatus is very simple. It consists of 
an ordinary irrigator, to which a rubber tube, about half a metre long and with a 
proper tip, is attached. Instead of the irrigator we can use an ordinary glass fun- 
nel, a " Hegar's funnel." We may very well use, for an end-piece to be introduced 
into the rectum, a long, soft, elastic oesophageal tube, which can easily be pushed 
quite high up. The fluids used for irrigation must always be warmed to about 
85° (30° C), and should be allowed to run in gradually and slowly. The amount 
of fluid used for one irrigation should be two or three pints (1-1£ litres), or 
sometimes more. The patient keeps on his back during the irrigation. The knee- 
elbow position, which is much more uncomfortable than the dorsal, is only occa- 
sionally necessary. The fluids most used are a one- or two-per-cent. solution of 
salicylic acid, solutions of salicylic and boracic acids, a one-per-cent. tannin solu- 
tion, or a solution of acetate of lead (1 to 1000). 

If there is painful tenesmus, it is usually relieved by suppositories of cocoa- 
butter and extract of opium. 

In chronic intestinal catarrh a careful regulation of the diet is of the greatest 
importance. Beside local treatment we must consider internal remedies, chiefly 
the astringents mentioned above, to which we may add alum, guarana, and kino. 



384 



DISEASES OF THE DIGESTIVE OEGANS. 



The different preparations of strychnine are also much praised by some physicians. 
Baths, like Carlsbad, Kissingen, Marienbad, or Tarasp, are often accompanied by 
good results, especially in cases where there is at times constipation. 

[Saratoga, Bedford (Pa,), and the Virginia Springs are those in chief repute in 
this country. The change of scene and regular life, to which patients will more 
readily submit in these and similar places than at home, have probably more effect 
than the water itself. 

I have known the Rockbridge alum-water, internally, render good service. A 
sea voyage is sometimes curative, and, in general, a sufferer from chronic diarrhoea 
should shun malarial regions. 

Treatment must often be patient and prolonged ; relapses are liable to follow 
imprudence of any kind. Time is, of course, required for the restoration of the 
intestine to its normal structure and function, and perseverance is not infrequently 
rewarded in full measure.] 

The symptoms which simulate a chronic intestinal catarrh often depend, as 
we have said, on abnormal processes of innervation. These are the cases which 
are associated with general nervous and nervous-dyspeptic symptoms. Internal 
remedies in such cases are of but little assistance, but judicious general treat- 
ment, cold-water cures, electricity, and massage may be attended with very good 
results. (See the chapters on nervous dyspepsia and habitual constipation.) 



CHAPTER II. 

CHOLERA MORBUS. 

{Cholera Nostras. Cholera Infantum.) 

By the name " cholera morbus " we mean an acute disease of the stomach and 
intestinal canal, of a definite form, whose symptoms in severe cases greatly resem- 
ble those of genuine Asiatic cholera. It is in the highest degree probable, from 
the whole course of the disease, that cholera morbus also depends upon an acute 
infection of the body by a specific, organized producer of disease, but this has not 
yet been definitely discovered. The statement of Finkler and Prior, that bacilli are 
found in the intestinal contents in cholera morbus which can not be distinguished 
from the comma-bacilli of genuine Asiatic cholera {q. v.), has not proved correct. 
Finkler's bacilli seem to have no pathogenetic significance in cholera morbus. 

Cholera morbus comes on usually as an epidemic, and almost exclusively in 
the hot summer months — June to August. Hence it is often termed summer 
cholera. Children in the first two years of life are chiefly attacked, especially 
those who are artificially fed or who have recently been weaned. The disease 
also attacks older children and adults, but much more rarely. 

[Special opportunities are afforded in this country for the study of cholera 
infantum. The causative conditions are, briefly, unsuitable food, a high tempera- 
ture, and bad hygiene — conditions which are all combined and attain their maxi- 
mum intensity in large cities. That a high thermometric range alone is not suffi- 
cient is shown by the comparative immunity of all country districts. Those who 
live in the country or have never been busied among the city poor have no idea 
of the atmosphere breathed by the children of the poorer classes, especially during 
the heated term, nor of the extreme difficulty — impossibility we can almost say 
— of getting a really good milk. Even if the milk was good at the start and has 
not been tampered with, the time which necessarily elapses after it is drawn from 



CHOLERA MORBUS. 



385 



the cow and before it reaches the consumer permits marked fermentative changes 
during hot weather. And milk is and must remain the main article of diet for 
children under two years of age. ] 

The symptoms of cholera morbus are those of a severe acute gastro-enteritis. 
The disease begins suddenly, or after some slight warning, with violent vomiting 
and severe diarrhoea. In some cases one of these symptoms predominates, and in 
others the other. The vomitus consists partly of the food taken, and partly of a 
slimy, watery substance. The stools at first retain their faecal character, but they 
soon become more colorless and more watery, so that they sometimes approach 
the well-known rice-water appearance of the stools in genuine cholera. Abdomi- 
nal pain is usually absent, but a feeling of pressure and constraint in the epigas- 
trium is often present. The diminished secretion of urine and the frequent mus- 
cular pains cause the whole type of the disease to resemble genuine cholera still 
more closely. 

The severe disturbance of the general condition is especially characteristic. 
The patient becomes extremely dull and has a wasted look, the voice is weak and 
hoarse, an unquenchable thirst sets in, the pulse is very small, the skin of the face 
and the extremities is cool and livid ; in short, we have the pronounced picture of 
a general collapse. The body heat also falls, although at the first stage of the 
disease there is often a rise of temperature. 

[The temperature is always high, even during the stage of collapse, when the 
skin and extremities are cool to the touch ; if the thermometer is introduced into 
the rectum — generally the best place, by the way, to take the temperature in 
young children — it will rise to 101° to 102°, and is more apt to reach 104° to 107°. 
This shows that inflammation plays a large part in the pathology of the disease.] 

The picture of a severe general disease is especially prominent in cholera infan- 
tum. In severe cases of this form of the disease the general restlessness, which at 
first exists, rapidly passes into somnolence. The child lies with sunken, half- 
closed eyes, the conjunctivae are slightly injected, the corneae are cloudy, the face 
is pale and cyanotic, the fontanel! es are depressed, the skin is cool, and the pulse 
is small and frequent and can scarcely be counted. Amid these symptoms, 
which are usually termed " hydrocephaloid " by specialists in children's diseases 
[Marshall Hall], death comes on in coma or with slight convulsions. 

The mortality of children with cholera infantum is very marked, especially in 
large cities, and among the poorer classes of society. Severe cases usually end 
fatally in a few days, but, on the other hand, many cases recover, either because 
the course of the disease from the first is not so severe, or because cases appar- 
ently hopeless take a favorable turn. In adults it is extremely rare to see cholera 
morbus terminate unfavorably. Patients also recover quite rapidly from appar- 
ently severe conditions, although the stomach and intestines often remain rather 
sensitive for a long time. 

The anatomical appearances in children who die of cholera infantum con- 
trast, from their insignificance, with the severe symptoms observed during 
life. The catarrhal affection of the gastric and intestinal mucous membranes is 
not at all prominent in the cadaver, and the solitary follicles and Peyer's patches 
show only a slight swelling. The other lesions which are most frequently seen 
are lobular atelectases in the lungs, and venous hyperaemia and oedema of the pia 
mater. 

The diagnosis of cholera morbus presents no difficulty if the characteristic 
symptoms of the disease are present. The distinction between it and genuine 
Asiatic cholera used to be occasionally quite difficult, and was possible only by con- 
sidering the aetiological factors, and by the evident connection between the individ- 
ual case and other cases of undoubted cholera. By Koch's discovery of the comma- 
25 



386 



DISEASES OF THE DIGESTIVE ORGANS. 



bacilli in Asiatic cholera the distinction between the two diseases has now become 
absolutely certain. In all suspicious cases, therefore, we must examine the dejec- 
tions for comma-bacilli, and upon the result of this examination depend the 
proper means of prophylaxis. 

The treatment of cholera morbus in adults must be first to take special care to 
limit the diet. The food should be only gruels, or at most broth, soft-boiled eggs, 
and milk. It is a good plan to give the milk iced, and in small amounts. The 
distressing thirst is best relieved by cracked ice. Wine (iced champagne) is to be 
given if the general weakness becomes marked. 

Among drugs opium is the most effective remedy, and, both in powder, as the 
extract, or in liquid form, as laudanum, is the first thing to use to relieve the diar- 
rhoea and vomiting. All other remedies which are recommended in cholera mor- 
bus in adults, like nitrate of silver, or calomel, are quite subordinate to opium. 
In other respects we may refer to the treatment of acute gastric and intestinal 
catarrh. 

We are more cautious in prescribing opiates for children, although here small 
doses of opium, one or two drops of laudanum according to the age of the child, 
may often be indispensable. In fresh cases calomel has obtained a great reputa- 
tion, a sixth of a grain (grm. 0*01) two or three times a day. Ice-cold cow's milk, 
given in teaspoonfuls, serves best as food, if the child can not be fed naturally by 
breast-milk. As soon as the signs of marked collapse appear, we must use hot 
baths of chamomile or mustard, hot packs, and also stimulants, small amounts of 
wine and injections of camphor. If the child's stupor increases we may under 
some circumstances use cool packs and shower-baths. 

We will pass over the many other remedies recommended for cholera infan- 
tum, like quinine, salicylic acid, and creasote, since in severe cases they unfort- 
unately almost always leave us in the lurch. In practice, of course, we are 
often obliged, to try one or another of these remedies. 

[Treatment must be prompt and judicious ; many a child is thus saved which 
would otherwise die. 

Calomel is less used in this country than in Germany, and I think rightly. It 
is not very often that a preliminary purgation is required ; the bowels have usu- 
ally been quite sufficiently unloaded before the physician arrives, and the indica- 
tion he has to meet is to check the vomiting and diarrhoea. Opium, either in the 
form of Dover's powder and combined with bismuth, or as paregoric, is nearly 
always in place before the stage of collapse ; precise directions should be given to 
omit the opium or diminish the dose if stupor comes on. Opium can also be given 
by enema if necessary. One should not wait till the symptoms are desperate 
before giving brandy, a good way to administer which is dropped on a teaspoon- 
ful of shaved ice. Improvement is shown by decrease or cessation of the vomit- 
ing, and greater consistency with less frequency of the dejections. While the 
symptoms are at their height there is but little use in trying to give nourishment, 
which can not be digested even if it is retained. 

A warm mustard bath aids in the re-establishment of the cutaneous circulation, 
and thus tends to relieve the gastro-intestinal tract. 

The diet is essentially the same as in the more chronic inflammatory and in 
the non-inflammatory diarrhoeas of young children. 

Details to complete the above brief sketch must be sought in works devoted to 
the diseases of children. It should, however, be added that removal to the pure 
air of the sea-shore in non-malarial regions will sometimes turn the scale in cases 
which are apparently hopeless. Pure country air is to be sought if the sea-side can 
not be reached ; but the latter is the better of the two.] 



INTESTINAL CATARRH OF CHILDREN. 



387 



CHAPTER III. 

INTESTINAL CATARRH OF CHILDREN. 

(Chronic Dyspepsia of Children. Pedatrophy.) 

The great frequency and the practical importance of the "dyspeptic condi- 
tions " in children in the first years of life, which conditions are associated with 
severe disturbances of nutrition, justify a short description of them, but we must 
refer to the special manuals on children's diseases for a detailed account. 

The reason why diseases of the. digestive organs play so large a part in chil- 
dren's troubles is owing, on the one hand, to the great sensitiveness which the 
digestive apparatus in children shows to the irritants which are brought in con- 
tact with it, and, on the other, in part to the too common foolishness and careless- 
ness which the child's parents and nurses show in its feeding. Of course it is 
not always ignorance and neglect, but often, unfortunately, poverty and want 
which cause children to be neglected, and explain the terrible frequency of infant 
mortality in the first years of life. 

The simple fact that by far the larger number of children who suffer 
from dyspeptic and atrophic conditions are fed artificially, leads us to the belief 
that the cause of most of the intestinal diseases in children is to be found in 
faulty and injudicious feeding. The food, which is not suited to the child's digest- 
ive powers, is only imperfectly absorbed ; it undergoes many processes of decom- 
position, whose products irritate the intestinal mucous membrane and give rise to 
increased peristaltic action. Thus the imperfect digestion, or " dyspepsia," excites 
a catarrh of the gastric and intestinal mucous membrane, by which again, in a 
vicious circle, the digestive power is still further reduced. Hence the boundary 
between " dyspepsia "and catarrh can be drawn only artificially. 

The anatomical changes of the intestinal mucous membrane in children 
who die of " chronic intestinal catarrh " are, as a rule, only slightly marked, 
and contrast, in their apparent insignificance, with the severe intestinal 
symptoms observed during life. We must remember, however, that most 
catarrhal conditions are generally hard to recognize in the cadaver from the 
disappearance of the hyperaemia. Sometimes the swelling of the follicles is 
especially marked — follicular catarrh. Follicular ulcers are also seen. In 
other cases the atrophy of the mucous membrane, which is often seen after 
chronic catarrhs, is the chief lesion. Chronic thickening and swelling of the mu- 
cous membrane is of rarer occurrence. In most of the severe cases the large intes- 
tine, and also the lower portion of the ileum, are the chief seat of the changes. We 
often find a swelling of the mesenteric lymph-glands, and also a fatty liver. In 
the lungs extensive atelectases or nodules of catarrhal pneumonia often develop 
from the imperfect respiration. 

The symptoms of chronic intestinal catarrh are, in the first place, those due 
directly to the intestinal trouble, and, secondly, the quite rapid disturbance of the 
child's general nutrition. 

The condition of the stools is the most important intestinal symptom. The 
normal dejection in children until they are weaned is of the color of the yolk of 
an egg, of rather a pasty consistency, and of a faintly sour smell. In intestinal 
catarrh the stools are more frequent, six or seven and even more a day. They are 
thinner, more watery, contain large flakes and lumps of undigested bits of case- 
ine and other remains of food, and smell badly. They very often have a green 
color, or acquire it on standing. We may find admixtures of mucus, sometimes 



388 



DISEASES OF THE DIGESTIVE ORGANS. 



in the form of the so-called u sago grains," especially in catarrh of the large intes- 
tine. In the severe forms we often find pus-corpuscles and epithelium under the 
microscope, beside remains of the food. The stools may contain small amounts 
of blood. 

There is no definite distinction in regard to the dejections in catarrh of the 
large and of the small intestines. On the whole, the rule holds that, in catarrh 
of the small intestines chiefly, the stools are more abundant, they are passed with 
more wind or gas, and show a more uniform consistency, while in catarrh of the 
large intestine they are more scanty but more frequent, ten or twenty a day, are 
passed noiselessly, are associated with tenesmus, and show a different consistency 
in their various parts, partly normal, partly thin, partly slimy, etc. Examination 
of the abdomen is in so far of importance that, in general, in catarrh of the small 
intestines, the abdomen is much swollen, while in catarrh of the large intestine it 
is often deeply sunken. 

We often find disturbances in the stomach, vomiting, eructations, etc., as well 
as trouble in the intestines. There may be thrush in the mouth, or the development 
of aphthous ulcers. 

In almost all long-continued cases, however, the general disturbance of nutri- 
tion, the atrophy (athrepsia) of the child, takes the first place in the picture of 
the disease. The muscles become shriveled and flabby, and the whole body finally 
becomes so much emaciated that the pale, dry skin hangs in broad folds and wrin- 
kles about the bones, whose prominences are everywhere visible. The face is 
sharp and has an aged expression from the many little folds of the skin. The 
eyes are dull, lusterless, and wide open ; the voice is merely a low, hoarse whim- 
per. The abdomen is deeply sunken, or in some cases it is swollen by meteorism, 
in peculiar contrast to the emaciation elsewhere ; and its surface is traversed by 
bluish veins. 

From this sad condition just described, unfortunately so common in practice 
among children, we can usually recognize the condition of things at the first 
glance, for by far the larger part of the cases called " pedatrophy " are due to 
chronic digestive disturbances. Very often it is combined with rachitic changes 
in the bones, of whose occurrence we shall speak further in the description of 
rachitis. Tubercular changes, too, are often found in the cadaver, especially in 
the lungs and the bronchial and mesenteric lymph-glands. In such cases, of 
course, the tuberculosis is usually to be regarded as the main disease, upon which 
the intestinal affection, which may be simple or even tubercular, has developed 
secondarily. During life tuberculosis in little atrophic children may very easily 
be overlooked and often not diagnosticated. 

If we would give a full account of the treatment of the atrophic conditions in 
children due to digestive disturbances, we must include in our consideration the 
entire hygiene and care of children in health and disease, for all children's physi- 
cians are united in the opinion that, as the cause of most intestinal diseases in 
children is to be found in improper feeding, so recovery from existing digestive 
disturbances can take place primarily only by a corresponding proper and judi- 
cious feeding. In what follows we can refer only to the most important princi- 
ples and general points which are here to be considered. 

The only proper and natural food for a child in its first year is breast-milk. 
All dyspeptic conditions are much rarer in children who are nursed than in bot- 
tle-fed children, and, when they do occur in children at the breast, they often 
are only of brief duration. They are then to be referred usually to certain dis- 
turbances in the mother, like disease, insufficient diet, or severe mental excite- 
ment. The return of menstruation or a new pregnancy has sometimes an unfa- 
vorable influence on the character of the milk. Finally, we may mention that, 



INTESTINAL CATAEEH OF CHILDREN. 



389 



in spite of the best of milk, if the breast is given irregularly and too frequently, it 
may cause anomalies of digestion in nursing children. 

Most of these slight disturbances may easily be readjusted, but sometimes it 
happens that, without any discoverable reason, the milk of a wet-nurse "does not 
agree " with the child. Then we must change the nurse. The atrophic conditions 
which develop and progress in children, in spite of plenty of normal food, are usu- 
ally due, not to simple digestive disturbances, but to deep-seated, general, constitu- 
tional diseases like tuberculosis, or syphilis. 

The great majority of cases of chronic intestinal catarrh and chronic atrophy 
are found, as we have said, in bottle-fed children. The first question, which every 
physician should ask a mother who brings him such a child for treatment, must 
therefore refer to the sort of feeding which the child has. If the mother, for any 
reason, can not nurse it herself, and if the bottle-fed child has digestive disturb- 
ances, we must invariably consider, in the first place, the possibility of procuring a 
wet-nurse. Feeding by the milk of a wet-nurse is the only remedy which, at least 
in many cases, by saving the child's life, repays the many annoyances and quite 
large expense which a wet-nurse causes. We must tell the parents this, and repre- 
sent to them, without reserve, the great dangers which threaten the life of every 
bottle-fed baby. Complete, and sometimes even quite rapid, recovery may be 
obtained through a wet-nurse, even in cases of quite severe chronic intestinal 
catarrh, although atrophy and weakness are already very far advanced. 

Often, however, it is impossible to hire a wet-nurse, especially in the poorer 
classes of society. We must continue bottle-feeding, and these are the cases 
where chronic intestinal catarrh demands its greatest sacrifice ; yet even here the 
physician can always do much good by instructing the parents. 

The best substitute for mother's milk is cow's milk. This must be as fresh as 
possible, and is usually given boiled. One part of the milk, according to its char- 
acter, must be diluted with two or three parts of boiled water in the first months, 
in children from four to six months old with equal parts of water, and in older 
children with about half as much water. From nine to twelve months the child 
may have undiluted milk. In general we give the milk warmed to about 85° 
(28° C), but children with gastro-intestinal catarrh often bear cold milk, given in 
small amounts, better than warm. Among the special additions to the milk, by 
which physicians have tried to make cow's milk more like human milk, we may 
mention as occasionally advantageous sugar of milk, as much as will go on the 
point of a small knife, added to the portion of milk given, and soda, a tablespoon- 
ful of a one- or two-per-cent. solution to a pint (half a litre) of milk. The much- 
practiced dilution of milk with salep, oat-meal, and barley waters is always inju- 
dicious, and it should be a principle, especially with children under three months, 
to avoid entirely any starchy food. It is not a bad plan to add veal-broth to the 
milk, as it is sometimes well borne even by weak children. 

Cow's milk, properly diluted, is better for children with chronic intestinal 
catarrh, in many cases, than any other food. In acute digestive disturbances only 
is it sometimes advisable to omit the milk entirely for a few days, and give instead 
of it only a little mucilaginous drink like decoction of salep. In chronic dyspep- 
sia, however, we must first try good cow's milk. If the milk is not well borne, if 
the diarrhoea increases, and if the child becomes still more emaciated, we may try 
to get milk from another and better source ; but it often happens that either we 
can not procure good milk, or that the child can not bear even the best cow's 
milk. We are then obliged to have recourse to one of the many " artificial foods " 
and " substitutes for mother's milk " in the market. We can not here go into par- 
ticulars concerning these. Each of these preparations has occasional good results 
to show, but none of them has an uncontested pre-eminence over the rest. We 



390 



DISEASES OF THE DIGESTIVE ORGANS. 



will mention the -preparations most in use at present, of whose usefulness in indi- 
vidual cases we have convinced ourselves : Swiss condensed milk, Nestle's and 
Frerich's infants' foods, Biedert's cream-mixture, Liebig's soups, and many others. 
Almost every physician has his special favorite preparation, which in his own 
personal experience has done him relatively the best service. 

If we keep fast to the principle that every intestinal catarrh in children is to 
be treated in the first place by a judicous regulation of the diet, in many cases we 
will not have to use any drugs. These may be of service only when we have also 
carried out the dietetic measures which are specially necessary. 

Calomel has obtained the greatest reputation in the treatment of intestinal 
catarrh in children. It deserves to be used in fresh cases, in doses of T \ to £ of a 
grain (grm. 0 '005-0 '01) in powder. If the diarrhoea lasts a long time, we may 
very well use opiates, although with great caution. The combination of calomel 
and opium often does good service. 



M. et ft. pulv. 

S. One such powder, three or four times a day. 

With little children we may put two to four drops of laudanum in three 
ounces (grm. 100) of liquid, like gum mixture, salep decoction, muriatic-acid 
mixture, etc., and give a dessertspoonful of this every two or three hours. 

Many attempts have been made to check the abnormal processes of decomposi- 
tion in the intestine by prescribing remedies which possess antiseptic and anti- 
zymotic properties. Creasote has been warmly recommended by many, four to 
six drops in two ounces (grm. 50) of water with half an ounce (grm. 15) of syrup, 
a teaspoonful every two hours. Muriatic acid, one-half to one-per-cent. solution 
of the dilute acid, and chloral hydrate, one-per-cent. solution, are also used with a 
like object. 

A number of other remedies, "astringents," are given to act directly on 
the diseased mucous membrane. Those most to be recommended in chronic 
diarrhoea are subnitrate of bismuth, one or two grains (grm. 0*05-0 -1) four to six 
times a day, which may be combined with opium, nitrate of silver (5 to 10,000 solu- 
tion), alum (5 to 1000 solution), guarana, five to fifteen grains (grm. 0 -3-1-0), three 
times a day, and many others. 

If a large amount of mucus in the stools points to a catarrh of the large intes- 
tine, we may sometimes employ irrigation of the colon with excellent results. We 
inject the fluid, one-per-cent. solution of tannin or alum, or solution of acetate of 
lead (1 to 3 to 1000), once or twice a day. The amount of fluid to be introduced at 
once, by a Hegar's funnel, with a gum-elastic catheter, may reach one or two pints 
(half a litre to a litre). 

In conclusion, we must mention the advantage of daily warm baths in atrophic 
children. We usually order some special " strengthening " additions to the bath- 
water, like salt baths, iron baths, or sweet-flag baths. 

[In view of the great importance of this malady, it seems desirable to remark 
on one or two points. 

In the first place, prophylactic measures are deducible directly from the aeti- 
ology. No child should be kept in a large city in summer, if it can be best pro- 
vided for at the sea-shore or in the country. The vast number who must perforce 
remain are to be kept under the best general hygienic conditions possible. Mothers 
should be encouraged to take their children to the relatively pure air of the public 



1J Calomel 

Extracti opii 
Pulv. acaciae 



gr. £ (grm. 0*01); 
gr. & ( " 0-002); 
gr. ss. ( " 0-03). 



TYPHLITIS AND PERITYPHLITIS. 



391 



parks as much as they can. The relation between diet and the diarrhoea of chil- 
dren should be dwelt upon whenever there is opportunity. 

The establishment of boards of health has done much, and will do more, to 
check the ravages of summer diarrhoea. 

Great advances have been made in the artificial digestion of cow's milk within 
a few years. By the aid of the preparations of Fairchild Bros. & Foster the caseine 
is digested in part, and the remaining portions coagulate in light flocculi ; at the 
same time no appreciable taste is imparted to the milk, provided that a moderate 
amount of care is exercised. The importance of preventing the formation of large, 
firm curds has long been recognized, and an older means of attaining this end was 
mechanically to separate the curd by adding to the milk a barley or other similar 
water-gruel. 

Mellin's, Horlick's, and Ridge's foods also deserve mention in this connection. 

The quantities of food, as well as the frequency with which it is given, must be 
determined in each case. 

The drugs most worthy of confidence are, in my opinion, opium and bismuth ; 
in mild cases the former is often not required ; the dose varies greatly with cir- 
cumstances ; the latter can safely be given in two-grain doses, every three hours, 
to a child of six months. Calomel does not now enjoy the reputation in this 
country that it does in Germany, though it has its advocates here. For more 
minute details see works on children's diseases.] 



CHAPTER IV. 

TYPHLITIS AND PERITYPHLITIS. 

{Typhlitis Stercoralis. Inflammation of the Ccecum.) 

iEtiology and Pathological Anatomy.— Inflammation of the caecum and its 
vicinity has a special place among the diseases of single portions of the intes- 
tines. The reason why circumscribed inflammation so often develops here is to 
be found in the peculiar anatomical arrangement of the caecum and its appendix, 
the vermiform process. This arrangement explains why faecal masses or foreign 
bodies are easily retained in the caecum, and give rise to an inflammation of it. 

Inflammation of the caecum is due, in most cases, to an accumulation of faeces 
in it, and hence it is usually termed typhlitis stercoralis. Since the causes pro- 
ducing the inflammation are usually permanent in their action, the anatomical 
inflammatory changes are generally much more intense in perityphlitis than in the 
other forms of intestinal catarrh. The inflammation attacks the whole intestinal 
wall, and sometimes even invades the surrounding connective tissue, being 
then called perityphlitis. 

The great majority of severe cases of perityphlitis do not start from the 
caecum itself, but from the vermiform appendix. This rudimentary portion of 
the intestine, so unimportant physiologically, plays a great part in pathology. 
Small faecal masses from the caecum often enter the vermiform appendix, and, 
under some circumstances, may remain there. The fluid in them is absorbed, they 
are very often incrusted with lime-salts, and thus the little so-called " faecal cal- 
culi " are formed. In many cases the return of faecal masses into the caecum is 
probably hindered by the valve at the orifice of the vermiform appendix, Gerlach's 
valve. Foreign bodies, like little seeds of fruit, or other seeds, often enter the 
vermiform appendix and give rise to the formation of a faecal calculus. These 



392 



DISEASES OF THE DIGESTIVE ORGANS. 



calculi often have such a rounded shape that they were formerly considered, very 
erroneously, to be retained cherry-stones. 

In many cases f aecal calculi may remain in the vermiform appendix for a long 
time without producing any further injurious results, hut, as a rule, they exert a 
mechanical irritation on the mucous membrane which leads to inflammation, and 
often, in some circumscribed spots, to a pressure necrosis, and later to ulceration 
of the vermiform appendix. If the ulcer does not cicatrize, as is always possible, 
the ulceration gradually deepens. When there is, finally, perforation of the ver- 
miform appendix, we have either a circumscribed or a general purulent peritonitis, 
according as adhesions have or have not formed in the vicinity. Although gen- 
eral peritonitis almost always ends fatally, the circumscribed purulent peri- 
typhlitis may, at least in a number of cases, finally recover (vide infra). 

Clinical History. — The symptoms of simple typhlitis stercoralis sometimes 
develop quite rapidly, but in other cases they are preceded by somewhat protracted 
prodromata. The latter are chiefly constipation, which may at times be inter- 
rupted by diarrhoea, and occasional dull pain in the ileo-caecal region. These 
symptoms gradually or suddenly increase. The pain in the ileo-caecal region, in 
particular, becomes more intense, and prevents the patient from making any con- 
siderable movement. Sometimes there is complete stoppage, but in other cases small 
amounts of faeces are still passed. The patient frequently vomits one or more times. 
The general health is also much disturbed. The patient, as a rule, is dull, has no 
appetite, and has a moderately high fever, somewhere between 101° and 104° 
(38'5°-39'8° C), the course of which has nothing characteristic. 

The most important signs for diagnosis come from the physical examination 
of the abdomen. The abdomen as a whole is often moderately swollen by meteor- 
ism. The collection of gas probably takes place chiefly in the ileum, above the 
part of the intestine which is narrowed by the accumulation of faeces. The 
meteorism is often entirely absent or is only slight, and then we often notice by 
mere inspection a marked prominence in the region of the caecum. If we examine 
more closely we often meet with very considerable sensitiveness and tenderness 
on pressure in the same region. We also feel a resistance, which is either diffuse 
or well-defined, exactly like a tumor, and which gives flatness or a dull tympanitic 
resonance on percussion. This characteristic ileo-caecal tumor, which usually 
confirms the diagnosis, is caused in part by the collection of masses of faeces, 
which often seem quite compressible, and permit us to determine approximately 
the portion of intestine affected, and in part by the materially thickened intestinal 
walls, and eventually by the inflammatory exudation in the vicinity. In their 
clinical relations there is no sharp distinction between typhlitis and perityphlitis, 
or inflammatory processes which rise from the vermiform appendix. The further 
course only can make the distinction, if it be possible. 

Most cases of simple typhlitis stercoralis take a favorable course. If the patient 
has timely care and proper treatment the pain and fever gradually disappear. 
Large dejections follow, and after ten days to three weeks complete convalescence 
sets in. The abnormal resistance in the region of the caecum from the thickened 
intestinal walls may often be felt, of course, for a much longer time. A tendency 
to constipation is also often present for a long time. Relapses are not uncommon, 
and it not infrequently happens that people who have once had typhlitis may be 
again attacked later on by the same affection. 

Typhlitis takes a more severe course in the happily quite rare cases where the 
intestinal stenosis as a result of retention of faeces is well-marked. The meteor- 
ism is more marked, the vomiting is more frequent, and finally assumes a marked 
stercoraceous character. The constitutional symptoms are much more severe. 
The patient is extremely dull, the skin is cool and livid, the pulse is small and 



TYPHLITIS AND PEEITYPHLITIS. 



393 



frequent. In such cases death may ensue with all the signs of general collapse, if 
we do not finally succeed in causing the evacuation of fasces and hence remov- 
ing the stenosis. 

The symptoms of perityphlitis are essentially the same as those of typhlitis, 
but they are usually of a higher degree of severity. The resistance to be felt in 
the region of the caecum is less sharply circumscribed and is deeper seated. As a 
rule, there is less meteorism where perityphlitis predominates than in typhlitis. 
The pain is usually very severe, and often shoots into the right leg, where there is 
often numbness and formication, but, on the other hand, there are cases in which 
quite extensive perityphlitic processes may cause very slight subjective symptoms 
for a long time. 

The course of perityphlitis is always tedious, but in favorable cases we may see 
complete absorption of the inflammatory products and recovery. Severe cases 
often end by forming abscesses, which may be ichorous. The local symptoms do 
not disappear, the fever continues and assumes a septic character. Finally, if 
the abscess tends to break externally, the swelling in the ileo-csecal region becomes 
more prominent and more sharply denned, the skin becomes thin and red, there 
is fluctuation, and the abscess breaks spontaneously, if it has not been opened 
previously. Beside perforation outward, we also meet with perforation into the 
abdominal cavity, with a consecutive general peritonitis, and sometimes perfora- 
tion into the ascending colon, with evacuation of pus into the bowels and final 
recovery. 

An unfavorable complication repeatedly observed in perityphlitis is an exten- 
sion of the inflammation to the ileo-csecal vein, which results in a purulent phle- 
bitis of this and also of the portal vein. A general pyaemic condition develops, 
with chills and marked elevation of temperature. This almost always ends fatal- 
ly, and at the autopsy we usually find many metastatic abscesses in the liver. 

The diagnosis of typhlitis and perityphlitis may easily be made in most cases 
from the peculiar localization of the swelling and tenderness, and by paying 
attention to the whole course of the disease. During life we can at most suspect 
whether the special origin of the inflammation is in the caecum or in the vermi- 
form appendix, but we can never determine this with certainty, since in both cases 
the type of the disease, as we have said, is almost precisely the same. The further 
course of the disease is the only means of deciding whether the inflammation has 
remained circumscribed, or has invaded the adjacent parts in the manner men- 
tioned above. 

Chronic cases may be confused with new growths, especially with cancer, aris- 
ing from the caecum or the vermiform appendix. Tumors of the right kidney, or 
the right ovary, and also psoas abscess, after caries of the vertebrae, have in some 
cases given rise to false diagnoses. In such doubtful cases we are usually able to 
form a definite opinion only after long and careful observation. 

We may mention here, in addition, that, in rare cases, there may be a closure 
in some part of the vermiform appendix. The portion behind this closure is then 
gradually more and more distended by the secretion of the mucous membrane, 
and thus the so-called dropsy of the vermiform appendix is developed, which may 
give rise to a tumor which can be felt in the ileo-caecal region. 

The prognosis in every case of typhlitis and perityphlitis is to be given with 
some reserve, since we can not foresee the further course of the disease. A favor- 
able termination, however, is by far the most frequent, and the rule is that the 
cases are mild and the inflammation is confined to the caecum. In severe cases of 
perityphlitis, which end in suppuration, all depends upon whether a general peri- 
tonitis ensues or not, and then, if the inflammation be limited, whether the 
patient's strength is sufficient or not to sustain him until the abscess finally heals. 



394 



DISEASES OF THE DIGESTIVE ORGANS. 



If his strength holds out, he may sometimes recover after the disease has lasted 
for months. 

The treatment of typhlitis has two tasks to accomplish : first, to remove the 
accumulation of fasces, which in most cases has caused and which still keeps up 
the inflammation, and, in the second place, to prevent, if possible, the further 
extension of the inflammation, when it has once appeared. Unfortunately, the 
accomplishment of these two tasks are opposed to each other, and thus, in a given 
case, it is often hard to decide whether to satisfy the first indication by prescrib- 
ing cathartics, or the second by prescribing opium. In general, as we believe, the 
fear of the harm which cathartics may do by tearing any adhesions formed, etc., 
need not be carried too far. In fresh cases of simple typhlitis stercoralis, which 
come on with manifest stoppage and a palpable faecal tumor in the region of the 
caecum, we may always prescribe cathartics like castor-oil or rhubarb with precau- 
tion. If there are copious dejections after a few spoonfuls of castor-oil, the pain 
and fever usually speedily disappear. If we do not wish to be imprudent in cases 
where marked tenderness leads us to suspect that the peritoneum is already 
involved, we may order large enemata of water instead of cathartics, and these 
often act well. In cases, too, where there are signs of intestinal stenosis, we may 
hope for the best results from large enemata repeated three or four times a day. 

If the inflammation has extended to the parts adjacent to the caecum, and if, 
accordingly, we have a perityphlitis, cathartics are no longer proper, and are even 
sometimes injurious. The treatment then is chiefly to give opium, half a grain to 
a grain (grm. 0-03-0"06) of the extract every hour or two according to the sever- 
ity of the case. By prescribing opium we soonest attain a cessation of the pain 
and a limitation of the inflammation. If we suspect a large accumulation of 
faeces beside the perityphlitis, or if symptoms of intestinal stenosis appear, the 
opium treatment can be combined very well with large enemata. 

The local treatment of typhlitis and perityphlitis is often of great service. 
In most cases an ice-bag on the ileo-caecal region is well borne and relieves the 
pain. If there is very much tenderness, we can employ local blood-letting, eight 
to fifteen leeches, in robust persons, with very good results. 

If the signs of a local abscess-formation appear, we may replace the ice-bags 
by warm compresses or poultices. We do not take the useless trouble of reducing 
the fever by quinine, but we try to keep up the patient's strength as much as pos- 
sible. If there is fluctuation externally, we must open the abscess and treat it 
antiseptically. We must refer to the text-books on surgery for all the details. 

[Perityphlitis has become a much less serious disease since the treatment 
inaugurated by the late Willard Parker has come into vogue. The early evacua- 
tion of inflammatory products, the presence of which is to be sought with the 
aspirator-needle long before fluctuation can be found, is here referred to. The 
needle should be long and of fine size— 3 or 4, French catheter scale— and the 
syringe itself must be "tight." After failure to find pus, the needle having 
been introduced in the iliac region, Bull advocates inserting the needle into the 
lumbar region. He has thus several times found the pus which was not detected 
by puncture directly into the iliac region or the tumor itself. 

Noyes, of Providence, has collected 100 cases treated by operation with a mor- 
tality of only 15 per cent.] 



PEKFORATING ULCER OF THE DUODENUM. 395 



CHAPTER V. 
PERFORATING ULCER OF THE DUODENUM. 

There is a form of ulcer in the duodenum, especially in its upper, horizontal 
portion, which is precisely analogous to the round gastric ulcer in regard to aeti- 
ology, pathological anatomy, and, very largely, symptomatology. The origin of 
the ulcer is probably also due in most cases to the action of the acid gastric juice 
on the duodenal mucous membrane, under conditions which have been mentioned 
more fully in the aetiology of gastric ulcer. We must mention here the note- 
worthy fact that, after extensive burns of the external skin, ulceration of the 
duodenum, rarely of the stomach also, has been repeatedly observed. This is 
probably due to the plugging of a duodenal vessel by an embolus from decom- 
posed masses of blood. 

Ulcer of the duodenum is much rarer than the round gastric ulcer, and, in dis- 
tinction from the latter, it has been found remarkably oftener in men than in 
women. 

Many cases of ulcer of the duodenum run their course entirely without symp- 
toms, or they cause symptoms when sudden haemorrhage appears, from erosion of 
the pancreatico-duodenalis, gastro-duodenalis, etc., with haematemesis and bloody 
stools, or the sudden signs of peritonitis from perforation. In many cases a type 
of disease exists for a long time whose symptoms, as we have said, are so like the 
clinical symptoms of gastric ulcer that we can very rarely distinguish the two 
forms with certainty during life. We notice especially continuous or neuralgic 
pain, which, in ulcer of the duodenum, has its chief seat in the right hypochon- 
drium. Severe gastric symptoms, especially vomiting, are not as common as in 
gastric ulcer. The general health and general nutrition may remain quite undis- 
turbed for a long time. 

Ulcer of the duodenum ends by cicatrization and recovery, or by cicatrization 
and the formation of stenosis, with secondary dilatation of the upper portion of 
the duodenum and of the stomach. In regard to the different adhesions and per- 
forations of the ulcer into neighboring organs we may refer to what has been said 
of gastric ulcer. 

The treatment must be governed by the same principles which were laid down 
in the treatment of gastric ulcer, especially as the diagnosis is usually doubtful. 



CHAPTER VI. 
TUBERCULOSIS OF THE INTESTINES. 

Tuberculosis of the intestines is in most cases a secondary disease, and is one 
symptom of a more extensive general tuberculosis. It develops most frequently 
in the course of chronic pulmonary tuberculosis, and depends here, as we have 
seen, upon an infection of the intestines by the tubercular sputum that has been 
swallowed. 

Intestinal tuberculosis, however, may also be a primary disease, and the source 
of further extension of tuberculosis over the body. " Tuberculosis of the abdomi- 
nal organs," which usually comes from the intestines, has a clinical significance, 
especially in children. It is not improbable that in such cases the first infection 
of the intestine comes from without, and that the tubercular poison is taken into 



396 



DISEASES OF THE DIGESTIVE OEGANS. 



tlie body with the food. Here we must think especially of the milk from cows 
with pearly distemper — that is, with tubercular disease. 

The anatomical changes in intestinal tuberculosis are precisely analogous to the 
tubercular changes in other mucous membranes. The tubercular new growth has 
its origin usually in the lymph-apparatus of the intestine, in the solitary follicles, 
and in Peyer's patches. The first miliary tubercles form beneath the epithelium, 
and soon fuse with one another into a diffuse infiltration. In its further course 
the infiltration on one side extends deeper into the surrounding tissue, so that it 
attacks the submucous and muscular coats even to the serous coat, and on the 
other side, by the destruction of the new growth which begins at the surface and 
constantly spreads, tubercular ulcers are formed. We can often make out with 
the naked eye single miliary tubercles or groups of them at the base or in the infil- 
trated edges of the ulcer. This is especially plain in deep-seated ulcers on the 
corresponding portion of the serous coat. The form of the larger tubercular 
ulcers is often irregular. In many cases the long diameter of the ulcer is parallel 
to the circumference of the intestine, so that the girdle-like ulcers, which are espe- 
cially characteristic of tuberculosis, are formed. 

Tubercular ulcers are situated both in the large and in the small intestines. 
They are usually most marked in the vicinity of the ileo-csecal valve. Tubercular 
ulcers in the stomach are extremely rare. Beside the intestinal tuberculosis there 
is very often tuberculosis of the mesenteric lymph-glands, and also frequently 
tuberculosis of the peritoneum. 

The symptoms of intestinal tuberculosis are usually quite subordinate to the 
symptoms caused by other co-existing tubercular affections. There may often be 
quite extensive tubercular ulcers without any marked symptoms, but, as a rule, 
the onset of diarrhoea turns the attention to the intestinal complication (see the 
chapter on pulmonary tuberculosis). 

Primary tuberculosis of the abdominal organs sometimes presents quite a char- 
acteristic type of disease, especially in children. This was termed by the older 
physicians tabes mesenterica. The chief feature of this type of disease consists of 
a progressive general emaciation and anaemia, which is usually associated with a 
persistent hectic fever, which obstinately resists all remedies employed. The abdo- 
men is usually swollen by meteorism, but it is sometimes flat or sunken. In some 
cases, but less frequently than was formerly believed, we can feel the swollen 
mesenteric lymph-glands through the abdominal wall during life. The liver may 
be enlarged and its lower border can often be felt. The bowels are irregular, 
and there is usually a moderate diarrhoea, persisting in spite of all remedies. 
The invariably fatal termination is due to an increase of the general marasmus, 
or from a final acute tubercular affection, like miliary tuberculosis or tubercu- 
lar meningitis. The autopsy shows tuberculosis of the intestines, peritoneum, 
lymph-glands, liver, etc., to a greater or less extent. The lungs may be quite free 
from tuberculosis. We will return to this affection in the description of tuber- 
culosis of the peritoneum. 

The treatment of intestinal tuberculosis can be only purely symptomatic. 
Beside the general dietetic treatment which seeks to keep up the patient's strength 
as far as possible, medical interference is demanded by the abdominal pain and 
diarrhoea. The chief remedy is opium, which, alone or in combination with tan- 
nin, acetate of lead, etc., acts most rapidly in relieving the intestinal, symptoms. 
Warm poultices and wet compresses give the best service for local applications. 

In other respects the treatment coincides with the general treatment of tuber- 
culosis (vide supra). 



SYPHILIS OF THE RECTUM. 



397 



CHAPTER VII. 
SYPHILIS OF THE RECTUM. 

In not very rare cases we see in the rectum, especially in its lower portions, 
extensive syphilitic ulcerations, which produce a severe and practically important 
type of disease. The more intimate relation between syphilis of the rectum and 
the general syphilitic process is not perfectly clear. According to quite a wide- 
spread opinion, the infection of the rectum comes from the secretion trickling 
down from the ulcers of the genitals. The facts seem to support this view, since 
syphilis of the rectum is seen much more frequently in women than in men. 
Some authors have even asserted that all the so-called " syphilitic " ulcers in the 
rectum have no connection at all with genuine syphilis, but are chancroids. It is 
in fact striking, even if it by no means proves such a hypothesis, that, at the 
autopsy of people who have died of " syphilis of the rectum," we rarely find defi- 
nite syphilitic changes in other internal organs, a fact which we also can confirm. 

The most characteristic mark of syphilitic ulcers in the rectum is their tendency 
to form cicatrices and stenoses. This result of the ulcer is also important in its 
clinical relations, since the chief symptoms of the disease usually begin with the 
development of the stenosis. The seat of the stenosis is usually so low down that 
we can conveniently reach it with the finger, on a digital examination of the rec- 
tum during the patient's life. The rectum narrows like a funnel upward, and we 
can feel the quite sharp edge of the ring-like cicatrix with the point of the finger. 
This funnel-shaped stenosis of the rectum is so characteristic of syphilis of that 
organ that, in almost all cases, we can make the diagnosis with perfect certainty 
from this alone. 

The rectum and the descending colon are usually dilated above the stenosis, 
and here extensive, irregular ulcerations, with undermined edges, are usually 
found in the mucous membrane. These are partly of a specific nature, and are 
partly diphtheritic ulcers caused by the pressure of the accumulated faecal masses. 

The symptoms of syphilis of the rectum usually develop quite gradually. At 
first the bowels are irregular and there are disturbances of defecation which stub- 
bornly resist the ordinary remedies employed. There are sometimes, in the first 
stage of the disease, frequent and severe haemorrhages with the dejections, as we 
have seen, and for a long time these may falsely be considered to be " bleeding 
from haemorrhoids." The symptoms become more marked as cicatrization of the 
ulcer increases and as stenosis of the rectum develops. There is usually a decided 
catarrh of the rectum, so that the thin stools contain a large admixture of mucus 
and pus. The patient's condition is extremely distressing, from the pains with the 
frequent but always scanty dejections, and from the severe tenesmus. Nodular 
thickenings and prolapse of the mucous membrane, and sometimes true haemor- 
rhoids form about the anus. The patient's strength constantly diminishes from 
the pain and the continual diarrhoea. He finally becomes emaciated, looks very 
pale and wretched, and has fever toward night. Death ensues from increasing 
general weakness, or rarely from a terminal peritonitis due to perforation, after 
the whole disease has lasted one and a half to two and a half years. 

This unfavorable termination unfortunately seems to be the rule in all the 
cases described ; hence the prognosis is to be regarded as very serious in all cases 
of syphilis of the rectum. Improvement worthy of mention, or even perhaps 
recovery, is possible only when the disease is recognized at the outset and properly 
treated. 



398 



DISEASES OF THE DIGESTIVE ORGANS. 



At the outset of the disease the treatment of course must consist chiefly of an 
energetic general treatment of the syphilis by mercurial inunction and iodide of 
potassium ; but, as soon as the characteristic funnel-shaped stenosis of the rectum 
has formed, we can not expect much from anti-syphilitic medication, since this can 
no longer exert any influence on the cicatrices and their results. We may now 
hope soonest for at least a palliation and improvement by slow mechanical dilata- 
tion of the stenosis by passing bougies. A corresponding local treatment by irri- 
gation is also of benefit to the catarrh and to the ulcers that still exist in the rec- 
tum. Internally, we may continue to use iodide of potassium. 



CHAPTER VIII. 
CANCER OF THE INTESTINES. 

The development of cancer is far more rare in the intestine than in the 
stomach. Carcinoma is seen with any frequency only at the lower end of the 
intestine, in the rectum. In other parts the points of election for the development 
of carcinoma are the colon, especially at its bends, the caecum and vermiform 
appendix, and the small intestine, especially in the region of the papilla duodenalis. 

Most cancers of the intestine appear in the form of ring-like swellings that take 
in the whole circumference of the intestine. More rarely we find a more diffuse 
papillary proliferation, extending over a larger surface of the intestine. There is 
often quite an extensive destruction of the new growth on the surface of the cancer, 
from which deep ulcerations arise. We sometimes find metastases in other 
organs ; for example, the lymph-glands, the abdominal cavity, or the liver. In 
its histological structure, cancer of the intestine is to be regarded as invariably a 
cylindrical-celled carcinoma, which sometimes shows a plainly glandular structure 
— adeno-carcinoma — and sometimes that of the other forms of cancer — scirrhus, 
medullary, or colloid. 

Cancer of the intestines, like all cancers, occurs chiefly if not invariably in 
advanced life. 

The clinical symptoms of cancer of the intestines are only in a part of the 
cases so pronounced that we can make a sure diagnosis of the disease. Cancer of 
the rectum, however, presents a characteristic picture. 

Cancer of the rectum begins usually with distress at stool and pain in the 
rectum, which at first comes only with defecation, but later becomes almost con- 
tinuous. The pains often shoot into the neighboring parts — the thighs, the genitals, 
etc. The local symptoms gradually increase, the stools often contain some mucus 
and blood, and diarrhoea alternates with obstinate constipation. The patient also 
becomes emaciated and constantly grows weaker and more miserable. Finally, 
we often find a complete paralysis of the sphincter ani, so that a mucous, bloody 
fluid constantly comes from the half -open anus. The diagnosis can almost always 
be easily and surely made by digital examination of the rectum. We feel the 
firm, nodulated proliferations of cancer, and we can usually make out with 
approximate accuracy its extent and its invasion of neighboring organs, like the 
vagina and bladder. Examination with the rectal speculum makes the diagnosis 
more accurate. In some cases the destruction of the new growth may cause per- 
foration into the organs mentioned, and we can easily understand the results of 
this, such as cystitis, purulent discharge from the vagina, etc. We may also have 
peritonitis from perforation. 



CANCER OF THE INTESTINES. 



399 



Carcinoma of the colon causes, as a rule, only very indefinite symptoms, that 
for a long time are hard to determine. These symptoms consist chiefly of distress 
at stool, obstinate constipation, dull pains in the abdomen, and the signs of slowly 
increasing general weakness and emaciation. In many cases the stools consist of 
peculiar, flat, compressed little lumps, which have a certain resemblance to sheep's 
dung. A similar appearance may also be seen in cancer of the small intestines. 
In many cases examination of the abdomen gives a negative result, but we can 
sometimes feel the new growth as an evident tumor through the abdominal wall. 
In such cases, however, it is almost always difficult to decide upon the seat of the 
tumor with certainty. It may be very easy to confuse this form with cancers 
arising from the stomach, the omentum, the mesenteric lymph-glands, etc. We 
may also be deceived as to the location of the tumor by the fact that the tumor 
which is felt in intestinal cancer is sometimes not the new growth itself, but 
corresponds to the faecal masses collected above it. Carcinoma of the caecum can 
often not be distinguished for a long time from the tumors caused by chronic 
typhlitis and perityphlitis. The patient's age, the tedious course and increasing 
severity of the disease, and sometimes the swelling of the inguinal glands, are the 
only things that make us think of a cancer. In a case seen at the surgical clinique 
here in Leipsic, a cancer arising from the vermiform appendix ruptured exter- 
nally through the skin. The rare cases of cancer of the small intestines cause still 
greater difficulties in diagnosis. In cases where the tumor can be felt externally 
we can sometimes make out a marked mobility of the swelling, corresponding to 
the different positions of the affected loop of intestine. Cancer of the duodenum 
in many of its relations resembles cancer of the stomach, especially of the pylorus. 
It also leads finally to dilatation of the stomach with its well-known results, 
as well as to dilatation of the part of the duodenum above the new growth. 
Cancers situated in the region of the papilla duodenalis usually cause intense 
and protracted jaundice. 

The prognosis of all intestinal carcinomata is absolutely unfavorable. The 
disease may sometimes last quite a long time, some two or three years, but in some 
cases the duration of the special symptoms is brief, a few months or even weeks, 
apparently because it has previously existed for a long time without symptoms. 
Intestinal cancer terminates with the signs of increasing loss of strength, or it per- 
forates, causing a terminal purulent peritonitis. Extensive ichorous processes in 
the surrounding connective tissue, phlebitis, and pyaemia, may follow intestinal 
cancer. A number of cases die with the signs of a slowly or rapidly developing 
intestinal stenosis {vide infra), but in some cases, upon ulceration of the cancer, the 
already pronounced symptoms of stenosis may disappear for a time. 

The treatment must be confined to relieving the patient's symptoms as far as 
possible. We must provide for easy dejections by a suitable diet and cathartics. 
Pain, if it is present, must be lessened by narcotics. Surgical treatment of intesti- 
nal cancer has shown good results as yet only in cancer of the rectum. The pallia- 
tion which lasts for a long time after scraping out the rectum is often quite 
marked, even in advanced cases. All the details are to be found in the text-books 
on surgery. 



400 



DISEASES OF THE DIGESTIVE ORGANS. 



CHAPTER IX. 
HEMORRHOIDS. 

By the name u haemorrhoids " we mean diffuse or varicose dilatations of the 
haemorrhoidal veins, especially of the venous plexuses at the lower end of the 
rectum. Haemorrhoids are single large varices, which usually rise from the sub- 
mucous layer, and push the mucous membrane out before them. If they are situ- 
ated outside of the sphincter ani we speak of external haemorrhoids, in dis- 
tinction from internal haemorrhoids, which lie above the sphincter. The size of 
the nodules varies with the fullness of the dilated veins ; but haemorrhoids, as a 
rule, do not consist exclusively of dilated vessels, for we often find, at the same 
time, quite a considerable thickening of the surrounding connective tissue, so that 
the whole mucous membrane has a swollen appearance, with a polypoid prolifera- 
tion in parts. The haemorrhoids usually present themselves as bluish tumors, 
from the size of a pea to that of a walnut, which surround the anus like a garland. 
Many of them have a broad base, while others are pedunculated. 

The cause of haemorrhoids is, chiefly, frequently-repeated stasis in the veins 
affected. The hindrance to the venous blood return has sometimes a purely local 
cause. Thus haemorrhoids quite frequently develop in people with habitual con- 
stipation, and hence in persons who lead a sedentary life. Haemorrhoids also 
occur as a result of stasis in the portal system, in cirrhosis of the liver, etc., and 
finally in general disturbances of the circulation, as in diseases of the heart and 
lungs. Quite often, however, we can discover no sufficient cause for the development 
of the disease, and we are then forced to the hypothesis of a local disease of the 
affected venous plexus, which is probably often connected with an individual, 
and apparently sometimes hereditary predisposition in the parts affected. We 
most frequently see haemorrhoids in men in middle life. 

Haemorrhoids sometimes cause only slight symptoms, or none at all, but in 
other cases they are a tedious, burdensome, and even distressing evil for the 
patient. The chief symptom is pain, which is felt as a constant burniug at the 
anus, but which increases to be very severe at each dejection. There is great 
pain when the haemorrhoids and the surrounding tissue gradually get into an 
inflamed condition. In the skin about the anus, erythema, excoriations, and some- 
times little, but very painful, fissures are formed. The mucous membrane at the 
lower end of the rectum is often found in a catarrhal state, which gives rise to the 
presence of pus and mucus in the dejections — "mucous haemorrhoids." Some- 
times there is a genuine phlebitis in individual haemorrhoids, which ends by form- 
ing an abscess. There is very severe pain if an internal haemorrhoid is pushed out 
by the strain and pressure at stool and is strangulated by the sphincter. Since all 
the conditions mentioned — marked temporary filling, inflammation, and strangu- 
lation of a haemorrhoid — must at times give rise to a great increase of the disturb- 
ance, we can understand why we often hear such troubles spoken of as " attacks 
of haemorrhoids." 

Haemorrhoidal bleeding is a frequent and familiar symptom, which rises 
from a rupture of the dilated veins and usually comes on at stool. The haemor- 
rhage is usually not very large, so that the loss of blood is iu itself very rarely 
dangerous. The swelling of the varices after the haemorrhages have ceased 
explains why the haemorrhoidal symptoms are usually less marked as long as 
there are haemorrhages than if there are none. Hence the old term of the 
" golden vein " for haemorrhoidal bleeding. 

Beside the local symptoms mentioned in the anus there are sometimes other 



HiEMOKRHOIDS. 



401 



symptoms which are due to an implication of the neighboring venous plexuses, 
the vesical, prostatic, and sacral plexuses. There is often pain in the sacral 
region, difficulty in micturition, and sometimes even blood in the urine — " vesical 
haemorrhoids — and in women vaginal catarrh, anomalies of menstruation, etc. 
Since the symptoms of some primary disease of the liver, or heart, or of other 
co-existing morbid conditions, like abnormal corpulency, or chronic gastro-intesti- 
nal catarrh, may be added to the general picture, we can comprehend why medi- 
cal superstition has found in haemorrhoids an abundant cause for forming the 
strangest ideas, Kke that of "transposed haemorrhoids" ! 

The treatment of haemorrhoids is usually no easy task, since the disease often 
has causal factors which can not be removed. In all cases where there are large 
haemorrhoids causing severe symptoms, there is only one radical cure — removal by 
operation — which is not dangerous and not hard to perform. It is best performed 
by squeezing the nodule with a clamp and burning it with the thermo-cautery. 
Details in regard to it may be found in the text-books of surgery. 

If single nodules are inflamed, we may apply ice locally, or under some circum- 
stances local blood-letting is to be preferred. If an abscess forms it must be 
opened. We try to replace strangulated haemorrhoids carefully and slowly with 
the oiled finger. 

The treatment of chronic haemorrhoidal symptoms consists chiefly in looking 
out for regular and easy movements of the bowels, because the local symptoms 
can thus be best relieved. "We must also attend to any underlying trouble, like 
disease of the liver or heart. The food to be prescribed depends upon the 
patient's physical constitution. It is usually wise to limit the supply of meat, and 
to recommend instead a more vegetable diet, fruit, vegetables, light farinaceous 
food, and rice. It is well to prescribe sufficient physical exercise, cool baths, under 
some circumstances sitz-baths, and rubbing. We must also consider cathartics, 
especially the bitter waters, the springs at Marienbad, and Kissingen, and also the 
regular use of cold enemata, rhubarb, aloes, etc. Sulphur is a remedy very often 
used in the treatment of haemorrhoids, the chief ingredient of most of the " pile 
powders " for internal use, as follows : 

5 Sulphuris loti, ) 



Haemorrhoidal bleedings, as has been said, are only exceptionally so severe as 
to require interference by means of styptics, like ice, chloride of iron, or tampon- 
ing the rectum. 

[Persistent and intelligent treatment will often bring about very great relief, or 
even complete cure, in chronic cases. There are many local applications, each of 
which has its warm advocates — so many that it is not possible here to go into 
details. Suffice it to say that an astringent with or without an anodyne may be 
used as an enema, in suppository or in ointment. The fluid extract of hamamelis. 
glycerine, and some other remedies given by the mouth, are reported to have 
afforded good results.] 




aa | ss. (grm. 15) ; 



aa 3 ijss. (grm. 10). M. 



26 



402 



DISEASES OF THE DIGESTIVE OEGANS. 



CHAPTER X. 
HABITUAL CONSTIPATION,, 

A PERSISTENT tendency to constipation is a frequent symptom in many different 
diseases, where it is almost always due to a diminution of the normal peristaltic 
movements of the intestines. In many conditions this diminished energy of peri- 
stalsis is only one symptom of general weakness of the body. Thus we see in all 
possible forms of chronic disease, which are associated with loss of flesh and 
strength, that the intestinal movements become sluggish, and hence the dejections 
are delayed ; yet many other causes usually have a similar action. The small 
amount of food taken, and its quality, as it is often composed largely of fluids and 
" non-irritating " substances, and also the rest in bed, or at least the slight amount 
of physical exercise taken — all these conditions play a part in the frequent con- 
stipation in patients with chronic disease. 

In other cases we have to do with disease of the intestine itself, as the cause of 
the habitual constipation. In chronic primary and secondary intestinal catarrh 
we often observe a persistent tendency to constipation, which is only occasionally 
interrupted by diarrhoea. Many factors also act here simultaneously. The chronic 
inflamed membrane, which is often covered with mucus, is less irritable, and 
hence it is more difficult to excite the intestinal movements by reflex action than 
if the intestinal mucous membrane is normal. The muscular coat itself often 
takes part in the morbid changes, and atrophy of it has been repeatedly observed 
as a result of chronic intestinal catarrh. The habitual constipation in chronic 
affections of the peritoneum is explained in a similar way, as the muscular coat is 
also directly affected by collateral oedema, etc. We must also mention here the 
constipation in all forms of chronic jaundice, which depends in part at least upon 
the absence of the irritation which the bile normally exerts upon the intestinal 
wall. 

We very often see chronic constipation in the different diseases of the nervous 
system, especially of the brain and spinal cord. Here we have to do with abnor- 
mal inhibition or direct disturbance of the nervous stimulus, which is necessary 
to cause the intestinal movements. Abnormal mental conditions are also of great 
influence. In many psychoses, especially in hypochondriasis, melancholia, and 
many forms of hysteria and neurasthenia, we very often see habitual constipation. 

While constipation, in the diseases so far described, is a symptom which is more 
or less subordinate to the other symptoms of the disease, there is a form of 
habitual constipation, extremely important practically, where the constipation is 
the chief or almost the sole symptom, and accordingly it may be regarded to a 
certain extent as a disease sui generis. Patients very often come to the physician 
who look perfectly well, and are entirely able to attend to their business, but 
who are constantly troubled because they can not have a movement of the bowels 
every day, like other people, but only every three or four days, or even less fre- 
quently. In some cases of this sort the patient's complaint is limited to the delay 
in the stools, but more frequently a number of other abnormal subjective sensa- 
tions and disturbances are added to the habitual constipation, which are regarded 
as a result of the constipation by the patient himself, and are usually observed 
with great care and excessive accuracy. These are the cases which may lead to 
the highest degree of hypochondriasis. The patient's whole thought and sense are 
busied almost exclusively with his own morbid condition, through which he has 
lost all energy and joy in life. He seeks aid from different physicians and from 
quacks, usually without any real confidence, and without having the necessary 



HABITUAL CONSTIPATION. 



403 



perseverance to follow out the directions given. Beside the trouble with the bow- 
els, such patients complain chiefly of dizziness in the head, pressure, coldness, and 
other abnormal sensations in the extremities, very often of cold sweaty hands, of a 
feeling of oppression in the chest, of disturbed sleep, etc. 

It is not always easy to interpret these cases correctly. The nervous affection, 
like hypochondriasis or neurasthenia, is often probably the primary disease, which 
is followed by constipation, while in other cases the habitual constipation leads 
secondarily to the nervous depression. The two conditions usually form a vicious 
circle, since each of them is able to keep up and to increase the other. The cause 
of primary habitual constipation can not usually be discovered. Probably we 
often have to do with a congenital weakness of the muscles or of the innervation 
of the intestines, since many cases date from early youth. 

The treatment of habitual constipation is a difficult and often a thankless task 
for the physician, and it demands patience and professional tact. It goes without 
saying that we must first of all look for the causal factors. If we succeed in 
improving the underlying disease — as, for instance, the chronic gastro-intestinal 
catarrh, the chronic affections of the heart or lungs, the anaemic conditions, or 
certain nervous troubles — a regulation of the bowels often follows of itself. In 
ordinary habitual constipation we must first attend to the patient's diet. Since 
most of these patients also suffer from symptoms of nervous dyspepsia, they 
are usually very careful in their diet, and take only a little, easily digestible, and 
chiefly liquid food. It is no wonder that no good dejections follow such food. 
Improvement can be obtained only by plenty of food which can irritate the 
intestine mechanically. Hence we must try to bring the patient to return to 
his ordinary former " household fare," to take, beside plenty of meat, a sufficient 
amount of bread, vegetables, etc. It is a very good thing to recommend espe- 
cially certain kinds of bread, like Graham-bread or rye-bread, and also larger 
amounts of butter, beside fruit, prunes and grapes, and honey. The well-known 
remedy of drinking a glass of cold water in the morning before breakfast is in 
common use. We should be very guarded in giving special cathartics, since the 
patient easily gets accustomed to them, and then must take them in larger doses. 
Of the milder laxatives, the different bitter waters, like Friedrich shall, do the best 
service. We usually prescribe one or two wineglassfuls. The other cathartics, 
like tamarinds, rhubarb, aloes, gamboge, or jalap, which may sometimes be used 
regularly for a long time, are prescribed in various combinations, as pills and 
powders. We may often have to change our remedies and our doses a number 
of times until we find the right ones. 

In the treatment of habitual constipation associated with hypochondriasis, the 
first rule is to treat the patient's mental condition properly. We should not make 
merry over his trouble, nor should we let him feel roughly that we do not con- 
sider his complaints so important as he himself imagines. The patient does not 
deserve to be scoffed at, since his subjective symptoms are to him of the most 
urgent nature ; but it is extremely important to divert his thoughts from his 
trouble. As in many other reflex processes, so in defecation, the voluntary 
attention abnormally directed to it has an inhibitory action. Hence we admon- 
ish the patient to think of his trouble as little as possible, and to begin his regu- 
lar activity again, and we try to convince him of the groundlessness of his 
fears. The cathartics, which most patients have already taken freely with- 
out the desired action, are usually of no advantage at all. On the contrary, it is 
almost always necessary to forbid the patient to use cathartics at all. Except by 
a proper diet (vide supra), we try to regulate the peristalsis by external remedies 
only. Methodical massage of the abdomen is most employed for this, and also 
electrical treatment, faradization of the abdominal walls, and faradization and gal- 



404: 



DISEASES OF THE DIGESTIVE ORGANS. 



vanization transversely through the abdomen. We must not omit a proper gen- 
eral treatment : cold sponging, baths, a country residence, and sufficient physical 
exercise. By these means only do we succeed in giving the patient renewed cour- 
age, and sometimes finally in attaining recovery even in severe and persistent 
cases. (Compare the chapters on nervous dyspepsia and on neurasthenia.) 



CHAPTER XI. 

STRICTURE AND OBSTRUCTION OF THE INTESTINES. 

./Etiology and Pathological Anatomy. — Different pathological processes may 
lead to stricture or complete obstruction of the intestinal tube in different parts. 
Since in this affection the purely mechanical effect of the intestinal stenosis is the 
chief cause of the clinical symptoms, the type of the disease is very similar in all 
the cases of this class, in spite of the manifold anatomical causes. Hence, after 
enumerating the single affections which may lead to stricture of the intestines, 
we can describe their symptoms in common. 

The anatomical causes of stricture or obstruction of the intestines are as fol- 
lows : 

1. Congenital closure of the intestines is found at the anus, atresia ani, and 
much less frequently in the colon or small intestines. The form first mentioned 
is the only one of clinical interest, since it may be relieved, at least in some cases, 
by operation. All the other forms of congenital closure of the intestines are 
incompatible with a long duration of life. 

2. Tumors and Cicatricial Strictures. — Cancer of the intestine is the only 
tumor that has any clinical significance. We have already described its most 
important anatomical relations and the possibility of intestinal stenosis from it. 

We see cicatricial strictures most frequently in the large intestine after recov- 
ery from dysenteric ulcers. The syphilitic stenosis of the rectum, which we have 
already described, is also of practical importance. Typhoid ulcers very rarely lead 
to cicatricial stenosis. Strictures as a result of tubercular ulcers of the intestines 
are also extremely rare. Stenosis of the duodenum after the healing of a duodenal 
ulcer {vide supra) resembles, in its clinical symptoms, stenosis of the pylorus, and 
not stenosis of the intestines. 

3. Intestinal Obstruction. — The most frequent form of intestinal obstruction 
comes from the impaction of faeces. From the different conditions which cause 
enf eeblement of the peristaltic movements, an accumulation of faeces (coprostasis) 
may arise, especially in the colon, and gradually gain in extent, and finally lead 
to the fully developed symptoms of intestinal stenosis. Since in such cases a 
paralysis of the muscular coat has been supposed to be the first cause of the con- 
stipation, the occasional stercoraceous vomiting which finally sets in has been 
termed " ileus paralyticus." We must also mention that, in intestinal stenosis 
from other anatomical causes, coprostasis is often an important factor in increas- 
ing the stenosis. 

We see obstruction of the intestines from other causes much less frequently 
than from impaction of faeces. In some cases impacted gall-stones have been 
found, especially in the lower part of the ileum, which almost completely stop up 
the lumen of the intestine. The very rare genuine intestinal calculi may excep- 
tionally lead to obstruction. We must also mention here the very rare cases where 
a large foreign body has been swallowed and wedged itself into some part of the 
intestine. Such a thing has been seen, especially in children and among the 
insane. 



STEICTURE AND OBSTRUCTION OF THE INTESTINES. 405 



4. Intestinal Constriction. — Although the mechanism of intestinal constriction 
in external hernias lies in the domain of surgery, we must mention here the chief 
causes of the so-called internal intestinal constriction, internal incarceration, or 
strangulation. In the abdominal cavity itself pouches and diverticula are found, 
either as normal or abnormal formations, in which single loops of intestine may 
be caught and constricted. The duodenojejunal hernia — the so-called Treitz's 
retro-peritoneal hernia — is worthy of special mention, and comes from the entrance 
of a loop of intestine into the duodeno-jejunal fossa. This hernia may become 
very large. It is sometimes found by accident in the cadaver, not having 
caused any symptoms during life, but in rare cases it may be the cause of acute 
internal constriction. We must also mention the hernia of the omental bursa — 
where a loop of intestine passes through the foramen of Winslow — the intersig- 
moid hernia, the subcascal hernia, etc. Diaphragmatic hernia is of greater practi- 
cal significance because it is somewhat commoner. By this name we designate 
both genuine protrusions into the diaphragm, and also the passage of abdominal 
viscera through congenital or acquired (traumatic) defects in the diaphragm. 
These hernias may exist without symptoms, or at least without causing any signs 
of severe disease, but in some cases they cause obstruction by constricting or twist- 
ing a dislocated loop of intestine. 

Those cases in which abnormal slits and holes in the omentum or mesentery 
give rise to internal constriction are to be added to the list of the internal hernias. 

Finally, abnormal fibers, membranes, and false ligaments in the abdominal 
cavity are a comparatively frequent cause of internal constriction. Such cords 
and bands are sometimes left as the results of a former peritonitis, and may cause 
actual constriction or bending of single loops of intestine. One form of such a 
false ligament, which must be specially mentioned, and which may cause intesti- 
nal constriction, is found as an addition to Meckel's diverticulum. By this we 
mean that diverticulum which must be regarded as the remains of the omphalo- 
mesenteric duct, still persisting, which has its seat, corresponding to the duct, from 
half a metre to a metre above the ileo-cascal valve. A firm cord sometimes arises 
from the free end of this diverticulum, the obliterated omphalo-mesenteric vein, 
which adheres to some part of the internal abdominal wall and may cause con- 
striction of the intestine. Adhesion of the free end of the vermiform appendix 
has been the cause of internal constriction in some cases observed. 

5. Twists (volvulus) and Knots of the Intestine. — Twists about the mesenteric 
axis, and complete constriction of a portion of intestine from this cause, are seen 
most frequently in the sigmoid flexure, especially if the mesentery of the flexure 
is unusually narrow congenital] y. The return from this abnormal condition is 
hindered by the weight of the loops of intestine filled with gas and masses of fasces, 
and by other portions of intestine lying on the place of twisting. Sometimes 
other portions of intestine wind themselves several times about the pedicle of the 
twisted loop so as to form a regular knot. Such twistings have been seen espe- 
cially between the sigmoid flexure and a portion of the ileum. External injury 
sometimes gives rise to the formation of a knot. In some cases abnormally great 
peristalsis, severe diarrhoea, precedes the appearance of obstruction. We have our- 
selves seen a case of volvulus in the upper part of the small intestines, as a result 
of very severe vomiting caused by a remedy for tape- worm given by a quack ! 

6. Invagination of the Intestine (Intussusception). — If a portion of intestine 
is pushed into the lumen of the portion that lies next below, we term the process 
invagination. The cause of this is probably to be looked for in a diminution or a 
complete absence of peristalsis in a circumscribed portion of intestine. If now 
there are energetic movements in the portion immediately above, they push this 
into the paralyzed portion. In other cases we may, perhaps, consider spasmodic 



406 



DISEASES OF THE DIGESTIVE OEGANS. 



states of the muscular coat. We find invagination of the ileum most frequently 
in the bodies of atrophic children. In such cases it is an ante-mortem symptom, 
due to the different periods of cessation of peristalsis in the different parts of the 
intestines. 

Beside this invagination, which has only an anatomical interest, sudden intus- 
susceptions are seen, especially often in children up to ten years of age, for which 
we can usually discover no certain cause, and which, in a short time, lead to the 
severest symptoms of intestinal stenosis. Such intussusceptions,, which ofteu 
involve quite long portions of the intestine, may have their seat in almost any part 
of the intestine. The invagination of the caecum and a portion of the lower part 
of the ileum into the colon (ileo-caecal invagination) is relatively the most fre- 
quent. These intussusceptions may sometimes reach such an extent in children 
that the invaginated portion of the ileum may finally reach the rectum, and some- 
times even project externally. Inflammation and adhesions usually appear in the 
part invaginated. Gangrene of the internal portion, from the constriction of the 
afferent vessels, is also common. The necrotic portion may be cast off and passed 
with the dejections, a process which, in some cases observed, has led to a sponta- 
neous healing of the intussusception and to a cure of the intestinal obstruction 
caused by it. 

We must mention intestinal polypi as a special cause of intussusception, as they 
gradually pull that portion of the intestine in which they are situated into the 
neighboring portion next below by their weight. This has been repeatedly con- 
firmed. 

7. Compression of the Intestine from without, by tumors of the uterus, ovarian 
cysts, pelvic abscesses, omental tumors, etc., has been observed in rare cases as a 
cause of intestinal stenosis. The symptoms of stricture in such cases develop 
either very gradually or sometimes quite suddenly. 

We must now mention certain pathological changes which may follow every 
obstruction, from whatever causes it may arise. 

The further changes in the intestine deserve the chief attention. Above the 
constricted point it is usually greatly swollen from gas and the accumulation of 
faeces. The whole intestinal wall is found in an inflamed condition, which is due 
in part to mechanical action, and in part to the great irritation caused by the 
abnormal transposition of the intestinal contents. A severe diphtheritic process 
often develops in the intestine, with ulceration above the stenosis. In the inflamed, 
softened intestinal wall, thin from its abnormal distention, a little tear easily 
occurs in some spot, or more rarely a genuine perforation following an ulcer. 
Some of the putrefying contents of the intestine thus enter the abdominal cav- 
ity, and an intense purulent or ichorous peritonitis is unavoidable. This is 
why acute peritonitis is so frequent a lesion in persons who die of intestinal 
obstruction. If the intestinal stenosis has lasted a long time, we usually find in 
the upper portion of the intestine, beside the signs of inflammation, a manifest 
hypertrophy of the muscular coat, the result of the abnormally active peristalsis 
by which the muscle has tried to overcome the obstacle. The intestine below the 
constriction, in contrast to the part just described, appears narrow, contracted, and 
empty. 

The changes in the other organs correspond to the general inanition. The 
frequent development of inhalation-pneumonia is easily explained, if severe vom- 
iting has preceded {vide infra). 

Clinical History. — In regard to the clinical symptoms we must distinguish the 
cases with a rapid, complete obstruction of the intestine from those in which the 
condition develops gradually, and where there is, therefore, merely a constriction 
of the intestine, at least for a time. 



STRICTURE AND OBSTRUCTION OF THE INTESTINES. 407 



The first symptom of the intestinal constrictions, which arise from cicatricial 
strictures and new growths, from partial blocking up of the lumen, from intussus- 
ceptions, etc., is usually a disturbance in defecation. The bowels are costive, 
they move only at long intervals, and their motion is often associated with pain 
and tenesmus. In the description of cancer of the intestines we have already 
mentioned that the faeces passed sometimes have a peculiar, flat, compressed, or 
scybalous form. Blood and mucus are often mixed with the dejections and are 
due to the character of the primary disease. In some cases there is no constipa- 
tion, and there may be even constant diarrhoea. We can easily understand from 
the physiological conditions that in stenosis of the small intestines, whose contents 
have an approximately fluid consistency, disturbances of defecation are less apt 
to take place than in stenosis of the large intestine, where the faecal masses have 
already assumed a more firm consistency. 

Physical examination of the abdomen often gives important and valuable 
information. The abdomen is usually swollen by meteorism, which arises from the 
accumulation of gas above the constricted portion. The intensity of the meteor- 
ism varies very much in different cases and at different times in the same patient. 
Meteorism is sometimes absent, especially in stenosis at the beginning of the intes- 
tine. There may then be gastrectasis. The marked peristaltic movements, plainly 
visible through the abdominal walls, are very characteristic of most intestinal 
constrictions. The contour of single loops of intestine is often marked, at times 
quite sharply, and then we can sometimes feel the thickened intestinal walls 
through the lax abdominal wall. We may often decide upon the seat of the ste- 
nosis from the location and course of the visible peristaltic movements. We must 
finally state that we have been repeatedly struck by the great extent and strength 
with which we could feel the pulsation of the aorta through the swollen loops of 
intestine. If we put our ear to the anterior abdominal wall we can often hear 
many gurgling and splashing noises, which sometimes have a distinct metallic 
quality. Eructations are frequent, and sometimes there is occasional vomiting. 

The duration of all these symptoms differs with the form of the primary dis- 
ease. Either gradually or sometimes quite suddenly the symptoms of intestinal 
constriction pass into those of obstruction. In this case the same type of disease 
develops as is seen in all acute internal strangulations. 

The symptoms of intestinal obstruction form one of the severest and 
most frightful conditions known to pathology. The patient's general condition 
in a short time undergoes a threatening change for the worse. The signs of gen- 
eral collapse rapidly develop ; the face sinks in and assumes a sunken and sharp 
expression, the extremities become cool and livid, the pulse is frequent and can 
scarcely be felt, the voice is weak and obscure. The temperature usually falls, 
but it occasionally rises. The abdomen is much swollen from meteorism, and is 
usually very tender on pressure from beginning peritonitis. The passage of 
faeces and the escape of flatus cease entirely. We often see the peristaltic motions 
of the intestines above the obstruction through the abdominal walls, but in 
some cases the muscular coat is so paretic that it is no longer capable of marked 
peristalsis. 

The most characteristic symptom of intestinal obstruction is the appearance of 
the vomiting of feculent-smelling masses, the so-called stercoraceous vomiting 
(ileus miserere). There is often frequent eructation at the beginning of the 
attack, which alternates with real vomiting. The vomitus at first is of the usual 
character, but it soon acquires a manifestly putrid, faecal odor. The old opinion 
is false that in this vomiting real faecal masses were forced backward from the 
large intestine into the stomach by an antiperistaltic action of the intestine. 
Stercoraceous vomiting occurs, not only when the obstruction is in the large 



408 



DISEASES OF THE DIGESTIVE ORGANS. 



intestine, but also in obstruction of the small intestines. In this case we have to 
do with a putrid decomposition of the contents of the intestine stagnating above 
the obstruction. Part of this putrid mass reaches the stomach in vomiting, since 
the pylorus gradually yields to the increasing swelling of the small intestines. 
The vomiting itself is probably caused in large part by the pulling on the perito- 
neum, and perhaps from the irritation of the abnormal matter which has entered 
the stomach. 

We must mention, finally, certain facts observed in the different forms of intes- 
tinal stenosis, which are of theoretical interest and also of diagnostic importance. 
In the contents of the intestine stagnating above the stenosis, large amounts of indol 
and phenol are formed, chiefly from the decomposition of the albuminous sub- 
stances, and also from the other products of putrefaction. These are in part 
absorbed and excreted with the urine. Hence, in stenosis of the small intestines 
we often find that the urine contains an increased amount of indican * (Jaffe) and 
phenol (Brieger), but in stenosis of the large intestine the amount of indican in 
the urine is not increased, because the albuminous substances capable of decom- 
position are no longer present in the contents of the large intestine to cause it. 

The course of intestinal obstruction differs according to the anatomical causes 
which exist in different cases. In many cases of acute internal strangulation the 
severe type of general disease above described develops in a very short time, and 
may lead to death in a day or two, but usually the course is somewhat longer and 
lasts a week. In intestinal obstruction which develops gradually from intestinal 
constriction, the disease may go on longer and show many variations in its inten- 
sity. In mere intestinal constriction we can make fewer definite statements as to 
the duration and course of the affection, since the symptoms of the disease depend 
entirely upon the form of the primary disorder. 

In a great majority of cases intestinal obstruction terminates unfavorably. 
Death results either from increasing collapse or from secondary peritonitis (vide 
supra), or in rare cases from further complications, like pyaemic conditions or 
pneumonia. Recovery may occur even after the severest symptoms, but it is very 
rare. The obstructions from impactions are most capable of recovery. Impacted 
gall-stones, faecal accumulations, etc., may be evacuated, after which the severe 
symptoms disappear. The possibility of recovery in intussusception, by throwing 
off the gangrenous internal portion of intestine, has been mentioned above. We 
can not wholly deny that internal strangulations are capable of restoration, 
although the prognosis must almost always remain doubtful on account of the 
uncertainty of the diagnosis in any individual case. 

In intestinal constrictions, too, the nature of the trouble causes an unfavorable 
termination in most cases, either from the primary disease itself or from the com- 
plete obstruction that finally follows, but the possibility of recovery can not be 
wholly excluded in certain conditions, like impaction or external compression. 

To go into details as to the clinical symptoms of the separate forms of intestinal 
constriction and obstruction would lead merely to repetitions. In most of the 
acute and many chronic cases the diagnosis can generally be made only as to the 
presence of a mechanical obstacle in the intestine, but the definite determination of 
the nature of the obstruction can at best be based on suspicion. Individual factors 
in reference to this, and in regard to the question of the seat of the stenosis, are 
contained in the account given above of the aetiology and symptomatology. 

[The diagnosis of the nature of an intestinal obstruction is so difficult in many 

* The indican test is performed in the following way : We mix equal volumes of urine and officinal 
hydrochloric acid (P. G.), and then add, drop by drop, a concentrated solution of calcic chloride, 
shaking it after each drop. If the urine contains much indican, a decided indigo-blue color appears. 



STRICTURE AND OBSTRUCTION OF THE INTESTINES. 409 



cases, and yet so important with reference to treatment, that the editor ventures to 
introduce tables of differential diagnosis of the more common forms of the condi- 
tion. These tables are based upon the masterly prize-essay of Treves, of London.] 



ACUTE INTESTINAL OBSTRUCTION. 

Chief Common Symptoms.— Sudden pain,' intermittent or constant, with exacerbations ; tends to become 
constant with time. Vomiting, early, severe, becoming feculent. Constipation, more or less abso- 
lute. Abdominal distention. Shock. 





Strangulation by Bands or 
through Apertures (25 
per cent, of all cases of 
acute obstruction). 


Volvulus of Colon. 


1;--;,. \ 

Acute Intussusception. 


Age and Sex . . 

Local Ten- 
derness 

Constipation. . 

Prostration . . 

Abdominal 
Wall .... 

Meteorism 


Young adults ; rare after 40. 

Previous peritonitis in 68 per 
cent.; previous attacks of 
obstruction in 12 per cent. 

Sudden in 70 per cent. 

Early, severe, continuous, 
with exacerbations. 

Absent at first, appears later. 

Early, marked ; in 60 per cent. 

becomes feculent ; affords 

no relief. 
Continuous and absolute ; no 

blood. 

Marked. 
Absent. 

Flaccid unless peritonitis. 
Very rare. 

Slight, appears about third 
day. 


Males as 4 : 1 ; 40 to 60. 
Previous constipation. 

Sudden. 

Early,less severe, intermittent 
at first, becoming constant 
with exacerbations. 

Early over distended coil, and 
constant. 

Less early, severe, and con- 
stant ; often affords relief. 

Early and absolute ; no blood. 

Rather less marked ; may be 

dyspnoea. 
In i5 per cent. 

Rigid from early peritonitis. 
Absent. 

Early, rapid, increases, and is 
extreme. 


More than 50 per cent, under 

10 years. 
Usually negative. 

Sudden in 75 per cent. 

Early and severe ; increasing 

and later subsiding ; at first 

paroxysmal. 
Common about a tumor. 

Still less early and severe ; in 
25 per cent, becomes fecu- 
lent. 

Absolute rare ; diarrhoea not 
uncommon ; blood in 80 
per cent. 

Marked. 

In 55 per cent., and often early. 

Flaccid unless peritonitis. 

In 50 percent.; invagination 
sometimes felt in rectum. 

Rare, unless marked consti- 
pation. 


N. B.— No trustworthy conclusions can be drawn from the seat of the pain as to the seat of the obstruc- 
tion unless local peritonitis comes on. The pain is usually referred in all forms to the region of the navel. 
In complete obstruction, the pain is constant, though with exacerbations ; intermittent pain shows that 
the obstruction is partial. Coils of intestine are not visible through the abdominal wall in acute cases. 

CHRONIC INTESTINAL OBSTRUCTION. 




Stricture of the Small Gut. 


Stricture of the Large Gut 


F^cal Accumulation. 


Age and Sex. . 
History 

Constipation. . 

Tenesmus 

Meteorism 

Coils of In- 
testine 


Adults, 

Cancer, trauma, tuberculosis ; 
disordered, imperfect, irreg- 
ular action of bowels from 
time to time, with intervals 
of comparative ease. 

Gradual. 
Intermittent. 

Late, scanty, feculent only to- 
ward end of acute attack ; 
may be provoked by food. 

May alternate with diarrhoea; 
blood points to cancer. 

Absent. 

Not marked, unless acute at- 
tack. 

Only in cancer, and then in 30 
per cent. 

Marked in proportion to ema- 
ciation. 


Adults. 

Cancer, trauma, tuberculosis, 
dysentery ; disordered, im- 
perfect, irregular action ox 
bowels from time to time, 
with intervals of compara- 
tive ease. 

Gradual. 

Intermittent. 

Less prominent, rarely fecu- 
lent or provoked by food. 

Form of faeces may be al- 
tered; blood points to can- 
cer. 

Often present. 

Often marked. 

Only in cancer, and then in 40 
per cent. ; may be felt in 
rectum. 

Marked in proportion to ema- 
ciation. 


Adults ; more common in fe- 
males ; the hysterical, luna- 
tics, hypochondriacs. 

Previous constipation. 

Gradual. 
Less prominent. 
Late, scanty, rarely feculent, 
often absent. 

Gradually increasing : may be 
spurious diarrhoea ; no 
blood. 

Absent. 

Late ; generally increases 

with obstruction. 
Common and distinctive ; 

most easily felt in caecum ; 

little or no tenderness ; 

sometimes movable, and 

can be changed in shape. 
Rarely seen. 



N. B.— In any form of chronic obstruction, the symptoms of acute occlusion may suddenly supervene. 



410 



DISEASES OF THE DIGESTIVE ORGANS. 



We would here make special brief mention of only one frequent form of in- 
testinal obstruction, on account of its practical importance. We mean that form 
which is caused by the accumulation of large masses of old faeces in the rectum. 
We sometimes find monstrous accumulations of faeces in the rectum, especially 
in old women who have previously suffered from habitual constipation, or in 
whom constipation is due to some other affection. Severe symptoms usually 
come on quite suddenly, after long-continued mild prodromal symptoms, and 
these severe symptoms are much like the picture of internal strangulation — severe, 
sometimes colicky, abdominal pain, great tenderness of the abdomen, which is usu- 
ally swollen, marked general collapse, loss of strength, a small pulse, an outbreak 
of cold sweat, vomiting, etc. If we try to give an enema in such cases, very little 
fluid runs into the rectum. On introducing the finger, it usually strikes solidly on 
old, hard, faecal masses above the sphincter, and there is often nothing left but to 
undertake the dirty task of removing at least a part of the scybala with our own 
hands. We may then succeed, by repeated enemata and by giving cathartics 
internally, in removing sometimes quite an incredible amount of accumulated 
faeces, and in obtaining thus a rapid recovery from the condition. 

Treatment. — As soon as the dangerous signs of intestinal obstruction are 
recognized by the physician, he must decide in the first place whether the stenosis 
is not accessible to direct treatment. Hence we first examine in the most careful 
manner the external points for hernia, that we may not overlook a strangu- 
lated hernia. Then we make a digital examination of the rectum in order to 
decide whether the stenosis may not have its seat here, as from coprostasis, rectal 
tumors, or perceptible intussusception. Beside that, we of course examine the 
rest of the abdomen, as far as the patient's condition permits, in order by this, 
and by any facts in the history, to decide as to the form of the stenosis, from oblit- 
eration or compression. 

Definite therapeutic measures sometimes follow from the conditions indicated. 
Strangulated external herniae require operative treatment as taught by surgery. 
We may obtain aid, in some cases of stenosis from impaction, by the prudent use 
of cathartics. The treatment of faecal impaction is of special importance. We 
have described the most frequent form of this in detail above. As has already 
been said, it is usually necessary to remove at least a part of the faeces with the 
fingers, or some instrument like dressing-forceps or a spoon. In the second 
place, we may use large enemata of pure water or soap-suds, which must often be 
repeated four or five times a day. until they have a satisfactory result. These 
are best given by a funnel and an oesophageal tube (" intestinal tube ") intro- 
duced as high as possible into the intestine. Cathartics administered internally 
serve as aids, especially castor-oil and rhubarb. 

In stenosis of the rectum from cicatrices and new growths we can also some- 
times employ a local surgical treatment, like dilatation or scraping. The treat- 
ment of faecal accumulations usually plays an important part here. Finally, the 
cases of ileo-caecal invagination, in which the lower end of the invaginated ileum 
reaches the rectum, may yield to local treatment. We may try a partial replace- 
ment by a "sponge-sound" (an elastic oesophageal tube to the end of which a 
sponge is fastened). Blowing in air by the bellows was also recommended for 
this purpose by the old physicians. As a rule, however, we use here large 
enemata of warm water, which sometimes seem to exert a favorable mechanical 
action. 

Very often we can not decide with certainty as to the anatomical cause and 
the seat of the obstruction at the bedside. In these cases nothing but a sympto- 
matic treatment is left for the physician. With constipation we usually try first 
cathartics, first the weaker, then the stronger, and finally, as a " last resort," regu- 



INTESTINAL PAKASITES. 



411 



line quicksilver, pure mercury in doses of five to ten ounces (grm. 150-300), 
which is sometimes claimed to act mechanically in " doubtful cases " by its weight. 
Except among- some defenders of mercury, the present opinion among physicians 
tends far more to the belief that cathartics are usually of no service, but are often 
directly injurious by increasing the resistance. Hence we have at present gone 
over to the treatment of severe internal incarcerations with large doses of opium. 
Opium acts favorably on the patient's pain, the vomiting is diminished, and, by 
quieting the peristalsis, the danger of increasing the stenosis and tearing the intes- 
tine is also lessened. In fact, the opium treatment has some favorable results to 
show. Sometimes the first dejection appears, even during the administration of 
opium. 

Since, therefore, there are many opinions against the internal use of cathartics, 
we may try to use large enemata in those cases where the seat of the stenosis is 
not known to be in the large intestine. They must be given with caution, but per- 
sistently, and they must often be repeated ; then they sometimes give good results, 
even in severe cases. In several recent cases (Kussmaul and others) washing 
out the stomach repeatedly was accompanied by good results. In fact, we may 
consider that emptying the stomach of its accumulated contents may be of service 
in stopping the increased peristalsis. 

We need not go into details as to the general treatment. It goes without 
saying that the patient's strength must be kept up as much as possible, and that 
in severe states of collapse all possible stimulants must be used, like hot, strong 
coffee, camphor, and ether. Local applications to the abdomen are usually ill 
borne on account of the tenderness, but we may try ice poultices or wet com- 
presses. Opium is the best remedy against pain and vomiting, but it must often 
be replaced by subcutaneous injections of morphine. 

[There is every reason to hope that the surgical treatment of intestinal obstruc- 
tion will prove of the greatest service. The safety with which laparotomy is now 
performed has stimulated the study of all affections in which the operation has 
any bearing. Internal strangulations and invaginations may be relieved, and the 
portion of intestine containing a non-cancerous stricture can be excised. An early 
operation offers much better chances, of course. In these days persons should not 
be allowed to die directly from intestinal occlusion without an attempt being 
made to restore the permeability of the canal by surgical means.] 



CHAPTEE XII. 

INTESTINAL PARASITES. 

(Helminthiasis.) 

1. Tape-worms. 

Natural History of the Tape-worm.— Three of the tape-worms (cestodes) whi-Sh 
are found in the intestines have a clinical significance : the tcenia solium, the 
tcenia mediocanellata, and the bothriocephalus lotus. 

1. The tcenia solium is, when fully developed, two or three metres long. Its 
head (Figs. 36 and 37) is about the size of that of a pin, and has four projecting 
cup-like suckers, and in front a beak with about twenty-six hooks. The top of the 
head is, as a rule, plainly pigmented. A small neck, about an inch long, is 
attached to the head, and then follow the single " joints " (proglottides) of the 
tape-worm, of which the youngest, lying near the head, are still very small and 



412 



DISEASES OF THE DIGESTIVE ORGANS. 



short. They gradually increase in length and breadth, and at about a metre 
from the head they have an approximately quadrilateral shape. The segments 
which lie farther down, and which have already reached puberty, have the form 




Fig. 36.— (From Heller.) Fig . 37.— (From Heller.) Head of cysticercus of 

Head of taenia solium. the brain. 



of pumpkin-seeds, and are nine or ten millimetres long and six or seven wide. 
The matrix or uterus runs through the middle of each mature segment (see Fig. 
38), and from it, on each side, go seven or eight side branches, which ramify like 
a tree. On one side, a little below the middle, lies the sexual orifice (Fig. 38, a). 
The male sexual organs consist of a number of little clear vesicles in the anterior 
portion of the segments. The thick-shelled eggs (Fig. 39, 
3) develop in the uterus, and contain an embryo with six 
hooklets. 

The taenia solium inhabits the small intestines of man. 
Its head clings to the mucous membrane so tightly, usually 
at some point in the upper third of the small intestine, that 
the neck is often torn off in trying to loosen the worm 
from the intestinal wall. The rest of the worm, which is 
in part in many coils, extends to the lower part of the 
ileum, but only exceptionally into the caecum. From the 
lower end long chains, or single mature segments, are often 
detached, mix with the contents of the intestine, and are 
passed with the faeces, together with some of the eggs from 
the uterus. 

The further development of the eggs of the taenia solium 
takes place in another " lodging," almost always in the hog. 
Hogs are infected by eating faeces, offal, etc., containing taenia eggs. The thick 
shell of the eggs is dissolved in the hog's stomach, and the free embryos pierce 
the walls of the stomach and intestines and travel with the blood-current, or 
through the tissues, into the different organs, especially into the muscles. Here 
they develop, in two or three months, into cysts something larger than a pea, from 
whose walls a newly developed taenia-head arises, a so-called scolex (nurse). 
These cysts are termed worm-cysts, measles, or cysticerci cellulosce. They live 
from three to six years ; then they die and become calcified. If a cysticercus gets 
into a man's stomach, from his eating raw or imperfectly cooked ham or pork, a 
new and complete taenia sprouts from the scolex, which forms mature segments in 
three or four months. 




Fig. 38.— (From Heller.) 
Taenia solium. Mature 
segment. 



INTESTINAL PAKASITES. 



413 



"We usually find only one tape-worm in man, but several specimens have been 
seen at the same time in the same intestine. The length of a tape-worm's life is 



2. 5. .4. 5. 




1. 8. 7* 6, 



Fig. 39.— Comparative view of the eggs of some of the commoner intestinal parasites. 1. Egg of dis- 
toma hepaticum. 2. Distomum lanceolatum. 3. Taenia solium. 4. Taenia mediocanellata. 5. 
Bothriocephalic latus. 6. Oxyuris vermicularis. 7. Trichocephalus dispar. 8. Ascaris lumbri- 
coides. 

not certainly known, but it has happened that some persons have lodged the same 
tape-worm for ten or fifteen years. 

Although the fully developed taenia solium is seen only in man, as we' have 
said, the cysticercus cellulosae has been found, in rare cases, in dogs, rats, and mon- 
keys, as well as in hogs. It is a particularly important fact that the cysticercus 
cellulosae itself may also occur, as such, in man. If tape-worms or mature seg- 
ments get into a man's stomach in any way, probably by auto-infection, by the 
finger, etc., the embryos travel into other organs. Cysticerci are often found in 
men, singly or in groups, especially in the skin, the brain, the eye, and the mus- 
cles. There is a special form of cysticercus of the brain, in which we find a whole 
chain of cysts, like a cluster of grapes, but sterile, the so-called cysticercus race- 
mosus. 

2. The taenia mediocanellata, or tcenia saginata (from saginare, to fatten), is 
even more common than the taenia solium in many parts of Germany. It is 
longer than the taenia solium, being about three or four metres long, and its indi- 
vidual joints are, on the whole, broader and thicker. The head (Fig. 40) has also 
four prominent cup-like suckers, but it has no crown of hooklets. The mature 
segments differ from the proglottides of taenia solium, in that the central uterus 
sends off many more (twenty to thirty) side branches, which divide dichotomously, 
and not like a tree. The sexual opening is also on the side (Fig. 41, a). 

The life-history of the taenia mediocanellata is, on the whole, like that of the 
taenia solium. The taenia mediocanellata, however, throws off single mature seg- 
ments much more frequently than the taenia solium. These segments are found 
in the faeces, and here they often exhibit a crawling motion. The cysticercus of 
taenia mediocanellata does not inhabit pork, but beef, so that the infection of man 
by this tape-worm comes from eating raw beef. In man the cysticercus of taenia 
mediocanellata, which is somewhat smaller than the cysticercus cellulosae, has 
never yet been observed. 

3. The bothriocephalus latus occurs in Holland, Switzerland (Geneva), Pome- 



414 



DISEASES OF THE DIGESTIVE ORGANS. 





Fig. 40.— (From Heller.) 
Head of taenia medio- 
canellata. 



Fig. 41.— (From Heller.) 
Taenia mediocanellata. 
Mature segment. 



rania, East Prussia, Hamburg, and Kussia (the German Baltic provinces). It "has 
not yet been observed in middle Germany. It is the largest tape-worm : it may 
be six or eight metres long, and sometimes has over four thousand joints. The 
head of the bothriocephalus (Fig. 42) consists of a little club-shaped swelling, with 
two slit-like depressed suckers on the sides. A long, 
thread-like neck joins the head to the youngest segments. 
The full-grown segments (Fig. 43) are short, but are' dis- 
tinguished by their great breadth. 
The largest segments measure in 
length about three or four millime- 
tres, and in breadth ten or twelve, 
but the last joints are longer and 
are not so broad, so that they have 
an approximately quadrilateral 
form. The uterus consists of a very 
tortuous canal in the center. The 
sexual orifice does not lie on one 
side, as in the tseniaB, but in the mid- 
dle of the abdominal surface, nearer 
the anterior border of the segment 
than the posterior. The eggs {vide 
supra, Fig. 39, 5) are of an oval 
form, and have a hood-shaped lid at one end. They are to be found in almost 
every dejection of persons affected with a bothriocephalus. Single joints of the 
tape-worm are not passed with the stools, but portions of the worm, several feet 
long, come away from time to time, especially in the spring and autumn. 

The noteworthy life-history of the bothriocephalus has been made perfectly 
clear by Braun, in Dorpat. The eggs develop only in fresh water. The embryo 
(Fig. 44). which is formed in them in. a few months, and is provided with six 
hooklets and with vibrating cilia, is swallowed by fishes, especially 
by pike and eel-pouts, and develops in their muscles and internal 
organs into cysticerci. The infection of man with bothriocephalus 
comes from eating such fish containing cysticerci. 

Symptoms and Diagnosis. —In many cases tape- worms are lodged 
in the intestines without causing any morbid symptoms. We can 
recognize their presence only by occa- 
sionally finding the joints in the dejec- 
tions. 

In other cases, however, tape- worms 
cause a list of disturbances which are 
often exaggerated by anxious, hypochon- 
driacal, and nervous persons, but which 
ought not to be too little regarded. The 
symptoms are referred chiefly to the 
intestinal canal. Sometimes there is 
quite severe abdominal pain, which may assume a colicky character. The 
patient also frequently complains of irregularity of the bowels, and of occasional 
diarrhoea, which alternates with constipation. Many general symptoms are also 
added to those mentioned — loss of appetite, or at times marked voracity, general 
languor, disinclination to work, mental disturbance, depression, etc. We can 
see that, under such circumstances, the general health may suffer considerably. 

We must also mention a number of symptoms which probably owe their origin 
to abnormal reflex processes. Among these we sometimes see marked salivation, 





Lat- 



Figs. 42 and 43.— (From Heller.) 
Fig. 42.— Head of bothriocephalus latus. 

eral view, enlarged, b. Natural size. 
Fig. 43.— Bothriocephalus latus. Mature segment. 



INTESTINAL PARASITES. 



415 



tickling in the nose, dilatation of the pupils, palpitation, vomiting, headache 
(migraine), etc. In some cases even severe spasms, and choreic conditions, have 
been referred to the presence of tape-worms in the intestinal canal, but it is hard 
to decide how far such a supposed connection can really be regarded as justified. 

Although many of the symptoms mentioned may arouse suspicion as to the 
presence of a tape- worm, the diagnosis can be made only by finding the joints or 
eggs of the tape- worm in the dejections. In many 
cases the patient himself brings some of the seg- 
ments found by him in the dejections to the 
physician, but in judging of them a certain cau- 
tion is always necessary, since shreds of mucus, 
remains of food, etc., are quite frequently pre- 
sented to the physician, under the idea that they 
are segments of tape-worm. If possible, we 
should take pains to decide definitely, from the 
segments laid before us, the species of tape- worm, 
which is usually not a difficult task if we follow 
the anatomical description given above. If we 
spread out the pieces of tape- worm on a micro- 
scope slide, the thicker, fatter segments of the 
taenia mediocanellata, with its many-branched 
uterus, may usually be distinguished without 
difficulty from the more tender and more trans- 
lucent segments of the taenia solium, with a smaller number of lateral branches 
to its sexual apparatus. The statement of many patients that single segments of 
tape-worm come from them at other times than when at stool, and that they find 
them on their underclothing, almost always points to the presence of a taenia 
mediocanellata in the intestine. 

If we suspect a tape- worm, without having secured the certain evidence of seg- 
ments in the dejections, it is a good plan to give the patient a mild cathartic, like 
castor-oil, or a dose of boiled pumpkin-seeds, since after this, if the intestine har- 
bors a tape-worm, single portions of it almost always come away. 

Treatment. — The "tape- worm cures," which are recommended in so great a 
number that we can by no means mention all of them here, but only the most 
important and the most serviceable, aim at killing or benumbing the worm, and 
then at removing it from the intestine in toto by cathartics. 

We usually begin with a so-called " preparatory treatment." This is to cleanse 
the intestine, especially the large intestine, from old faecal masses, in order to pre- 
pare as free a passage as possible for the worm. For this purpose we give the 
patient a mild laxative, or, better still, a large enema of cold water. We also forbid 
for a day or two the use of vegetables, black bread, etc., and prescribe instead a 
limited diet of white bread, some meat, milk, and coffee. It is a wide-spread prac- 
tice to take during the preparatory treatment certain articles of food to " make the 
worm ill." Among these a salad of finely chopped and very salt herring with 
onions and garlic is especially recommended. A similar action is also ascribed to 
strawberries, cranberries, and bilberries. Hence, on the day, and especially on 
the afternoon, before treatment, we have the patient take a large amount of the 
articles of food mentioned, such as herring salad. 

On the next morning, after everything has been prepared, after the bowels 
have moved the night before, etc., the patient takes no breakfast, or only some 
strong sweet cafe noir. Then he takes the special anthelmintic, and in two or 
three hours, if he feels a great pressure in the abdomen, he also takes a few spoon- 
fuls of castor-oil or rhubarb. 




Fig. 44. — Embryo of bothriocepba- 
lus latus, w'ith its ciliated coat. 
(Leuckart.) 



416 



DISEASES OF THE DIGESTIVE ORGANS. 



The number of anthelmintics recommended is, as we have said, very great. 
At present the following are most in use : 

The bark of pomegranate-root {cortex radicis Punicce granati) is one of the 
most efficient remedies. In the clinique here in Leipsic it has been given for 
years, in combination with the ethereal extract of male fern, in the following pre- 
scription : 

5 Granati radicis corticis 1 iv-v (grm. 120-150) ; 

Aquae Oij (grm. 1000). 

Macerate for twenty-four hours, and boil until it is reduced to § v (grm. 150). 
Add : Oleoresinae filicis 3 j (grm. 5). 

The whole amount is to be taken in three or four doses as near together as 
possible. In order to obviate the bad taste of the remedy and to increase the 
action by introducing a larger amount at once, it has been recommended to intro- 
duce the whole amount of a still stronger decoction of pomegranate-root at once 
into the stomach by means of an oesophageal tube. As a rule, it is well to avoid 
this procedure. 

A second remedy, which has often proved successful, is kousso-flowers. We 
give in three or four powders a drachm (grm. 5) of powdered kousso-flowers in 
white wine, giving a glass of wine containing one powder about every half -hour. 
Rosenthal's " kousso tablets " are more agreeable to take and are very good, but 
they are more expensive. Twenty of these, up to fifteen grains (one gramme), 
may be taken without danger within an hour with cafe noir or lemonade. Dur- 
ing the period of treatment the patient must lie as quiet as possible in order to 
avoid vomiting. Up to the present time we have not had sufficient experience of 
the koussine or kosseine, prepared from the alcoholic extract of kousso-leaves, 
which is said to be very efficient in doses of thirty to forty-five grains (grm. 2-3). 

Of the other remedies we may mention kamala, one to three drachms (grm. 
5-10) of the powder in wine or water, and oil of turpentine, one or two ounces 
(grm. 40-60) in two doses in milk — an efficient but rather dangerous remedy in 
these doses — and picro-nitrate of potassium. We may also prescribe male fern in 
powders up to a drachm (grm. 4), taking it in three or four powders within an 
hour. 

The treatment is to be regarded as absolutely successful only when we find the 
head of the tape-worm, as well as its joints, in the patient's dejections. We may 
best search for the head in the faeces by diluting the dejection with water, stirring 
it repeatedly, and pouring off the water. The tape-worm then remains at the 
bottom of the vessel. 

Every tape-worm treatment is rather a violent procedure, and hence it is 
well, after the treatment is over, to recommend the patient to be prudent in his 
diet, and to be careful about his digestive tract for some time. In persons who are 
very weak, or who have some other disease, we do not willingly undertake to 
remove a tape-worm without urgent reasons, but in people who are otherwise 
healthy it is always well to get rid of a tape-worm, even if it causes no severe 
symptoms. Of course only the taenia solium is attended with the serious danger 
of the possibility of cysticerci invading the brain (see diseases of the brain). The 
best time for undertaking a treatment is when joints or large pieces of the worm 
come away quite frequently of their own accord. We should never prescribe a 
treatment on the mere statements or suspicions of the patient. We must always 
convince ourselves with complete certainty of the presence of a tape- worm in the 
intestine. 

We must finally mention that the only efficient prophylaxis against acquiring 



INTESTINAL PAEASITES. 



417 



a tape-worm is in entirely avoiding* the use of raw or half -cooked beef or pork. 
The more widely spread the taking of raw meat is, as in Abyssinia, the more com- 
mon are tape-worms in man. Certain callings, like 
those of cooks and butchers, are also especially ex- 
posed to infection. 

2. Round-worms. 

(Ascaris lumbricoides.) 

Natural History. — Ascarides are pale-reddish, 
cylindrical worms, pointed at both ends, with the 
sexes in different individuals. The females are 
thirty or forty centimetres long, the males about 
twenty-five. At the cephalic end of the worm are 
found three lips furnished with fine teeth. The 
tail is straight in the females and curved in the 
males. In the female sexual organs (Fig. 45) sixty 
millions of eggs may develop, at a safe estimate. 
These are often found in the faeces of people who 
have round- worms in their intestines (see Fig. 39, 
8). They have a great capacity of resisting external 
influences, and a worm-like embryo develops in 
them in a few months. Their further fate, and the 
form and manner in which infection usually takes 
place in man, are not yet accurately known. 

The round-worms inhabit chiefly the small in- 
testine. In severe vomiting they often reach the 
stomach and are vomited up. In individual cases 
they have been found in the bile-ducts, in the air- 
passages, and, after perforation of the intestine, in 
the abdominal cavity. The number of round- worms 
existing at the same time in the intestines may be 
very considerable. We find them most commonly 
in children and in adults from the lower classes. 
Eound-worms have been repeatedly observed to 
crawl out of the anus, the mouth, or the nose of 
children during sleep. 

The round-worm is also common in hogs and 
cattle as well as in man. 

Symptoms.— In general, the round-worms are 
innocent parasites, which may exist in large num- 
bers in the intestines without any bad results. In 
other cases they cause symptoms similar to those 
ascribed to taeniae — abdominal pain, languor, itch- 
ing of the nose, burning in the eyes, etc. — symptoms 
which are all ambiguous and whose definite con- 
nection with the presence of round-worms it is 
hard to make out. The cases recorded in literature are quite numerous in which 
severe nervous symptoms have been caused by round-worms and have disappeared 
after the removal of the parasites. However cautious we may be in accepting 
such statements, nevertheless their credibility can not be wholly denied, espe- 
cially if we have to do with convulsions, epileptiform seizures, choreic and cata- 
leptic conditions, contractures, and temporary mental disturbances, which are 
27 




Fig. 45.— (From Heller.) Ascaris 
lumbricoides. Female, 143 milli- 
metres long. a. Vagina, b. In- 
testine, c. Boundary between 
the uterus and oviducts, d. 
Longitudinal bands, e. Coil of 
oviducts and ovaries. 



418 



DISEASES OF THE DIGESTIVE ORGANS. 



Fig. 46. — Oxyuris vermicularis. 

1. Female. 2. 



Natural size- 
Two males 



eg 



claimed to be excited by ascarides. Milder nervous attacks — like headache, vertigo, 
dilated pupils, and chills — are quite frequently seen in children with ascarides. 

In some cases the presence of ascarides may excite much more severe symp- 
toms by unfortunate accidents, as, for example, sudden suffocation from the 
entrance of a round- worm into the larynx. When a very large number of round- 
worms have been present in the intestine, severe symptoms of intestinal stenosis 

have been observed from their rolling together into a 
^^^^^^^m haM. If a round- worm crawls into the bile-ducts, it 

J may give rise to jaundice, and even to the develop- 

ment of an abscess of the liver. In the abscesses of 
S B the anterior abdominal wall, usually termed u worm 

abscesses," the round-worms probably play a purely 
■ accidental part. We have to do in such cases with 

y| perityphlitic abscesses or with inflamed herniae, 

which have perforated externally, by which the 
round-worms which are accidentally found in the 
intestines pass out, without having any causal re- 
lation to the origin of the abscess. 

Treatment. — The oldest and most approved 
remedy against ascarides is worm-seed — santonica. 
This is best given in the form of an electuary — 
santonica, a drachm (grm. 5) ; jalap, fifteen grains 
(grm. 1) ; and syrup, an ounce (grm. 30), to be taken 
in three doses — in combination with a cathartic. 
Of late, worm-seed, on account of its bad taste, has 
been almost wholly replaced by santonin, which is 
derived from it. This is prescribed in one- or two- 
grain (grm. 0*05-0 "10) powders, or still more fre- 
quently in the form of santonin troches (" worm- 
tablets"), which may be had of any apothecary. 
It is also well to give santonin in connection with 
a cathartic, like calomel. We let the patient take 
V * ijflfl one or ^ wo doses of santonin in the morning for 
vMl Bin three days, and on the fourth we give a cathartic. 

jfcfy g evere symptoms of poisoning — spasms — have been 
seen only occasionally from the careless use of it. 
Milder symptoms, like a yellowness of the urine 
and conjunctivas, and xanthopsia, or seeing every- 
thing as yellow, are somewhat more frequent. 

3. Oxyuris vermicularis. 

(Seat-worms. Pin-worms.) 

Natural History. — The oxyures are little round 
worms, the females ten or twelve millimetres long, 
the males only three or four (see Figs. 46 and 47). 
The eggs, when they reach the human stomach, 
develop very rapidly. The embryos, set free, collect 
in the small intestine and later in the caecum, where 
they soon become mature. The impregnated female 
usually crawls down into the rectum, deposits her 
eggs there, and either crawls out of the anus herself, 
or, like the male, is evacuated with the faeces. The whole development of the 
oxyuris occupies about a fortnight. The total number of oxyures present in the 



Fig. 47.— (From Heller.) Oxyuris 
vermicularis, enlarged. a. 
Mature female, not yet im- 
pregnated, b. Male. c. Female 
containing eggs. 



INTESTINAL PARASITES. 



419 



intestine at the same time may be very considerable, so that " the whole mucous 
membrane of the large intestine is covered with them like fur. 1 ' 

The infection by the eggs of the oxyuris prol^ably takes place as a rule from 
one man to another, since the eggs stick to the hands (in scratching the anus), 
and are thus communicated to food, bread, fruit, etc. In children and dirty adults 
auto-infection may often be repeated in an analogous manner. 

Symptoms and Treatment.— The oxyures found in the upper portions of the 
intestine and in the caecum cause no symptoms whatever, but in the lower part of 
the rectum their presence causes local symptoms, especially a very severe feeling 
of itching and burning in the anus, which makes the child constantly scratch and 
dig with his fingers. This itching of the anus is most severe at night in bed. In 
girls the oxyures frequently travel into the vagina, by which an intense itching is 
also set up there, which sometimes leads to masturbation. In some cases in boys 
and men oxyures have been found to be the cause of abnormal sexual irritation. 

The diagnosis of oxyures is not difficult. Our attention is called to the itching 
of the anus, and we look for worms. Single worms are easily found in the dejec- 
tions, and often on the skin about the anus. The diagnosis is made more certain 
by finding the eggs (Fig. 39, 6) in the faeces under the microscope. 

Treatment can remove the oxyures from the rectum with ease, but only with 
difficulty from the upper portions of the intestine, especially from the caecum and 
the vermiform appendix. Santonin is generally used, but we must also prescribe 
large enemata of cold water and cathartics internally. Instead of ordinary water 
we may use soap-suds, vinegar- water, and, in severe cases, a weak solution of cor- 
rosive sublimate (1 to 10,000) in the enemata. The itching of the anus is relieved 
by rubbing on a little mercurial ointment. 

[Enemas containing infusion of quassia, alum, eucalyptol, tannin, etc. , are much 
in use. A plain enema should be given first, to unload the rectum and clean the 
membrane as far as possible, so that the anthelmintic may reach the worms when 
introduced.] 

4. Anchylostomum duodenale. 

(Dochmius s. Strongylus duodenalis.) 

The anchylostomum duodenale is a worm first observed in upper Italy and in 
Egypt, which, singly or in large numbers, inhabits the upper portion of the small 
intestine, especially the duodenum. The male is six to ten 
millimetres long, the female ten to eighteen. At the 
cephalic end (Figs. 48, 49) is found a bell-shaped mouth- 
capsule, which is provided with two small teeth on its dor- 
sal edge, and four larger curved teeth on its ventral edge. 
With this sucking and biting apparatus the worm fixes 
itself firmly, like a wet cup, on the intestinal mucous 
membrane, and is nourished by 
the blood which it sucks out. The 
places in the intestine to which an 
anchylostomum has fastened may 
be recognized in the cadaver as little 
ecchymoses. The worms sometimes 
bore completely into the inner part 
of the mucous coat. 

If an intestine harbors many 
anchylostoma, the small but con- 
stant loss of blood caused by them 
is not without influence on the organism. The symptoms of a severe anaemia 
gradually develop. Griesinger first made the discovery, in the year 1854, that 



id 




Fig. 48.— Anchylostomum 

duodenale. Natural 
size. a. Male. b. Fe- 
male. 



Fig. 49. — (From Hel- 
ler.) Anchylostomum 
duodenale, enlarged. 
Head with bell-like 
mouth. 



420 



DISEASES OF THE DIGESTIVE ORGANS. 



the disease long known by the name of " Egyptian chlorosis " was caused by the 
anchylostomum duodenale. Since then confirmatory observations have been 
made in many parts of the tropics. Of late years the anchylostoma disease has 
been especially known, because it occurred with great frequency among the Italian 
laborers employed in building the St. Gothard tunnel. In Germany, too, cases 
have repeatedly been detected with certainty, especially among brick-makers who 
work in wet clay-pits. The infection probably takes place chiefly from drinking 
impure, muddy water, in which the eggs of the anchylostomum are found. 

The symptoms of the disease consist of a gradually increasing general anaemia, 
for which no special organic disease can be made out objectively as a cause. The 
patient also suffers from very great general weakness and languor, constraint in 
breathing, palpitation, headache, etc. The disease may last for months, or even 
years, and it often ends fatally, if it be not recognized and treated in time. 

The diagnosis is easy if we only think of the possibility of anchylostoma. Many 
eggs may be found in the faeces, without great trouble ; these are quite like the 
eggs of ascaris lumbricoides, only they are a little smaller. After using cathartics 
the full-grown worms have often been found in large numbers in the patient's 
dejections. 

If the trouble is correctly diagnosticated, treatment will usually give good 
results. We prescribe the same anthelmintics as for the other intestinal para- 
sites, especially santonin and male fern, and also cathartics and enemata. In 
this way we often succeed in removing the parasites entirely from the intestinal 
canal, and thus bringing about a complete cure, even in severe cases. 

5. Trichocephalus dispar. 

( Whip-worm.) 

The trichocephalus dispar is a worm four 
or five centimetres long, whose anterior part 
is very thin, but whose posterior part is de- 
cidedly thick (Fig. 50). 

The chief dwelling-place of the trichoceph- 
alus is the caecum, where it is often found 
singly or in large numbers. It seems to have 
no clinical significance. At the most, if present 
in very large numbers, it may give rise to faecal impaction, typhlitis, etc., but, up 
to the present time, such an observation has never been made with certainty. 




Fig. 50.— {From Heller!) Trichocephalus 
dispar. 



SECTION VI. 
Diseases of the Peritoneum. 
CHAPTER I. 
ACUTE PERITONITIS. 

iEtiology— There are two ways by which inflammatory agents most frequently 
reach the peritoneum : one is from the gastro-intestinal tract, and the other— in 
women — is from the genitals. 

All the diverse forms of ulceration which attack the digestive canal may 
involve the serous layer. In such a case an inflammation arises which is at first 
limited, but may under certain circumstances become more extensive. This 



ACUTE PERITONITIS. 



421 



inflammation may be regarded as analogous to that of the pleura in pneumonia ; 
but the anatomy of the stomach and intestine is such that very often an ulcer in 
their walls ends in a complete perforation. If this occurs, the inflammatory 
germs contained in the prima? viae at once escape into the peritoneal cavity and 
there excite an inflammation ; which, from the specific character of its cause, is 
invariably purulent, and very frequently is at the same time septic or ichorous. 
The possibility of a peritonitis due to perforation, as a result of the various ulcera- 
tive processes of the stomach and intestines, has been frequently referred to in the 
previous sections of this work. Thus, it may occur in simple ulcer and in ulcerat- 
ing cancer of the stomach ; in typhoid, tubercular, or dysenteric ulceration of the 
intestine; in ulceration of the intestine above intestinal stenoses of many varie- 
ties ; and in the small ulcers of the vermiform appendix due to the pressure of 
hard substances. 

The female organs of generation are the other frequent source of peritonitis. 
In labor and premature delivery the genital tract is often directly infected. The 
infection may also occur, although much less frequently, at other times ; for exam- 
ple, during menstruation. The various forms of inflammation which are thus set 
up, including endometritis, metritis, and parametritis, may in several different 
ways reach the peritoneum and excite peritonitis. A septic inflammation of the 
endometrium may involve the peritoneum by direct extension up the Fallopian 
tubes. In other cases it is through the lymph-vessels that a purulent metritis or 
parametritis spreads to the peritoneum. The larger parametritic abscesses may 
break into the peritoneal cavity. It is to be particularly noticed, however, that in 
many cases of septic puerperal peritonitis the uterus and its appendages are in a 
perfectly normal condition, having served merely as a gateway to the inflamma- 
tory agents without suffering any harm themselves. 

Beside these two chief sources of peritonitis, numerous others are possible, 
although much less frequent. 

Sometimes peritonitis is due to an extension of inflammation from other 
abdominal viscera. Hepatic abscess, suppurating hydatid cysts of the liver, ulcer 
of the biliary ducts, splenic abscess or infarction, purulent nephritis or pyelitis, 
abscess near the bladder or in the prostate, suppurating ovarian cysts, tubal preg- 
nancy, psoas abscess, and Pott's disease — all these may produce peritonitis, either 
by direct extension or by perforation. 

It is worthy of note that peritonitis may occur as a sequel of pleurisy. The 
pleural and peritoneal cavities are directly connected by the lymph-vessels of the 
diaphragm ; and empyema as well as tubercular pleurisy (see next chapter) may 
spread to the peritoneum. 

Penetrating wounds of the abdomen are a fruitful source of acute peritonitis. 
Surgical operations upon abdominal organs come under the same head. A large 
number of laparotomies proved fatal before Listerism was introduced, because the 
inflammatory germs thus admitted excited a diffuse septic peritonitis. Even tap- 
ping the abdomen for ascites may cause acute peritonitis if the trocar is not asep- 
tic. Abdominal injuries in which the walls are not penetrated very rarely, if 
ever, give rise to peritonitis. One way in which they have been said to produce 
it is by exciting internal haemorrhage. 

Two diseases still remain to be mentioned, in the course of which acute peri- 
tonitis may be developed, although the occurrence is a rare one — acute articular 
rheumatism and nephritis. It may either be one of the symptoms of these dis- 
eases or an independent complication. We are somewhat in doubt as to how it 
arises. In acute articular rheumatism it must be regarded as analogous to the 
pleurisy and pericarditis which occur in the course of this disease, for they also 
involve serous membranes. We should likewise bear in mind the possibility that 



422 



DISEASES OF THE DIGESTIVE ORGANS. 



the inflammation may extend from the pleura to the peritoneum through the 
lymphatics. Acute peritonitis has now and then been observed in the various 
forms of nephritis, both acute and chronic, inclusive of amyloid disease. It usu- 
ally proves fatal in these cases. Possibly the retention of urinary impurities in 
the blood plays some part in the development of this form of peritonitis. 

Pathology. — Like the analogous inflammations of the pleura and pericardium, 
peritonitis is divided into different varieties according to the character of the 
inflammatory exudation. The nature of the exciting cause of most cases of peri- 
tonitis is such that by far the most frequent variety is the fibrino-purulent. If the 
process involves the entire peritoneum — that is, if there is a " diffuse general peri- 
tonitis " — we generally find upon opening the abdomen that the parietal layer of 
the peritoneum and the outer surface of the intestinal coils are distinctly reddened, 
from marked vascular injection. There may even be small ecchymoses here and 
there. The serous membrane is clouded, a result partly of desquamation of its 
endothelium, and partly of the more or less abundant fibrinous exudation which 
covers the peritoneum with a sheet of coagulated fibrin. Very often the coils of 
intestine have formed numerous adhesions with one another (compare pleuritic 
adhesions). In cases of brief duration these can still be easily broken up, but after 
a prolonged illness they are extremely firm. There is usually also some free, fluid, 
fibrino-purulent exudation in the abdominal cavity. Its amount varies greatly. 
Sometimes there is only a small amount of opaque fluid in the dependent por- 
tions of the cavity ; sometimes there are many quarts, causing great distention of 
the abdomen. The exudation seldom inclines to a sero-purulent character. It is 
usually predominantly purulent. Very often the purulent exudation undergoes 
decomposition into the offensive sanious fluid of septic peritonitis. This is par- 
ticularly apt to occur when the disease originates from an intestinal perforation 
or from puerperal poisoning. The perforation through the walls of the intestine 
is sometimes so large as to admit considerable amounts of intestinal gases and 
faeces into the peritoneal cavity. It is also possible that the putrefaction of peri- 
toneal exudations may generate offensive gases. In rare instances the exudation 
is hemorrhagic ; but most cases of hseniorrhagic peritonitis do not belong here, 
but come rather under the tubercular form {vide infra). 

In severe and protracted cases of peritonitis the intestine is involved to a cer- 
tain extent. There is a collateral inflammatory oedema of its walls, causing some- 
times a considerable increase in thickness, while at the same time they may be 
non-resistant and easily torn. The weakness of the muscular layer of the intes- 
tine may amount to complete paralysis, and thus permit excessive intestinal tym- 
panites, either diffuse or local. 

Milder forms of general peritonitis with sero-fibrinous, or chiefly serous, exu- 
dation are relatively infrequent. Under this head would come certain apparently 
primary and usually chronic cases with favorable issue, and also the peritonitis 
which sometimes occurs as a sequel of an ascites, which has existed for some time 
before (see next chapter). Those rare cases in which a peritonitis arising in the 
course of acute rheumatism has ended in recovery, also probably produce a sero- 
fibrinous exudation. 

We have spoken thus far of diffuse general peritonitis, but cases are not 
rarely seen of circumscribed or " encapsulated " peritonitis. Here also we have 
mild varieties with fibrinous exudations on the one hand, and on the other puru- 
lent inflammation. The milder inflammation is a result of the extension of the 
most varied forms of inflammation in neighboring organs. Thus, deep intestinal 
ulcers, for example, give rise to a mild circumscribed inflammation of the corre- 
sponding portion of the serous layer. A similar condition results from superficial 
splenic infarctions ; from various hepatic diseases, when they reach the surface 



ACUTE PERITONITIS. 



423 



of the liver ; and from numerous pathological conditions of the female genitals. 
In many of these cases the peritonitis takes a chronic course and leads to adhe- 
sions, and hence is called adhesive peritonitis. 

Circumscribed purulent peritonitis has precisely the same aetiology as the 
general form, with this single difference, that firm adhesions are quickly formed 
around the spot whence the inflammation proceeds, limiting it and preventing it 
from involving the entire peritoneum. It occurs most frequently as a purulent 
perityphlitis (q. v.) consequent upon perforation of the vermiform appendix ; and 
also as pelvic peritonitis, which is a possible sequel of most of the forms of puer- 
peral inflammation to which the uterus and its appendages are liable. It may 
also follow perforative gastric or intestinal ulcer, hepatic abscess with perforation, 
and analogous affections. So-called sub-diaphragmatic abscess is a form of encap- 
sulated purulent peritonitis. 

Histologically considered, acute peritonitis is perfectly analogous to the 
inflammatory processes which attack other serous membranes. The endo- 
thelium becomes degenerated, and, for the most part, is cast off. There is an 
exudation from the blood-vessels of a fibrinous fluid, which is partly coagulable, 
and with this exudation round cells escape in greater or less abundance. In the 
further progress of the disease there is an inflammatory new growth of vascular 
connective tissue, to which it is probable that the escaping cells mainly con- 
tribute ; but it also seems likely that new blood-vessels are formed by a budding 
of the capillaries in the serous membrane. Thus arise the adhesions of connect- 
ive tissue and the false membranes found in chronic cases between the different 
coils of intestine. They lead in process of time to marked thickening and retrac- 
tion of the omentum and mesentery. Most cases of purulent peritonitis prove 
fatal in the early acute stage. If a case recovers, the exudation undergoes fatty 
degeneration, and its cellular constituents are thus disintegrated and then are 
absorbed. 

The results of circumscribed purulent peritonitis are detailed in connection 
with the clinical history. 

Clinical History. 1. Acute General Peritonitis. — The following description 
applies chiefly to the severe purulent form, the one by far most frequently met with. 
It occurs in most instances after perforation, in puerperal cases, and after external 
injuries, like operations. In most of these cases the peritonitis is a secondary 
disease, so that it must obviously be greatly modified in its general characteristics 
and behavior by the original trouble. In the first place, the onset is modified. 
Many cases of peritonitis due to perforation begin abruptly, the patient having 
been previously in perfect health. Thus, as already mentioned, the first indica- 
tion of a gastric or duodenal ulcer may be given by perforation. Most cases of 
perforation of the vermiform appendix present equally sudden and unexpected 
symptoms. 

There are many other cases where the symptoms of peritonitis supervene upon 
those of some grave disease already existing. For example, typhoid fever, 
intestinal tuberculosis or intestinal stenosis, may, by causing perforation, excite 
a peritonitis. Here the symptoms of this secondary disease may be more or less 
completely veiled by the other grave local and constitutional disturbances. 

Again, an acute general peritonitis may, as we have already said, be the sequel 
to a local and circumscribed inflammation of the peritoneum. Thus, a purulent 
perityphlitis, or a purulent puerperal pelvic peritonitis, may finally become uni- 
versal. In such unfortunate cases the change in symptoms is often gradual, and 
is not clearly pronounced. 

We have now indicated certain variations from the general course of the dis- 
ease ; but, with these exceptions, almost every case of acute general peritonitis, 



4:24: 



DISEASES OF THE DIGESTIVE ORGANS. 



whatever its aetiology, presents clinical symptoms which are so characteristic and 
typical that a general description of the disease will be both easy and advanta- 
geous. 

The symptoms of acute peritonitis form two groups, the local and the constitu- 
tional. The latter are the result of the local disturbance acting upon the gen- 
eral condition of the patient. 

Of the local symptoms, pain deserves to be named first. It is usually the 
earliest symptom ; and, as the disease progresses, it is generally the excruciating 
abdominal pain which attracts most attention. The localization of the pain in 
the beginning of the illness may be of diagnostic value in doubtful cases, if such 
as to indicate the possible starting-point of the inflammation, for example, the 
vermiform appendix or a gastric ulcer. Later the pain extends over the whole 
abdomen. As a rule, there are brief remissions followed by fresh exacerbations. 
The pain is aggravated by voluntary movements, by deep inspirations, and prob- 
ably by intestinal peristalsis. The abdominal tenderness is often extreme in 
peritonitis, and is very characteristic. The gentlest palpation is torture, and often 
the slightest pressure of the bed-clothes is almost unbearable. Frequently the 
greatest tenderness is in the umbilical region. 

Acute peritonitis seldom exists without pain. The exceptions to this rule are 
chiefly seen in patients who are extremely prostrated, and whose sensibility and 
intelligence are much impaired. Here the peritonitis itself may escape notice. 

Physical examination of the abdomen greatly aids the diagnosis in many ways. 

As a rule, the abdomen is distended. This is an early symptom, and gradually 
becomes more and more pronounced. It is due mainly to the intestinal tympa- 
nites, which we have already mentioned, and which sometimes becomes very 
great if the muscular fibers of the intestine are paralyzed. In the later stages the 
liquid effusion into the peritoneal cavity of course contributes to the prominence 
of the abdomen, but even then the distention is seldom as uniform or as broad as 
in ascites. In peritonitis, coils of distended intestine can often be recognized by 
their characteristic contour through the abdominal wall. In general, if the 
abdominal wall is yielding and thin, the peritonitic distention will be greater, so 
that it is most marked in puerperal cases, where the preceding pregnancy has ren- 
dered the walls lax. In a person with powerful muscles and tense abdominal 
walls the convexity of the abdomen is seldom great. In some cases there is no 
convexity whatever. The walls may be as hard as a board, and the abdomen flat 
or slightly concave. In such cases diagnosis may be difficult. 

Percussion over the distended intestinal coils yields a resonant and usually 
tympanitic sound. It is not till a considerable amount of liquid effusion has col- 
lected that there is dullness, most marked in the dependent portions of the 
abdomen. If there is much tympanites, however, quite a large effusion may exist 
without being detected on percussion. Usually there is too much pain to permit 
a careful examination of the change of dullness consequent upon change of decu- 
bitus. In general, the numerous adhesions between the separate coils of intestine 
not infrequently interfere with the free motion of the peritonitic exudations. 

Percussion not only gives information about purulent effusion, but is also of 
value in determining the level of the diaphragm, as affected by abnormal abdomi- 
nal distention. The upper limit of hepatic dullness is raised to the fifth or even 
the fourth rib. The heart is also pushed up. There is tympanitic resonance above 
the margin of the ribs on the right side. The area of hepatic dullness is not only 
displaced upward, but is also evidently diminished. This is due in part to coils 
of distended intestine overlapping the anterior edge of the liver, and in part to 
the organ being tilted upward in such a way that its area of contact with the 
anterior wall of the body is less than normal. Various authors formerly laid 



ACUTE PEEITONITIS. 



425 



great stress upon the total disappearance of hepatic dullness, regarding it as a sure 
sign that gas has escaped from the intestine into the abdominal cavity. The infer- 
ence is not always correct. The liver may be displaced backward by coils of 
intestine, and hepatic dullness be thus abolished, although there is no air free in 
the peritoneal cavity. 

If there is a considerable effusion, it is possible, as in ascites (q. v.), to get a 
sensation of fluctuation by gentle, quick palpation. 

As a rule, auscultation of the abdomen does not throw much light on a case 
of peritonitis. In the distended coils of intestine we not infrequently hear all 
sorts of gurgling and splashing sounds. Sometimes we hear a peritonitic friction- 
sound, coincident with the movements of respiration and due to the rubbing 
against each other of two rough surfaces under the impulse of the diaphragm. 

In almost every severe case of peritonitis there are gastro-intestinal symptoms. 

As to the stomach, vomiting is the most frequent and important symptom. 
Vomiting is often seen early in the disease, and recurs frequently as the illness 
progresses. It sometimes is spontaneous, and sometimes follows the ingestion of 
food. If spontaneous, the vomitus consists of watery mucus, usually of a green- 
ish tinge. Why vomiting is so prominent in peritonitis we do not know abso- 
lutely. Apparently it is in part a reflex action, excited by the inflammation of 
the serous membrane. Possibly the external pressure of the exudation also affects 
the stomach. The vomiting usually is accompanied by frequent eructations. 

Of the intestinal symptoms, the reader has already become acquainted with the 
tympanites and also with the fact that it is due mainly to a paresis of the mus- 
cular fibers of the intestine. This same muscular weakness furnishes an obvious 
reason for the persistent constipation usually observed in peritonitis ; but we may 
have diarrhoea instead, from increased peristalsis and secondary intestinal catarrh. 

The pushing up of the diaphragm has a noteworthy effect upon the thoracic 
organs. The lower lobes of the lungs are compressed, so that considerable dyspnoea 
results. The heart is likewise crowded upward, so that the apex-beat is usually to 
be felt in the fourth intercostal space. 

Every case of acute peritonitis that is at all extensive has marked constitutional 
effects. These are in part the result of the wakefulness due to pain, and the rest- 
lessness and fever. But in all probability there are also decided reflex inhibitory 
influences, originating in the irritation of the peritoneal nerves and affecting 
chiefly the heart, just as Goltz in his well-known experiment killed a frog by 
blows upon the abdomen. There is no other disease, except internal strangulated 
hernia — and the effect of that is perfectly analogous — which produces general col- 
lapse so quickly as does peritonitis. The countenance is rapidly altered, the cheeks 
fall in, and the eyes become hollow. The nose grows sharp and cool, the lips dry 
and cyanotic. The skin of the extremities is also cool and bluish, as a result of 
impaired circulation. The patient is extremely feeble. The chief cause of all 
these symptoms is the excessive weakness of the heart. The peritonitis has hardly 
begun before we find the pulse small and soft. In many severe cases the pulse 
finally becomes almost imperceptible. At the same time the pulse-rate increases, 
as is usual in collapse from any cause, so that 120 to 140 beats per minute is not 
an exceptional rapidity. 

The temperature varies greatly in different cases. It may be high in the 
rectum, although the skin feels cool. Still, very high fever is not usual ; and 
there are often considerable remissions. We even frequently observe the subnor- 
mal temperature of collapse. The number of respirations per minute is usually 
30 to 40. This increased rate is due not only to the compression of the lower 
lobes of the lungs, but also to the pain caused by full inspirations and to the 
impeded circulation. 



426 



DISEASES OF THE DIGESTIVE ORGANS. 



The intellect remains in most cases almost unimpaired to the end. There may 
exceptionally be mild delirium, or an approach to stupor, toward the close. 

The course of acute general peritonitis in the great majority of cases is unfa- 
vorable. With the appearance of the grave symptoms just depicted, the prognosis 
becomes almost hopeless. The course of the disease is also comparatively rapid. 
Marked variations in the intensity of the symptoms are infrequent. The grave 
local and constitutional symptoms persist, and as a rule the patient dies at the end of a 
few (two to six) days. Still, it is not well to make general dogmatic statements as to 
the clinical history, for the aetiology of each individual case impresses upon it indi- 
vidual characteristics. A peritonitis resulting from gastric or intestinal perforation 
is usually quickly fatal. The same is true of almost all cases of puerperal septic 
peritonitis. In a few cases, however, the inflammation is limited, by the encapsu- 
lation of the exudation. These may finally end in recovery through perforation 
of the abdominal walls or perforation into the intestinal canal. Now and then 
an acute general peritonitis may assume a chronic form. The effusion is mostly 
reabsorbed, and the newly-formed adhesions and false membranes contract into 
firm bands of connective tissue. The liver, spleen, and other abdominal viscera 
acquire a tough coating of connective tissue. The omentum and mesentery are 
shortened and thickened. Indeed, the omentum may roll itself almost completely 
up. Although the clinical symptoms become less severe, weakness usually per- 
sists, with gradual exhaustion and death. Often the intestine is so bent or pinched 
as to give rise to grave symptoms from stenosis. 

Recovery from acute general peritonitis is very rare. If seen, it is usually in 
mild cases, such as sometimes occur after menstruation, abortion, or labor. Peri- 
tonitis as a complication of acute articular rheumatism is a very rare event. Its 
termination is generally favorable. In all cases of this kind the inflammation is 
probably not purulent, but sero-fibrinous. 

2. Acute Circumscribed Peritonitis. — The local symptoms of this are essen- 
tially the same as we have just ascribed to the general form ; except that, a 
smaller extent of tissue being involved, they are correspondingly limited. The 
pain and tenderness are confined mainly to one region, but its boundaries are never 
sharply defined. On palpation of this region, we find an increased resistance 
which is sometimes almost like that produced by a tumor. If there is an encap- 
sulated effusion, we may detect fluctuation, particularly if the abscess is going to 
point outward. On percussion over the affected spot, there is either dullness or a 
muffled tympanitic resonance. 

The constitutional symptoms are likewise those of general peritonitis, only usu- 
ally less severe. Reflex vomiting does occur, but is seldom so persistent as in the 
diffuse inflammation. The physical weakness and symptoms of collapse are 
decided, but do not usually become extreme. There is generally an irregular 
fever, which may now and then assume an intermittent,, pysemic character. 
Most cases run a chronic course. If the illness be very much prolonged, death 
may finally ensue from general debility. Recovery is possible if the pus can be 
let out. This may be accomplished either by the surgeon or by Nature. Spontane- 
ous discharge of the abscess may take place through the abdominal walls, into the 
intestine, or even in rare instances through the pleura into the lungs. But if the 
pus finds its way into the general peritoneal cavity, the peritonitis becomes diffuse 
and causes death. 

To describe in detail each separate variety of circumscribed peritonitis would 
occupy too much space, and would also lead to useless repetitions. We have 
already spoken at some length of one especially important form — namely, peri- 
typhlitis. Perimetritis and pelvic peritonitis are chiefly puerperal affections, and 
are fully discussed by writers on gynaecology. 



ACUTE PERITONITIS. 



427 



Abscesses which are very deeply situated — as, for instance, behind the stomach 
or in front of the spinal column — may prove very difficult to diagnosticate, being 
so far out of reach. Sub-diaphragmatic abscesses containing air deserve a brief 
mention. They are sometimes observed as a result of perforation of the stomach 
or transverse colon. Lying between the liver and the diaphragm, they crowd the 
latter upward, and are liable to be mistaken for pyo-pneumothorax. Finally, there 
is a rare form of circumscribed purulent peritonitis to be noted, to which children 
seem especially exposed. It declares its presence by a painful fluctuating tumor 
above the left groin, which usually points into the rectum and ends in recovery. 

Diagnosis. — The diagnosis of peritonitis is in many cases an easy matter, when 
we have the characteristic symptoms of tenderness and tympanites, vomiting, and 
collapse. Often the starting-point of the inflammation is equally obvious, in 
cases of secondary peritonitis supervening upon some disease which we have 
already recognized with certainty, such as typhoid fever, gastric ulcer, or puer- 
peral diseases. But where the peritonitis is apparently primary we must inquire 
carefully into the previous history and the earliest symptoms of the attack in 
order to form even a surmise as to aetiology. 

The diagnosis is sometimes greatly obscured by the fact that under certain cir- 
cumstances very similar symptoms may be excited by other disorders affecting 
the intestines. Thus, in typhoid fever there may be great tympanites and grave 
constitutional symptoms, with abdominal pain, so that peritonitis may be diagnos- 
ticated, while the autopsy, if there be one, discloses no signs of it. Deep ulcers of 
the intestine, however produced, may give rise to so great abdominal tenderness 
as likewise to simulate peritonitis. The grave symptoms of acute intestinal 
obstruction are often of such a character that it is impossible to determine whether 
the intestinal disorder has already induced a peritonitis or not. On the other 
hand, we have already mentioned that peritonitis attended by stupor and general 
depression may hide itself from the keenest eye, because the abdominal distention, 
tenderness, and other chief symptoms are absent. 

It is not always easy to diagnosticate circumscribed peritonitis, even where the 
trouble is not deep-seated and therefore inaccessible. It is not infrequently mis- 
taken for a new growth ; and prolonged observation is often necessary before we 
can be certain of our diagnosis. Caution should be exercised in satisfying our 
diagnostic curiosity by the use of the aspirating needle. 

It is well to remember that a pregnant uterus and a distended and therefore 
painful bladder have each repeatedly been mistaken for peritonitis ! 

Treatment. — Although severe cases are generally almost hopeless, yet we must 
try to meet the symptomatic indications, and must do all in our power to promote 
a limitation of the process, if it be still possible. 

External counter-irritants or " revulsants " are seldom of much use. Painting 
with tincture of iodine and mercurial inunctions seem so utterly purposeless that 
they may be discarded. The local abstraction of blood can not be employed in an 
extensive peritonitis with constitutional prostration. It is only in a circumscribed 
peritonitis which is very painful, and where the general condition of the patient 
remains comparatively favorable, that local bleeding is to be considered. Under 
these circumstances, the application of eight to fifteen leeches sometimes causes 
decided abatement of the pain. The local application of ice to the abdomen is 
universally in vogue. It usually moderates the pain, and it may also have a 
beneficial influence in quieting peristalsis. Still, some patients can not bear ice, 
and sometimes hot cloths and poultices give great relief. 

Of all internal remedies, there is but one of great value — namely, opium. This 
in large doses (a grain [grm. 0'05] of extract of opium every hour) almost always 
proves beneficial. It moderates both the pain and the vomiting or eructations ; 



428 



DISEASES OF THE DIGESTIVE OKGANS. 



and, by diminishing the peristaltic movements of the intestine, opium further con- 
tributes to assuage the pain and possibly to limit the spread of the inflammation. 
Experience shows that almost all patients bear even very large doses of opium 
remarkably well in peritonitis. Perhaps this is because the drug is only slowly 
absorbed. To substitute injections of morphine for the opium is to be recom- 
mended only in cases where we wish to produce narcosis as rapidly as possible, or 
where the vomiting does not prove amenable to the ordinary treatment. 

Sometimes particular symptoms demand special attention. For vomiting we 
may employ, beside opium, bits of ice, or small quantities of " sherbet." If tym- 
panites is excessive, we may try to remove some of the gas through a rectal tube 
passed as high up as possible. Many physicians also puncture the distended intes- 
tinal coils with a fine trocar. Collapse and cardiac failure require the exhibition 
of stimulants, such as champagne or other alcoholic liquors, or doses of ether or 
camphor given subcutaneously. It is generally very difficult to nourish the 
patient. As a rule, small quantities of ice-cold milk are the best of anything, as 
food. 

The treatment cf circumscribed peritonitis should conform in general to the 
above indications. In suitable cases operative interference may be of great value ; 
but upon this point we refer to works on surgery. 

[The author does not seem to be acquainted with the opium treatment intro- 
duced by Prof. Alonzo Clark, and employed by him and others with the greatest 
success. This treatment is based upon the principle that an acutely inflamed part 
requires rest, and consists, first, in the alimentation of the patient by such articles 
as are digested and absorbed by the stomach; and, second, the administration of 
opium in some form — whatever form is selected should not be changed thereafter 
without cogent reasons for so doing — up to the point of almost narcotizing the 
patient. The respiration should be reduced to twelve per minute, and alarm need 
not be felt if it fall still lower. The amount required varies much in different cases. 
More than thirty grains of sulphate of morphine per diem has been given by Clark 
with the best results. His plan is to begin with a moderate dose of opium (grs. 
2-3), or its equivalent in morphine, and note the effect after two doses; if then 
opium symptoms are present, the dose is to be repeated ; if they are absent, the 
dose is to be increased by one grain, and so on at intervals of two hours until the 
tolerance of the patient is ascertained. The duration of the treatment may be only 
two or three days ; it may be two or three weeks. No other treatment is needed ; 
the bowels can safely be left ten days or a fortnight, and should not then be urged 
more strongly than by an enema. 

Under this management peritonitis has become a tractable disease, instead of 
one of the most dreaded. Puerperal peritonitis is to be combated on precisely the 
same principles. 

The reader is referred to Prof. Clark's masterly contribution to Pepper's " Sys- 
tem of Medicine," vol. ii, p. 1132. 

It is probable that the future has much in store for us in the surgical treatment 
of acute diffuse peritonitis, especially that form caused by perforation of the stom- 
ach or intestine and the like. Eeported cases are not yet numerous, but a reason- 
ing from analogy seems perfectly justifiable.] 



CHRONIC PERITONITIS. TUBERCULAR PERITONITIS. 429 



CHAPTER II. 

CHRONIC PERITONITIS. TUBERCULAR PERITONITIS. 

JEtiology. — Chronic peritonitis, not tubercular, is a rather rare disease. It is 
found most frequently in post-mortem examinations of patients who have had for 
a long while ascites due to venous stasis — for example, in chronic cardiac or 
hepatic cases. The chronic peritonitis, however, is not, as a rule, the direct result 
of the passive hyperemia in such cases, but is, as already hinted, due to the punc- 
turing- of the abdomen during life for the removal of the ascitic fluid. Exception- 
ally, a chronic peritonitis occurs as a sequel to some severe intestinal disorder, such 
as ulceration. Thus, chronic peritonitis is sometimes observed to follow typhoid 
fever. 

Chronic peritonitis may furthermore be the result of an acute peritonitis. The 
latter seldom terminates in this way, but still it may, when rather mild and not 
quickly fatal. The encapsulated exudations of peritonitis usually persist a long 
while, as was implied in the preceding chapter. 

In a few instances we can find no satisfactory cause for chronic peritonitis. It 
is sometimes ascribed to an injury. Alcoholic excesses are also said to predispose 
to the disease. Many of the apparently spontaneous cases, however, finally turn 
out to be tubercular. 

The tubercular is the most frequent form of chronic peritonitis. It is often 
merely a part of the tuberculosis of serous membranes in general {vide pages 244, 
304), of which mention has been already repeatedly made. In these cases it is usu- 
ally due to a conveyance of the process from the pleura through the diaphragm. 
Another way in which tubercular peritonitis may arise is by infection from neigh- 
boring tubercular organs. Tubercular intestinal ulcers are among the chief 
causes of this kind, the ulcer extending to the peritoneum ; or the peritonitis may 
be excited by tubercular retroperitoneal or mesenteric lymph-glands. In women 
a tubercular peritonitis may be developed in consequence of tuberculosis of the 
genital organs. A tuberculosis of the uterus sometimes affects the Fallopian tubes 
by direct extension, and thence the virus enters the abdominal cavity and excites 
its specific inflammation. In conclusion, we have to mention that, in general mili- 
ary tuberculosis, the peritoneum also may be the seat of numerous tubercles, 
although these do not as a rule give rise to important symptoms. 

Pathology. — After well-marked cases of chronic peritonitis, the peritoneum is 
usually found to be considerably thickened. The intestinal coils are joined to 
one another and to the neighboring organs by numerous and extensive adhesions. 
It is often a hard matter to disentangle the confused mass into which the intes- 
tines have been rolled. Sometimes the liver and spleen are covered by firm, 
tough capsules. The omentum and mesentery are much shrunken ; hence the 
name peritonitis deformans. The mesentery may indeed be transformed into a 
single thick cord. As a rule, there is little liquid effusion, and perhaps none. In 
simple chronic peritonitis, such fluid as may be present is usually a cloudy serum, 
pus being seldom seen. 

The milder forms of simple chronic peritonitis occur oftenest, as we have 
said, in cases of ascites due to venous stasis, after repeated tappings. It is fre- 
quently possible to detect the points where the trocar has pierced the internal layer 
of the abdominal wall, by adhesions, minute haemorrhages, or other lesions. The 
false membranes which exist in these cases are often very numerous, but they are 
usually not dense and are easily separable. The serous liquid found in the abdomi- 
nal cavity is partly a transudation, but contains clumps of fibrine in more or less 



430 



DISEASES OF THE DIGESTIVE ORGANS. 



abundance. In rare instances a peculiar form of chronic peritonitis has been 
observed as a sequel to punctures for ascites, called by Friedreich " chronic 
haemorrhagic peritonitis with haematoma." In it almost the entire peritoneum is 
covered by a newly formed membrane permeated with large ecchymoses. 

Tubercular disease of the peritoneum may be divided into two forms : tuber- 
culosis of the peritoneum, which may be acute or chronic ; and tubercular peri- 
tonitis, which is usually chronic. In tuberculosis the peritoneum is covered 
with numerous tubercular nodules, varying in size from a millet-seed up to 
a pea ; but there is not much coincident inflammatory change. In genuine 
tubercular peritonitis, on the other hand, the inflammatory changes above 
described are well marked, while sometimes it requires a microscopic examination 
to demonstrate the tubercular nature of the inflammation, by the detection of 
tubercles and cheesy degeneration in the newly formed tissue. Tubercular peri- 
tonitis is usually rather chronic, so that the adhesions are numerous and strong. 
The amount of liquid effusion varies, being sometimes considerable and some- 
times scanty. Just as in tubercular pleurisy, it is not rare for the exudation to be 
bloody. Tubercular peritonitis is quite often accompanied by hepatic cirrhosis 
(q. v.). _ 

Clinical History — Diagnosis. — If an acute peritonitis becomes chronic, the 
violent symptoms gradually abate, while another group of symptoms takes their 
place. In other cases the chronic disease develops gradually and insidiously. 

The sensitiveness of the abdomen is never so extreme as in the acute inflamma- 
tion. Sometimes, to be sure, the patient complains of dull pains and a sense of 
abdominal oppression, but quite often the pain is either constantly or at times 
insignificant. On physical examination, we usually find moderate distention of 
the abdomen. Frequently this is not perfectly uniform, certain coils of intestine 
being especially prominent. Occasionally there is no abdominal distention what- 
ever, the belly is flat or concave, and the walls are tense and unyielding. 

In many instances palpation furnishes very characteristic signs ; for sometimes 
the thickening of the omentum and the numerous fibrous inter-intestinal bands 
above described can be felt through the abdominal walls as peculiarly resistant 
masses or uneven prominences. Indeed, if the omentum is rolled up, it may 
closely simulate a new growth. Not infrequently, particularly in tubercular peri- 
tonitis, the liver is enlarged so that its lower edge can be felt. But in other cases 
of chronic peritonitis there are no changes discoverable by palpation ; or they may 
be concealed by an effusion or by the tenseness of the abdominal walls. A large 
exudation can be demonstrated by the great distention, or by its causing fluctua- 
tion, or by the signs yielded on percussion. In general, uncomplicated cases do 
not give rise to great accumulations of fluid. Such accumulations are almost 
invariably present when tubercular peritonitis and cirrhosis of the liver are com- 
bined ; and here there are usually also passive congestion and enlargement of the 
spleen. It has been already stated that the distortions and flexions which the 
intestines may undergo in chronic peritonitis may result in obstruction. In the 
same way the duodenum or the ductus choledochus may be so occluded as to 
occasion persistent jaundice. 

The objective signs of both the simple and tubercular forms of chronic peri- 
tonitis have been embraced in one description, because the abdominal signs of the 
two are identical. To differentiate between them, other factors must be considered. 
We regard the patient's constitution and general appearance, and inquire into his 
family history, or discover if there are other serological factors, such as previous 
tubercular disease. A careful thoracic examination is extremely important. If 
we find the signs of coincident pulmonary tuberculosis, and particularly of pleurisy, 
then it is almost indubitable that the peritonitis is tubercular. The character of 



CHRONIC PERITONITIS. TUBERCULAR PERITONITIS. 431 



the exudation is also of some importance, for if hemorrhagic, as already stated, 
the peritonitis is probably tubercular. Whether tubercle bacilli may be present 
in the exudation has not yet been determined, as far as we are aware. 

To diagnosticate simple tuberculosis of the peritoneum, when not attended by 
marked inflammatory changes, is generally a difficult matter. Often it is abso- 
lutely impossible. Frequently there is no abdominal pain or tenderness whatever. 
The abdomen is usually but moderately distended, as a result of the effusion 
present. 

Particular notice should be given to the chronic peritonitis of children. The 
occurrence of ascites in children, between the ages of two and ten years, has 
been observed repeatedly, both by other authors and by ourselves. The ascites, 
which may be quite considerable, can not be traced to any cause, and after a 
few months completely disappears. The child, during this time, is usually 
rather pale and languid, but not much emaciated, nor does he suffer great local 
discomfort. Since the cases recover, their pathological anatomy remains obscure. 
Probably they are a mild form of simple chronic peritonitis. 

In children tubercular peritonitis plays an important part in general tubercu- 
losis of the abdominal organs, a condition known as tabes mesenterica. In these 
cases the tuberculosis probably originates, as we have already said, in the intes- 
tine, so that usually we find the intestine, peritoneum, liver, and abdominal lymph- 
glands all simultaneously involved. The clinical symptoms are often mainly due 
to the peritonitis. The abdomen is distended and painful, and there is an effusion. 
Often there is also obstinate diarrhoea, as a result of tubercular intestinal ulcers, 
with persistent fever of an intermittent character, emaciation, and ansemia. The 
tubercular process may eventually involve the lungs, pleura, meninges, and other 
organs, or it may never extend beyond the abdomen. 

As to the course of chronic peritonitis we have little to say. The simple 
chronic peritonitis may terminate in recovery, although, on account of other 
co-existing lesions, this event is rare, except in the special form which children 
present. Most cases of tubercular peritonitis prove fatal in a few months or 
weeks. In some instances, however, chronic tubercular peritonitis has a favorable 
issue, or at least there is very great abatement of all symptoms. This is particu- 
larly apt to be the case in what is called primary tuberculosis of the serous mem- 
branes in general {vide supra). If, in this disease, there is no simultaneous 
tuberculosis of the lungs, intestines, or other organs, then the final reabsorption 
of the exudation is possible, just as in tubercular pleurisy. It must be confessed 
that often the recovery is not permanent, for the tubercles may appear later, in 
some other part of the body. 

Treatment. — The means by which we can exercise a favorable influence upon 
the course of chronic peritonitis are scanty. Attention to nourishment and 
hygienic surroundings are very important ; but, beyond this, treatment is mainly 
symptomatic. The chief local applications are poultices or fomentations, perse- 
veringly employed. There is seldom such persistent and severe pain as to demand 
opiates, but they may be required for the diarrhoea which is liable to occur. Or, 
on the other hand, enemata and mild laxatives may be indicated. Among special 
remedies, the preparations of iodine should be mentioned ; iodide of potassium 
and syrup of the iodide of iron sometimes are of apparent benefit. Arsenic may 
also be tried. Iron and syrup of the iodide of iron are also employed in the 
chronic peritonitis of children. 



432 



DISEASES OF THE DIGESTIVE ORGANS. 



CHAPTER III. 

ASCITES. 

(Hydroperitoneum.) 

The name ascites is given to a collection of transuded serum in the abdominal 
cavity, due to venous stasis. The peritoneal veins belong to the portal system, so 
that among the diseases which lead to ascites those which impede the portal cir- 
culation are chief. As we shall see in the next section, ascites is, therefore, of fre- 
quent occurrence in cirrhosis of the liver, syphilitic disease of the liver, compres- 
sion of the portal vein by tumors, thrombosis of the portal vein, and similar 
disorders. Ascites is also frequently present as one of the dropsical symptoms in 
general circulatory disturbances, such as cardiac disease or pulmonary emphysema, 
and in the various acute and chronic renal affections. 

The clinical significance of ascites is due partly to the local discomfort occa- 
sioned by the presence of any considerable amount of fluid within the abdominal 
cavity. Small quantities of serum are often unnoticed by the patient ; but, where 
many quarts (fifteen to twenty, or even more) of transudation exist, the abdomi- 
nal walls become greatly distended, and the patient has a very troublesome feeling 
of pressure, weight, and tension. What is of still greater importance is the crowd- 
ing upward of the diaphragm. Respiration is thereby not a little impeded. If 
the ascites is great, the lower lobes of the lungs are so compressed that a consider- 
able degree of atelectasis is produced. 

To demonstrate ascites by physical examination is possible only when a con- 
siderable accumulation exists. Then the belly is prominent, its walls are tense 
and shining, and, the base of the thorax being gradually distended by the pressure 
of the liquid, the lower part of the thorax seems much broader than the upper. 
Distended veins are usually visible through the skin of the abdomen, like blue 
lines, here and there. As soon as the abdominal tension has attained a certain 
degree, fluctuation can be perceived, by laying both hands upon the abdomen and 
imparting gentle but quick impulses to the fluid through the walls. Percussion 
gives a dull sound everywhere that the fluid is in contact with the abdominal 
walls. Gravity, of course, leads the liquid to occupy the dependent parts. In the 
dorsal decubitus, and when the transudation is of medium amount, the dullness is 
bounded in the central and upper parts of the abdomen from a region of tympani- 
tic resonance by a line concave toward the head of the patient. The surface of 
the liquid being horizontal, of course the dullness reaches nearer to the thorax 
along the sides of the abdomen than in the central line. We would add, that 
where the layer of ascitic fluid is thin we can obtain dullness only by light, super- 
ficial percussion. If the pleximeter or finger is pressed deeply in, the fluid is 
crowded to one side, and we get a tympanitic sound from the underlying coils of 
intestine. A factor of great diagnostic value is the change of dullness on change 
of position of the patient. If he lies upon one side, the fluid seeks the dependent 
portions of the cavity, and gives rise to extensive dullness there, while the oppo- 
site side now yields a tympanitic resonance. Or, if he changes to the other side, 
it in turn becomes dull, and the side previously dull becomes tympanitic. Similar 
differences are found between the results of percussion in a horizontal and in a 
sitting posture. It is only when the accumulation is very abundant that there is 
dullness over the entire abdomen. 

The signs mentioned enable us in most cases to make a diagnosis of ascites 



ASCITES. 



433 



with ease and certainty. It is, indeed, not always easy to distinguish a transuda- 
tion of serum from the exudation of chronic peritonitis, for, of course, either sort 
of fluid would yield the same physical signs. Only, the change in the area of 
dullness consequent upon a change of position is less pronounced in case of an 
exudation, because the peritonitic adhesions impede the movements of the fluid ; 
and we have, besides, all the other symptoms to guide us : there may be pain, 
or thickenings of the peritoneum discoverable on palpation, or signs of tuber- 
culosis ; or, on the other hand, there may be some cardiac or hepatic disease, 
which would render ascites probable. If the fluid is drawn off, its character will 
sometimes aid us in diagnosis. Ascites yields pure serum, containing almost no 
morphological constituents. Its specific gravity is usually less than that of a peri- 
tonitic exudation, because it contains less albumen. We may say that the specific 
gravity of the fluid found in peritonitis is generally above 1018, and that of ascites 
about 1012, or even lower. 

There may be equal difficulty in the exclusion of ovarian cysts, particularly 
since the cysts are sometimes so large as to fill the whole abdominal cavity. We 
must first map out accurately the dullness on percussion, and also see if it varies 
with changes of position. In cases of ovarian tumor, change of position does not 
make much difference. The resonance on percussion of the deepest and most 
dependent portions of the abdomen may be misleading, in this way, that even in 
ascites a narrow zone here may be tympanitic. This should be remembered. 
Thus, just above the symphysis, there is sometimes a tympanitic resonance in 
ascites which might readily be mistaken for a proof of the existence of an ovarian 
tumor. The explanation is that in the places indicated a coil of intestine with a 
short mesenteric attachment may remain in contact with the abdominal wall in 
spite of ascitic accumulations. Further aids in the differential diagnosis are to 
be obtained from the history of the case (place where the swelling began), from a 
consideration of possible causative diseases, and from a vaginal examination. In 
ascites the uterus is freely movable, while in case of ovarian tumors it is often 
bound down by adhesions. Further particulars may be sought in books on 
gynaecology. 

The treatment of ascites, of course, depends largely upon the disease of which 
it is a symptom. As to the symptomatic treatment of ascites itself, we will con- 
fine ourselves to a few words about tapping. This operation is indicated when 
the local disturbances caused by the ascites are great ; that is, if there is an unbear- 
able sensation of pressure and tension, and, above all, if the crowding up of the 
diaphragm causes much dyspnoea. The instrument to be used is a common trocar 
of medium size. Usually the patient is tapped lying on his side in bed, at the 
most dependent point in the lateral portion of the abdominal walls ; but it is also 
a good way to make the puncture in the median line, about half way between the 
umbilicus and the pubes, with the patient in a chair. The operation is easy, and 
almost free from danger. We may allow large amounts of liquid (five or ten 
quarts, or more) to flow slowly away at one tapping. Over the puncture we put 
a piece of sticking-plaster, or, if great caution is to be exercised, an antiseptic band- 
age. Often the fluid trickles out through the opening, because the abdominal 
walls have lost their elasticity on account of the persistent distention. We may 
then employ a " circumvoluted suture " to close it. After tapping, the laxness of 
the walls is favorable to palpation of the abdominal organs. 

Inasmuch as tapping does not remove the cause, there is in most cases a very 
rapid reaccumulation of fluid. Thus the system is deprived of much albumen 
and nutrition is impaired, so that not infrequently the operation is followed by 
decided loss of strength. Therefore, we should not tap in ascites, as a rule, unless 
the indications for the operation are urgent. 
28 



434 



DISEASES OF THE DIGESTIVE ORGANS. 



[Before puncture the precaution should always be observed to see that the 
bladder is empty. 

If, as is very frequently the case, the fluid continues to drain away through the 
puncture after the trocar is withdrawn, good rather than harm results, provided 
the danger of irritation of the skin and of bed-sores is kept in mind and guarded 
against, and an instrument of moderate size is used. 

Flint advocates early and repeated tappings if the fluid causes discomfort and 
does not yield to diuretics or cathartics. The pressure is removed in a measure 
from the abdominal and thoracic organs, and nutrition is thus promoted. The 
fluid is likely to return, but does not always do so, or may do so only slowly. He 
reports cases in which, after repeated removal, the fluid ceased to return and the 
patient remained apparently well. The result must depend, of course, chiefly on 
the underlying cause, which is sometimes very obscure. 

In cases of cirrhosis the same principles govern Flint's treatment.] 



CHAPTER IV. 
CANCER OF THE PERITONEUM. 

Carcinoma is the only new growth of any practical importance to which the 
peritoneum is liable. Primary endothelial cancer, analogous to the growth which 
attacks the pleura, is very rare. Cancerous growths here are usually secondary 
to cancer of the stomach, intestine, pancreas, liver, or some other organ. Often 
the secondary nodules are numerous and almost as small as peas, presenting what 
is called miliary carcinosis of the peritoneum. Separate nodules of larger size are 
less frequent. These may be found in the omentum, in Douglas's pouch, around 
the navel, or in other situations. Colloid cancer attains the most diffuse and exten- 
sive development of any variety. The retroperitoneal lymph-glands may also 
present at the same time large cancerous growths. Often the development of 
cancer in the peritoneum is attended with pronounced inflammatory disturbances 
— that is, we have a cancerous peritonitis. 

The symptoms of peritoneal cancer resemble in many points those of chronic 
tubercular peritonitis. Simple miliary carcinosis may be very insidious and give 
rise to no special symptoms, so that it often is unsuspected. In many cases a 
moderate amount of fluid collects in the abdomen, and this, if we are aware of the 
existence of a primary cancerous growth, may lead us to surmise a secondary peri- 
toneal carcinosis. The symptoms are much more pronounced if there is cancer- 
ous peritonitis. In that case there is usually very severe pain, marked abdominal 
distention, and constipation. We may sometimes feel the larger nodules in the 
omentum or upon the inner surface of the anterior wall of the abdomen, or even 
those in the lowest part of the abdomen, by palpation through the vagina. If the 
exuded fluid be drawn off, it is sometimes merely serous, but it may be haemor- 
rhagic. When the new growth has been diffuse, and particularly in case of colloid 
cancer, the exudation has repeatedly been found to present a milky opacity. 
Sometimes this fluid also has been tinged with blood. The opacity is due to fat, 
from fatty- degenerated and disintegrated cancer cells. Occasionally the micro- 
scope reveals characteristic cancerous elements in the fluid. 

The diagnosis can not be made with any positiveness unless, as a sequel to a 
primary cancerous growth already demonstrated, we observe the evident tokens 
of peritoneal disturbance, such as free fluid and pain. Other points are the 



CATARRHAL JAUNDICE. 



435 



patient's age, cancerous cachexia, and secondary glandular enlargements, particu- 
larly in the groins. 

Treatment must be confined to efforts at mitigation of the suffering. Warm 
applications, morphine, and supporting measures are chiefly employed. 



SECTION VII. 
Diseases of the Liver, Bile-ducts, and Portal Vein. 
CHAPTER I. 

CATARRHAL JAUNDICE. 

{Icterus catarrhalis. Gastro-duodenal Catarrh with Jaundice.) 

jEtiology. — When discussing intestinal catarrh, we mentioned that inflamma- 
tion of the duodenum may invade the secretory ducts of the liver, and, above all, 
the ductus choledochus communis. This complication would be of little clinical 
importance did it not in many instances prevent the flow of bile into the intes- 
tine. Such an obstruction at once gives pathological interest to a catarrh of the 
bile-ducts, because it entails a series of very important clinical symptoms. In this 
case the cause of the biliary stasis is purely mechanical, and any closure of the 
hepatic ducts, however produced, gives rise to identical symptoms, which vary, if 
at all, only in their duration and intensity. Catarrhal jaundice is, therefore, only 
one form, though the most frequent form, of what is called hepatogenous jaundice. 
Accordingly, we will in this chapter describe in detail the general phenomena 
common to all cases of hepatogenous jaundice, that we may avoid needless repeti- 
tions hereafter. 

The causes which may excite gastro-duodenal catarrh, and thus a catarrh of 
the common duct, are the same as have been enumerated under the aetiology of 
intestinal catarrh in general. In most cases it is some mechanical or chemical 
irritant contained in the ingesta which gives rise to the catarrh. We have 
already more than once pointed out that infectious agents are probably to be 
included under this head ; and in catarrhal jaundice some facts render this 
idea still more plausible. Experience has repeatedly shown that often, particu- 
larly in spring and autumn, this disease comes like an epidemic. The infectious 
nature of the jaundice is still more probable in those cases where the disease is 
decidedly endemic. In barracks, prisons, and some houses quite important 
endemics of jaundice have been seen, the only explanation for which could 
be found in assuming the existence of some local source of infection. 

Another cause is the rather frequent occurrence of duodenal catarrh as a result 
of passive congestion. This is seldom very intense. It is especially frequent in 
heart disease. Again, the slight jaundice quite often seen in the course of many 
acute diseases, and of lobar pneumonia in particular, must be ascribed to catarrh. 
Sometimes catching cold is said to produce jaundice. This is doubtful ; but it is 
impossible absolutely to deny that great emotional excitement, such as violent 
anger, may excite the disease. Pronounced gastric disturbances may certainly be 
thus produced, as shown by anorexia, vomiting, and cardialgia, so that such an 
aetiology for catarrhal jaundice does not seem very unlikely. 

Pathology.— As in catarrhal affections of most other mucous membranes, the 



436 



DISEASES OF THE DIGESTIVE ORGANS. 



post-mortem signs of catarrh of the bile-ducts are not always striking, for the 
swelling and injection subside considerably after death. The usual method of 
testing the patency of the common duct is by pressing upon the gall-bladder to 
see if its contents can be squeezed out into the intestinal canal. If a catarrh has 
closed the common duct, the bile is not discharged at once. A firmer pressure 
drives out from the opening of the duct a plug of tough, white mucus, upon which 
the bile follows ; but such a plug is not present in every case, by any means, for 
even a simple swelling of the catarrhal membrane suffices to obstruct the flow of 
bile. 

If the biliary passages are slit open, the common duct is found more or less 
filled with tough white mucus. Usually the portion which lies in the intestinal 
wall, the so-called intestinal portion, is most affected. Behind the occluded part 
the ducts are distended, if the biliary retention has been chronic. This distention 
may involve even the smallest ducts, which lie in the liver itself. As a conse- 
quence, the liver is somewhat enlarged and has a diffuse bilious tinge. If the 
obstruction persists for a long while, which is very exceptional in simple catarrhal 
jaundice, a portion of the hepatic cells are destroyed by the pernicious influence 
of the retained secretion. The lost parenchyma is replaced by new-formed con- 
nective tissue. For further particulars see the chapter on biliary cirrhosis. 

Clinical History. — Inasmuch as catarrh of the ductus communis is almost 
always consequent upon a gastro-duodenal catarrh, the first symptoms are usually 
referable to the latter disease. It is indeed seldom that the attack begins with 
marked gastric disturbances, like violent vomiting and gastralgia, but almost inva- 
riably the jaundice is preceded for a variable period by indisposition, as shown by 
malaise, languor, anorexia, a bad taste in the mouth, nausea, gastric oppression, 
eructations, and sometimes tenrporary vomiting. Then comes the first evidence 
that the catarrh has invaded the common duct, in a jaundiced hue of the skin and 
of the visible mucous membranes. 

The pressure in the secretory ducts of the liver is extremely low, so that even 
the catarrhal swelling of the mucous membrane and the collection of viscid mucus 
in the common duct suffice to impede in a marked degree the further outflow of 
bile into the intestinal canal. As a rule, however, the retention of bile is not com- 
plete, or, if so, only for a time. Still a considerable amount of bile collects, and 
distends even the intra-hepatic ducts. As soon as this stasis has reached a certain 
point, the stagnant bile is absorbed by the hepatic lymph- vessels. Thus the bile 
and all its constituents are poured into the blood by way of the thoracic duct and 
carried to all parts of the body. 

No more than a few days need elapse before the bile-pigments are absorbed 
into the tissues, and give rise to the evident yellow color of the skin and mucous 
passages which we call jaundice. Usually the yellowness of the conjunctiva is the 
first thing to attract attention. Later the entire skin becomes yellow, and the same 
color is plainly visible in the mucous membrane of the mouth and throat, espe- 
cially after we have produced temporary anaemia by pressure, as in the lips. Of 
course, the internal organs, which we can not see, are likewise stained. Any 
abnormal collection of liquid will also have a marked yellow color. The cornea, 
the peripheral nerves, and the cartilages alone escape unstained. In other parts 
we may not only find this diffuse impregnation with the biliary pigments, but 
even solid granules of the latter. 

A jaundiced patient often presents other indications of the presence of biliary 
coloring matter than the color of his skin. If the jaundice is at all chronic, there 
is almost invariably an itching of the skin, which may be very troublesome. It 
may be so bad at night as to disturb sleep. The scratching thus induced often 
causes numerous excoriations and fissures, which may even occasion quite large 



CATARRHAL JAUNDICE. 



437 



furuncles. Urticaria is also sometimes observed. A peculiar disease of the skin, 
which, has been chiefly described by English authors in connection with jaundice, 
is called xanthelasma. It presents bright-yellow spots, usually somewhat elevated, 
which are found mainly on the eyelids, though also on other parts of the body. 

The remaining symptoms of hepatogenous jaundice may be divided into two 
groups. The first group comprise the symptoms excited by the presence of the 
biliary constituents, and particularly of the biliary acids, in the blood, while the 
second group are due to the lack of bile in the intestinal canal. 

"We have seen that, when the biliary outlets are occluded or narrowed, the con- 
stituents of the bile are absorbed by the lymphatics. We have already learned in 
part what becomes of the bile-pigments thus conveyed into the blood-vessels. The 
presence of the bile-acids in the blood is also of considerable clinical importance. 
Physiology has shown that these acids possess certain poisonous properties, and, 
among others, the power to destroy red blood-corpuscles. But in reality few if 
any blood-corpuscles are destroyed by the bile-acids in the blood, because they are 
too much diluted, and, besides, seem in large part to be quickly decomposed after 
absorption. These acids do really, however, excite certain nervous centers in a 
way to give rise to decided clinical symptoms. The most frequent effect is that 
produced by the cholate of sodium upon the cardiac ganglia, or possibly also upon 
the center for the vagus, and it is evinced by a slowing of the pulse. This is an 
almost invariable phenomenon, provided there be no fever or other complication, 
and is seen, not only in simple catarrhal jaundice, but in all cases of hepatogenous 
icterus. The pulse-rate is from 64 to 50, or even less. Slight irregularity in 
the heart's action is not infrequent. There are certain other nervous disturb- 
ances often seen in jaundice and referable to the presence in the blood of biliary 
constituents, and in particular of biliary acids. Sometimes there is a striking lan- 
guor and muscular weakness, or headache, or the patient is " out of sorts.'* Grave 
nervous symptoms, sometimes seen in jaundice and grouped under the name of 
cholamiia, are discussed in another chapter. It also deserves a brief mention here 
that many cases with marked jaundice have a noticeable tendency to bleeding — 
that is, a sort of " hemorrhagic diathesis." Haemorrhages into the skin and in 
the viscera are quite often seen, and also epistaxis and analogous occurrences. 

We now come to the second group of symptoms, which result from lack of bile 
in the intestinal canal. It will be easy to understand these if we briefly review 
the physiological functions assigned to the bile which is poured into the aliment- 
ary canal. Bile plays an important part in the digestion of fat, emulsifying it, 
and promoting its absorption into the chyle-ducts. Now, in hepatogenous icterus 
this work remains undone, as is shown by the fatty stools. From time imme- 
morial the white clay-colored stools of jaundice have been well known, and are 
employed as the best measure of the completeness of biliary retention. The light 
color of the stools is partly due to the lack of biliary pigment, for it is that chiefly 
which imparts to normal faeces their dark-brown color; but the characteristic 
white clay color is due exclusively to the presence of undigested fat in large 
amounts. We have ourselves performed the experiment of putting a patient with 
extreme hepatogenous icterus upon a diet containing as little fat as possible, and 
have found that the stools then became light brown, and not at all like clay. 
Upon microscopic examination of the faeces in jaundice, sheaf -like aggregations 
of crystals are not infrequently observed. These were formerly supposed to be 
tyrosine, but Oesterlein has shown them to be in reality magnesia-soap. 

The retention of bile has some further effects beside retarding the digestion 
of fat. Bile possesses decided antiseptic properties, and thus, to a certain extent, 
protects the contents of the primae viae from putrefaction. In hepatogenous jaun- 
dice, therefore, the processes of decay are abnormally active ; the faeces are unusu- 



438 



DISEASES OF THE DIGESTIVE ORGANS. 



ally offensive, and there is an excessive generation of gas, often leading to flatu- 
lence and tympanites. The bile also undoubtedly stimulates peristalsis, and so in 
jaundice there is often constipation. 

One important function of the bile remains to be considered — namely, that by 
precipitating pepsine it terminates peptic digestive action. Kuhn has shown how 
necessary this is to the normal processes, because pepsine will destroy pancreatine 
and therefore interferes with pancreatic digestion. Hence we are justified in 
assuming that in well-marked jaundice the digestive action of the pancreatic juice 
on fat and albumen is probably disturbed, even though the pancreas itself secretes 
normally. Often, and in catarrhal jaundice probably as a rule, the pancreatic 
duct is obstructed as well as the biliary, so that not only the bile, but also the 
pancreatic juice is retained. Just how far the digestive disturbances are to be 
ascribed to the lack of each of these secretions we are of course unable to 
determine. 

We must now inquire what becomes of the absorbed bile. As to the biliary 
acids, we have already said that they probably undergo decomposition. Of the 
other constituents, including the taurine and cholesterine and the pigmentary 
matters, we know the fate of the last-named only — that is, we have learned how 
Nature seeks to rid herself of this foreign substance. As soon as the amount of 
bile-pigment in the blood and tissues becomes considerable, excretory efforts are 
made, in which the kidneys take the chief share. Certain changes take place in 
the urine almost simultaneously with the first appearance of a jaundiced hue in 
the skin ; and these changes are due to the urine containing excreted biliary color- 
ing matter. 

The urine of jaundice is generally recognizable from its color, which is a dark 
brown, like beer. The foam caused by shaking it is not white, but distinctly 
yellow. A bit of white filter-paper dipped in the urine is stained yellow. If the 
urine is mixed with chloroform in a test-tube, the chloroform dissolves the pig- 
ment, and, on being allowed to collect at the bottom of the tube, displays a deep- 
yellow color. This is known as the " chloroform test. " Another reaction which 
usually gives a satisfactory result, but not always, is Gmelin's. If urine contain- 
ing bile-pigment is slowly poured down the sides of a test-tube containing some 
fuming nitric acid, the zone between these two liquids exhibits a fine play of colors. 
The effect of the acid upon the biliary pigment is to produce a number of colored 
rings, the highest and most characteristic of which is green ; next comes blue, then 
violet and red. 

The biliary acids also may be detected in the urine of jaundice; but the process 
is somewhat tedious, and the knowledge gained is of no practical importance. 

The urine very often contains morphological elements which are characteristic. 
Nothnagel was the first to describe minutely the icteric casts — that is, hyaline casts 
which usually have a yellow tinge and quite often are completely covered with 
dark-yellow granules. The mine may contain a little albumen also, but this is not 
constant. 

[The presence or absence of albumen depends largely on the amount of the 
biliary constituents and on the length of time they continue in action on the kid- 
neys; their effect on these organs is more or less that of an irritant.] 

The sweat-glands also take part in the excretion of bile-pigment. The latter 
can be demonstrated in the perspiration of jaundiced persons, as well as in their 
mine. Not infrequently the patient's linen is colored yellow by the sweat. On 
the other hand, no bile-pigment is found in the tears, saliva, gastric juice, or secre- 
tions other than those mentioned. 

Having now considered the phenomena common to all cases of hepatogenous 
icterus alike, we revert to the subject of simple catarrhal jaundice. The prodromal 



CATARRHAL JAUNDICE. 



439 



gastric symptoms usually last a few days, more rarely a week or two, when the 
skin becomes evidently jaundiced and the other results of the icterus are also seen. 
The urine grows dark with biliary pigment, the stools become light-colored and 
more or less clay-colored. The nervous system is not usually seriously deranged, 
but still most patients feel very languid and have anorexia and a tendency to con- 
stipation. The pulse becomes somewhat slower than normal, and sometimes the 
temperature also is subnormal, say 97° or 98° (36°-36'5° C). 

In most cases the physical examination of the liver is of interest, the organ 
being, as already mentioned, enlarged from the retained bile. Accordingly the 
lower boundary of hepatic dullness usually extends two or three finger-breadths 
below the edge of the ribs, and not infrequently the lower margin of the organ 
can be plainly felt. Often the gall-bladder is so distended, both by bile and by the 
mucus which it itself secretes, that it projects from under the edge of the liver. In 
such cases, as Gerhardt tells us, we may sometimes make out by percussion a con- 
vexity in the lower line of hepatic dullness, which corresponds to the gall-bladder. 
If the abdominal walls are lax, we may even feel the distended viscus. As a rule ? 
there is not much distress in the hepatic region, although now and then there is a 
certain sensation of pressure or tension. 

The symptoms depicted seldom last longer than a few weeks. Usually a 
patient who takes proper care of himself begins to feel better in even less time. 
The urine grows lighter colored, the stools darker, and the pulse more rapid. The 
yellow color of the skin often remains visible for quite a while, although gradu- 
ally diminishing, even after the patient feels perfectly well ; but at last the jaun- 
dice disappears also, and recovery is complete. Relapses are indeed possible, par- 
ticularly after errors in diet ; but they are rare. 

The termination of catarrhal jaundice is, therefore, almost invariably favorable. 
The entire course of the disease occupies about three to six weeks, rarely a longer 
period. It is a very exceptional occurrence, but one which we must always think 
of as possible, for this apparently mild and secure condition to be suddenly merged 
into the grave, pernicious variety of jaundice. (See the chapter on acute yellow 
atrophy of the liver and pernicious jaundice.) 

Diagnosis. — Catarrhal jaundice is usually easily diagnosticated. The diagnosis 
is made chiefly from the course of the disease — the development of jaundice, pre- 
ceded by gastric symptoms, in a previously healthy person, and generally in a 
youthful individual. It is very important to exclude other conditions which 
might occasion jaundice. We must consider, therefore, whether the history of 
the case suggests the presence of gall-stones (hepatic colic), and be vigilant in our 
physical examination to detect a possible cirrhosis or new growth. In the case of 
elderly patients, particularly, it is not rare for what was at first regarded as an 
attack of ordinary catarrhal jaundice eventually to disclose itself as a grave 
chronic disease. We should not make a diagnosis of catarrhal jaundice until we 
have carefully weighed all the rational and objective signs. 

Treatment. — Most cases of catarrhal jaundice terminate favorably and require 
no active treatment. Rest and prudence are indicated, and the diet should be 
carefully regulated, that the gastro-duodenal catarrh may not be aggravated. Fat 
must not be eaten, for, as we have seen, it is not assimilated, and only excites 
abnormal processes of decomposition in the intestinal canal. Lean meat, bread, 
soups, if not too rich, vegetables, preserves, and lemonade or tamarind- water are 
allowable. 

We should also employ internal remedies to mitigate the catarrh. The various 
stomachic tonics are frequently prescribed. Rhubarb is a favorite drug. A very 
good medicine is Carlsbad water, or the artificial Carlsbad salts, of which latter 
the dose is half a teaspoonful to a teaspoonful, in a tumbler of warm water, before 



DISEASES OF THE DIGESTIVE OEGANS. 



breakfast. The alkalies not only exert a direct beneficial influence upon the 
gastric mucous membrane, but are also useful as laxatives. More obstinate con- 
stipation may call for castor-oil, calomel, or rhubarb. 

Lately much enthusiasm has been displayed about the treatment of catarrhal 
jaundice by large enemata of cold water. The injections are said to overcome the 
biliary retention by exciting peristalsis and possibly by also promoting the secre- 
tion of bile. Once a day a quart or .two of water, at 60° to 70° (12°-18° E.), is 
injected, and is retained as long as possible. The good effect is said to be observ- 
able in a few days, both in the general condition of the patient and in the dimin- 
ished amount of bile-pigment in the urine, as well as the darker color of the stools. 

The effort has also been made to empty the gall-bladder by manipulation. 
Gerhardt states that sometimes the distended viscus can not only be felt through 
the abdominal walls (vide supra), but it can be so firmly compressed as to squeeze 
its contents into the duodenum. Sometimes the obstruction is said to yield sud- 
denly, as if a plug were driven out. This method has not been universally 
adopted. It seems applicable only in certain cases, and is probably not free from 
danger. Several authorities have recommended external faradization as a means 
to stimulate the gall-bladder to contract and discharge its contents. We believe 
that few will adopt the suggestion. 



CHAPTEE n. 

BILIARY CALCULI. 

(Hepatic Colic. Cholelithiasis.) 

JEtiology. — Although gall-stones are of very frequent occurrence, we do not 
yet possess much information as to their causation. It is only possible to state a 
few factors which very probably promote their formation. 

Biliary retention certainly acts in this way, both directly and by leading to an 
increased consistency and increased concentration of the bile. As a result, certain 
constituents which were before held in solution are thrown down. And yet this 
cause, however potent, can not be regarded as the only one. The chemical exami- 
nation of gall-stones leads plainly to the conclusion that their formation must be 
preceded by certain abnormal chemical processes of decomposition and of trans- 
formation. We can not otherwise explain why the constituents of gall-stones 
should differ, as they do in many ways, from the matters which normal bile holds 
in solution. For example, the pigment in gall-stones is never found unchanged, 
but invariably exists in composition with lime. Now, normal bile contains only 
a trace of lime, so that long ago Frerichs suggested that the lime comes from the 
mucous membrane of the gall-bladder. It is an important fact that the choleste- 
rine, and probably also a portion of the pigmentary matters, are held in solution 
in normal bile by the combination of sodium with the biliary acids which it con- 
tains. If this sodium salt were decomposed from any cause, the matters named 
would naturally be precipitated. The decomposition of the salts formed by the 
bile-acids is greatly promoted if the bile acquires an acid reaction ; but of the cir- 
cumstances in which this last-mentioned change occurs we do not yet have any 
accurate knowledge. Possibly fermentation may have something to do with it. 
The idea that often a clump of mucus forms the nucleus of a biliary concretion 
lacks chemical confirmation, for mucus is never found in the stones. 

We have rather more knowledge as to predisposing causes than about the 
chemical processes involved in the formation of gall-stones. 



BILIARY CALCULI. 



441 



Age seems to be an important factor. The great majority of patients are over 
forty. Gall-stones are much less frequent between twenty and forty years of age ; 
and in children they are very rare, although they have been observed in the new- 
born. One reason why elderly people are so liable to this trouble is said be the 
senile weakness of the muscular fibers of the gall-bladder. Thus stagnation and 
retention of bile are promoted. It has also been suggested that in old age the 
bile may contain an excessive amount of cholesterine and lime. 

Sex also has a decided influence. All authors agree that gall-stones are more 
frequent in females than in males, the proportion being about three to two. An 
explanation of this fact has been sought in the sedentary life of women, and 
particularly in the mechanical effect of tight lacing, impeding the outflow of bile. 

Much has been said about certain peculiarities of bodily temperament in rela- 
tion to cholelithiasis. Obesity, gout, and chronic endarteritis are said to favor the 
formation of gall-stones. A like influence is ascribed to excessive indulgence in 
meat and fat, as well as to gluttony in general, and to lack of exercise ; but the 
real importance of these various influences is not at all definitely determined. 

Diseases of the liver and bile-ducts do undeniably promote cholelithiasis, for 
they interfere hi many ways with the discharge of bile from the ducts and from 
the gall-bladder. Thus they may cause compression or obstruction of a duct, or 
may lead to degenerative changes in the tissues of the gall-bladder. The view is 
quite generally held, but is apparently incorrect, that even a simple chronic 
catarrh of the bile-ducts tends to cause gall-stones. Gall-stones and catarrh of the 
ducts are indeed often found to co-exist, but it is probable that the catarrh is not 
the cause, but the result of the presence of gall-stones. 

Occurrence, and Chemical and Physical Properties of Gall-stones.— The place 
where gall-stones are most frequently found is the gall-bladder. We may find in 
it any number, from one or two up to a hundred and more. The size varies from 
that of a grain of sand up to that of a hen's egg. The large stones may completely 
fill the gall-bladder ; and sometimes the smaller stones are numerous enough to 
fill it also. The stones usually lie free in the bladder, although exceptionally 
they may be found adherent to its walls. Rarely the bladder presents a diverticu- 
lum, in which a stone has been formed. The lining membrane of the viscus often 
suffers such mechanical irritation from the stones as to present quite a severe 
catarrhal inflammation. Sometimes there is even a more or less extensive necrosis 
or ulceration (vide infra). 

Stones which are found in the larger bile-ducts were not formed in them, but 
have become wedged in them while on their way to the intestine. This condition 
is described as an impaction of gall-stones. Gall-stones are quite often found in 
the liver itself, and frequently in large numbers. These concretions may measure 
half a centimetre to a centimetre in diameter. In such cases the small intra- 
hepatic bile-ducts are usually a good deal widened ; or occasionally they present 
niches in which the stones lie. As a rule, the hepatic parenchyma surrounding 
the stone is in a state of chronic or acute purulent inflammation (vide infra). 

In form, gall-stones vary infinitely. The smallest are irregular masses, well 
described by the name of " gall -sand." The larger stones are more or less round, 
or oval, or polyhedral. The polyhedra are usually due to the mutual rubbing and 
pressure of a number of stones upon one another. In color, the stones vary accord- 
ing to the amount of pigment they contain, from almost black or dark brown to a 
lighter greenish or bright yellow shade. A fresh gall-stone always sinks in 
water ; but when dry, gall-stones contain air and generally float. On cross-sec- 
tion, they are found to be either homogeneous or composed of layers. As a rule, 
there is a nucleus, darkly pigmented, which is surrounded by a lighter-colored 
envelope, itself either made up of concentric layers or evidently crystalline. 



442 



DISEASES OF THE DIGESTIVE OKGANS. 



Often the outermost layers are still distinguishable as peculiar darker and harder 
strata. 

As to chemical composition, gall-stones are usually divided into several groups. 
By far the most frequent variety is made up of cholesterine and pigment mixed 
together in greatly varying proportions. The pigment is part of it in its natural 
state, and part of it combined with lime. On the average, stones contain about 
seventy to eighty per cent, of cholesterine. Beside these two chief ingredients, 
most stones also contain lime and magnesium. In color, they are light or dark 
according to the smaller or greater proportion of coloring matter they contain. 
Less common are stones of pure cholesterine. These are usually found singly, are 
soft, and often are almost transparent. Most cholesterine stones have a nucleus of 
pigment and lime in combination. Pure pigmentary concretions are rare and are 
generally small, like coarse sand. A still greater rarity is a stone made up entirely 
of lime. Such a stone is small and very hard. 

Pathological and Clinical Consequences of Gall-stones.— Gall-stones may remain 
for a long while in the gall-bladder, and even in the liver, without causing the 
slightest unpleasant symptom. It is not at all unusual to find gall-stones unex- 
pectedly at an autopsy. 

In other cases, however, gall-stones occasion severe suffering, and sometimes 
even death. These grave phenomena may be due either to certain mechanical 
conditions, like impaction, or occlusion of the bile-ducts • or to secondary inflam- 
mation, resulting from their presence. These two kinds of disturbance must now 
be discussed in detail. 

Gall-stones not infrequently leave the place where they were formed. Stones 
formed in the liver are gradually driven onward by the current of the bile, and 
pass through the hepatic duct into the common duct and the intestine. The more 
numerous concretions formed within the gall-bladder also often change their 
location. What should make them move is not perfectly determined. Probably 
there are various factors ; in the first place, contraction of the muscular coat of 
the gall-bladder ; and then probably the weight of the stone ; and the pressure 
of the diaphragm and the abdominal walls, as in breathing, defecation, and 
vomiting. When once a stone has entered the biliary passages, we must regard 
the secretion behind it as the chief propulsive power ; for neither the cystic nor 
the common duct possess muscular fibers. 

Small calculi may effect their escape without exciting any attention ; but the 
passage of larger ones produces a very characteristic set of symptoms, known 
under the name of hepatic colic. Attacks of pain are frequently, though not 
always, the first symptom of the passage of gall-stones. ' The intensity of the suf- 
fering varies greatly in different cases. It may be so mild and ill-defined as not 
to suggest its true cause, or it may be unbearable. 

A typical attack of hepatic colic either begins suddenly, or it has for prodromata 
nausea, chilliness, and mild constitutional disturbance. The most frequent time 
for its occurrence is a few hours after dinner. The pain may be violent from the 
start ; or, if at first less severe, it quickly reaches an extreme degree. It is usually 
felt chiefly in the epigastrium and the right hypochondrium, but radiates thence 
backward and toward the shoulders, or even into the right arm. The pain comes 
in paroxysms, being worse each time till it becomes extremely severe. General 
convulsions have been repeatedly observed as a result of the pain, particularly in 
nervous individuals. Quite often there is a severe rigor. Vomiting is also com- 
mon. Usually there is constipation. As a rule, there is great constitutional dis- 
turbance ; there is extreme languor and weakness, with an appearance which 
suggests collapse. The pulse is small and somewhat accelerated ; less frequently, 
it is slower than normal. The temperature is normal. During the rigor, how- 



BILIARY CALCULI. 



443 



ever, it may be elevated to 104° (40° C.) or more. On physical examination, the 
liver is more or less enlarged ; and sometimes it is possible to feel a full and dis- 
tended gall-bladder, or at least to find a dullness on percussion corresponding to 
it. Jaundice often appears toward the end of the attack, but not invariably. Of 
course it can be caused by a calculus only when it blocks up the hepatic or com- 
mon ducts. Occlusion of the cystic duct would not produce it. 

The duration of an attack is, in mild cases, only a few hours, and in severer 
ones seldom more than one or two days. Probably the pain ceases the instant 
the stone has successfully passed the final narrow portion of the common duct, 
just above its opening into the intestine. Perhaps relief is sometimes due to the 
stone's slipping back again into the gall-bladder. If the faeces are carefully 
examined after an attack is ended, we often find one or more calculi. The best 
method of search is to pour the faeces upon a sieve, after adding water to them. 
In one or two instances, gall-stones have passed into the stomach and been 
vomited up. The interval between different attacks varies. Sometimes months 
or years intervene, sometimes only a little while. Not infrequently there is a 
quick succession of attacks, and then none for years or even for a lifetime. In 
the intervals the patient may feel perfectly well, but he may have a slight jaun- 
dice or an enlarged liver or chronic digestive disturbance. 

Permanent impaction of a stone at any point in the biliary passages gives rise 
to quite different symptoms. Usually the violent symptoms of hepatic colic per- 
sist for some days, but then abate, leaving behind only a dull pain subject to occa- 
sional exacerbations. Sometimes the symptoms almost all vanish, in case the 
passage is not entirely occluded. If, however, no bile whatever can pass, further 
trouble is to be expected. If the calculus lies in the cystic duct, mucus collects in 
the gall-bladder and gradually distends it. The coloring matter of the retained 
bile is gradually absorbed, so that finally the contents of the gall-bladder is an 
almost colorless mucous fluid. This condition, of course, arises just the same from 
occlusion of the cystic duct due to any other cause. It is termed dropsy of the 
gall-bladder. Sometimes the distended viscus can be felt through the abdominal 
walls. If a gall-stone lodges in the hepatic duct, or, as is much oftener the case, 
in the common duct and dams up the bile, chronic jaundice is inevitable. 

Another series of very important symptoms is due to the secondary inflamma- 
tion or ulceration resulting from the impaction. A gall-stone may excite a sec- 
ondary inflammation, no matter where it lodges, whether in the gall-bladder or the 
ducts, or the liver itself. The phenomena are quite analogous to the inflammation 
which a faecal calculus excites in the vermiform appendix (vide supra). The 
first effect of the stone is purely mechanical. Its pressure causes a simple necrosis 
of the mucous membrane. The inflammation and ulceration are developed 
secondarily around the necrosed tissue ; but once started, they may spread. The 
germs which excite the inflammation are probably in all cases derived from the 
intestinal canal. As long as the ulcerative process is confined to the mucous 
membrane there are no special symptoms ; but quite often it gradually involves 
the deeper tissues or invades neighboring organs. In such cases the number of 
possible events is almost infinite. We shall mention here only a few of the most 
frequent and important. 

If the gall-bladder or one of the large ducts is perforated, the bile flows into 
the abdominal cavity. Gall-stones also have more than once escaped in the same 
way. Such a perforation is almost invariably followed by a purulent and usually 
quickly fatal peritonitis. This is not excited by the bile itself, for normal bile 
does not provoke inflammation, but it is due to septic matter (or decomposed bile), 
which also gains access to the peritoneum. Rarely there is perforation outward, 
The inflamed gall-bladder forms adhesions to the abdominal walls, the ulceration 



444 



DISEASES OF THE DIGESTIVE OEGANS. 



slowly progresses, and finally reaches the surface of the body. Thus a genuine 
" external fistula of the gall-bladder " may be formed, through which bile and cal- 
culi are discharged. More frequent than either of these occurrences is perfora- 
tion into neighboring organs, and into the duodenum in particular. Virchow, and 
more lately Fiedler, have pointed out that we can not explain the appearance of 
large gall-stones in the fasces on any other supposition than that of duodenal per- 
foration; for it is hardly supposable that calculi the size of a walnut or even 
larger should pass through the bile-ducts if in a normal state. Of course, the bile 
can also escape through this same abnormal opening, whereupon the symptoms 
of biliary retention and those due to lack of bile in the intestines cease. There 
have been a few cases of similar perforation into the stomach and the colon, and 
even into the portal vein and the urinary passages. 

The clinical symptoms of all these secondary inflammatory and ulcerative pro- 
cesses may, of course, vary greatly. Sometimes the symptoms are for a long time 
so indefinite that no diagnosis can be made with any degree of certainty. There 
are abdominal pain, occasional febrile attacks, constitutional derangement, and 
anorexia — symptoms which, to be sure, indicate some serious trouble, but do not 
reveal its nature. The case is different if there be a previous history of colic, 
jaundice, the appearance of gall-stones in the stools, or similar more definite indi- 
cations. If perforation into the abdominal cavity takes place, acute and severe 
peritonitis is, as we have said, almost inevitable. If a perforation into other 
organs occurs, the only sign by which it can be recognized is the discharge of 
gall-stones through some unusual channel, for instance, through the abdominal 
walls, or the oesophagus, or the urinary organs. The " biliary abscesses " which 
may be produced in the liver by gall-stones will be considered under the general 
head of hepatic abscesses. It is worth while to mention that in rare instances 
large gall-stones which have reached the intestinal canal cause obstruction of the 
gut. There have also been a few cases of secondary inflammation and ulceration 
of the intestine due to gall-stones. 

Diagnosis. — It is evident from what has been already said that often the diag- 
nosis of cholelithiasis is easy and indubitable, while in other cases the symptoms 
and course of the disease are obscure and ambiguous. The most characteristic 
symptom is hepatic colic, but it alone is not enough to base a diagnosis upon. 
There must also be jaundice, or the presence of gall-stones in the stools. Other- 
wise we are liable to confound the disease with cardialgia, intestinal colic, the 
passage of renal calculi, or that rare disease, neuralgia of the hepatic subdivision 
of the cceliac plexus. We should, therefore, avoid making too hasty a diagnosis 
in doubtful cases. Further consideration or further developments may greatly 
aid us. 

It is but seldom that physical examination of the liver here yields decisive 
results. Still it is possible, as has been said, that a gall-bladder distended with cal- 
culi may be felt through the abdominal walls. Sometimes we can even hear with 
a stethoscope the friction of the stones upon each other. 

Prognosis. — We have already enumerated the manifold dangers which are 
incident to cholelithiasis, but on the whole these untoward results seldom occur. 
As a rule, the termination is favorable. Either the calculi escape in some way, 
and there is complete recovery; or at least the symptoms abate, and the patient 
feels as well as ever, although the possibility of a relapse hangs over him. 

As to the separate symptoms, the colic itself is very seldom dangerous. In a 
very few cases of extreme severity there has been a fatal collapse. Permanent 
obstruction of the common duct is worse, because it greatly impairs nutrition, and 
also leads to secondary changes in the liver {vide infra). The most favorable 
direction for a perforation to take is into the small intestine. It would seem that 



BILIAEY CALCULI. 



445 



the fistula thus caused may even heal up perfectly. The ulcerative process may 
cause an unfavorable result by entailing a cicatricial closure of the common 
duct. 

Treatment. — Our first efforts must be directed to a relief of the symptoms 
excited by the gall-stones. We must further endeavor to promote their discharge 
from the body and to prevent the formation of new ones. 

It is the hepatic colic which most often demands therapeutic interference. The 
most important and indispensable remedy is opium or morphine. If there is 
violent pain, a grain of opium (0*05 grm.) is usually required every hour or two. 
If there is vomiting, or if immediate relief is called for, a sixth to a third of a 
grain (0*01-0 '02 grm.) of morphine may be injected subcutaneously. Other nar- 
cotics, like chloral and belladonna, are seldom needed. In the way of external 
applications to the hepatic region, warm or hot poultices serve the best purpose. 
Some few patients get more relief from an ice-bag. Usually some relief can be 
obtained from a mixture of equal parts of chloroform and olive-oil rubbed gently 
in over the liver. Sometimes relief is obtained by a prolonged warm bath. For 
violent emesis, opium, potassic bromide or bits of ice may be administered. In 
collapse, we must exhibit such stimulants as wine, strong black coffee, or even 
ether or camphor subcutaneously. After the colic is over, some mild laxative, 
such as a mineral-water, is generally given, to favor the evacuation of such calculi 
as may have entered the intestinal canal. 

[When giving repeated doses of opium for biliary or renal colic, it should be 
remembered that the pain will cease abruptly as soon as the stone ceases to obstruct 
the passage, and that some toxic effects of the drug may then appear. In bilious 
colic the distance to be traversed by the stone is relatively short, and in that affec- 
tion especially the inhalation of ether or chloroform is sometimes the best, and, 
indeed, the imperative treatment. 

The brilliant results of surgical treatment at the hands of Tait and others in 
cases of multiple or impacted gall-stones demand mention. 

Mr. Tait has opened the gall-bladder twenty-one times up to February, 1886, 
and removed the actual or potential cause of obstruction without a single death 
or other ill effects. For an analysis by Massen of thirty-five cases, see " American 
Journal of the Medical Sciences," 1884, vol. ii, p. 383. 

Cases not infrequently come under observation in which the patient, either on 
his own notion or following ignorant advice, has taken large doses of olive-oil ; 
most of the oil is passed in lumps, which have a superficial resemblance to gall- 
stones, and are sometimes called such.] 

The second indication, namely, to prevent the formation of fresh concretions, 
is best met by certain alkaline mineral- waters. Just how they act is uncertain, 
but that they do exert a favorable influence has been satisfactorily established by 
experience. The springs of Carlsbad have gained the highest reputation of any. 
If the patient's circumstances permit, it is always best to send him to Carlsbad. 
During the " cure " there it often happens that a large number of gall-stones are 
passed with comparatively little discomfort, and the patient not infrequently 
returns home to enjoy for years, or even for life, freedom from his old trouble. 
Vichy is good, as are also Kissingen, Homburg, Marienbad, and Ems. If the 
patient can not travel, he must drink Carlsbad water at home for a month or six 
weeks. 

All the other remedies are of dubious efficacy. " Durande's remedy," which is 
a mixture of three parts of ether and two parts of oil of turpentine, is much in 
vogue : twenty or thirty drops are to be given two or three times daily for a long 
while. The internal administration of ten or fifteen drops of chloroform in muci- 
lage three or four times a day has also been recommended. 



4A6 



DISEASES OF THE DIGESTIVE OKGANS. 



If perforation, peritonitis, or any other special complications arise, they are to 
be treated on general principles. 



CHAPTER III. 

SUPPURATIVE HEPATITIS. 

(Hepatic Abscess.) 

JEtiology. — Exclusive of traumatism there are two ways by which bacteria 
may penetrate into the liver, there to excite a suppurative inflammation — namely, 
by the blood and through the bile-ducts. In the circulatory system the main route 
is by way of the portal vein, by which germs from the intestines reach the liver. 
This explains why many ulcerative processes in the intestine, like severe dysen- 
tery, are followed by hepatic abscess ; and why purulent pylephlebitis (q. v.) and 
other suppurative processes within the portal system may have a similar sequel. 
In general pyaemia, the germs must take a very circuitous route in order to reach 
the liver. They must, on leaving the primary abscesses, first enter the veins and 
the lungs, and then gain the liver by way of the hepatic artery. It has been well 
known for a long time that suppurating wounds of the head are followed by 
hepatic abscess with comparative frequency. Perhaps it may exceptionally hap- 
pen that infectious matter enters the hepatic veins by "retrogressive embolism" 
from the vena cava. 

The germs which make their way into the liver from the bile-ducts invariably 
originate in the intestine. In these cases the hepatic inflammation is almost 
invariably preceded by disease of the biliary passages. The most frequent cause 
by far of this variety of hepatic abscess is the formation of gall-stones. The two 
most essential factors are the mechanical injury caused by the concretion, that is, 
necrosis from pressure, and the decomposition of the retained bile. 

Among us, hepatic abscesses are rarely occasioned in other ways than those 
indicated ; but in the tropics it is said that quite a large number of apparently 
primary hepatic abscesses are met with. Their origin is not yet explained. 

Pathology. — The smallest and as yet imperfectly developed abscesses best illus- 
trate the mode of formation. We find the blood-vessels choked with micrococci, 
and the cells of the surrounding parenchyma void of nuclei and in process of dis- 
integration. Along the course of the blood-vessels nuclei are very abundant. 
These are due to white corpuscles which have escaped through the vascular walls. 
The cells and the liquid exudation rapidly increase, and there is complete destruc- 
tion of the hepatic parenchyma, and the formation of an abscess in its place. This 
may extend indefinitely in all directions. Large abscesses may at last involve 
an entire lobe. In other cases the suppurative process is limited by encapsula- 
tion. Sometimes quite large portions of the liver become necrotic and slough off, 
under the influence of what is called " sequestrating " suppuration. We almost 
invariably find some shreds of hepatic tissue in the pus of hepatic abscesses. 
Where the abscess is due to gall-stones, the latter are found in the pus. 

Small abscesses may be absorbed, but they are often merely symptomatic of 
pyaemia or some such disease, which is itself incurable. Larger abscesses may 
point into neighboring organs. If they are discharged into the abdominal cavity, 
diffuse peritonitis follows. The most favorable termination, and one repeatedly 
observed, is perforation through the abdominal walls, after these walls and the 
liver have been joined by adhesions. They may also break into the pleural cavity, 
the pericardium, the intestine, and the pelvis of the right kidney. 



SUPPURATIVE HEPATITIS. 



Clinical History. — An absolutely complete clinical description of hepatic 
abscess is impossible, because, as we have seen, it may be a symptom of such 
diverse pathological processes. Hepatic abscesses are often found post mortem 
which had given no previous indication of their presence ; this is frequently the 
case in pyaemia. In other cases there are symptoms, in part directly referable to 
the seat of inflammation, and in part due to its influence upon neighboring 
organs. 

Enlargement of the liver can often be made out by percussion or even by pal- 
pation. It is the result of swelling and hyperaemia involving the entire organ. 
Extensive abscesses may give much more definite signs of their presence, however, 
if situated near the anterior edge of the organ. They are sometimes felt through 
the abdominal walls as hemispherical and actually fluctuating tumors. It is not 
so very rare for tropical hepatic abscess to attain these dimensions. 

Pain in the right hypochondrium, although it may be entirely absent when 
the abscesses are small, even if they are numerous, is often violent and persistent 
when the abscess is large. It is excited by the tension of the peritoneal covering 
of the liver, or by a perihepatitis. The pain often radiates. Physicians have long 
been accustomed to associate pain in the right shoulder with hepatic abscess. 

The course of the fever may prove a strong diagnostic point. When the abscess 
is chronic and encapsulated there may, it is true, be no fever whatever; but, as a 
rule, fever does exist, and often presents a very characteristic intermittent char- 
acter. There are great elevations, usually ushered in by a chill, and succeeded 
by deep depressions of temperature accompanied by perspiration. If the hepatic 
trouble is merely a symptom of general pyaemia, then the fever is to be ascribed 
to the latter ; but if there are signs of a severe local hepatic disease, such as pain, 
enlargement, and jaundice, and if these febrile attacks come on at irregular inter- 
vals, we should always consider the possibility of abscess of the liver. In the 
cases of large tropical abscess this sort of fever is the rule. It is most frequent 
with us in cases of purulent pylephlebitis and of abscess excited by gall-stones. 
The ^fievre intermittente hepatique" of the French is in most instances due to 
the presence of gall-stones in the liver, with secondary suppuration. 

Among the secondary symptoms of hepatic abscess jaundice is prominent. It 
is not invariably present, however, occurring only when the abscess has com- 
pressed some large biliary duct, and has thus given occasion to the absorption of 
bile by the lymphatics. In rare instances the abscess compresses the portal vein 
and thus causes ascites. There may be pulmonary symptoms of considerable 
importance, even when there are no actual pulmonary complications. This is 
because the right half of the diaphragm is crowded up by abscesses projecting 
from the convex surface of the liver. Hiccough is sometimes a source of distress, 
and may be due to the pressure of the abscess upon the stomach. Vomiting is 
also a rather common and often very troublesome symptom. 

There is almost always great constitutional disturbance. The patient has no 
appetite, and loses flesh, particularly if there are frequent febrile exacerbations. 
Often there are severe nervous attacks. Very exceptionally, the disease remains 
latent for a long while, and does not disturb the general health to any great 
extent. 

The course of the disease depends mainly upon the nature of the original dis- 
turbance. Severe pyaemic cases, in the course of which hepatic abscesses develop, 
are generally brief, and are almost invariably fatal. Abscesses due to gall-stones, 
and the large abscesses which are apparently idiopathic, are generally chronic, 
lasting for weeks, or even for many months. Cases exhibit manifold diversities, 
according to the position, size, number, and sequelae of the abscesses. Among the 
possible results we would once more call attention to perforation into neighboring 



us 



DISEASES OF THE DIGESTIVE OEGANS. 



organs. If the pus is discharged externally, recovery may ensue; as also if the 
pus reaches the intestinal canal or the bronchi, which seldom happens. Perfora- 
tion into the abdominal cavity always excites a fatal acute peritonitis. As a gen- 
eral rule, hepatic abscess finally proves fatal, recovery being exceptional. Death 
is due either to the gradual loss of strength or to some complication. 

Treatment.— Local bleeding, counter-irritation, purgatives, and emetics are 
among the remedies which are advocated, but we can hardly expect them to exert 
much influence upon a hepatic abscess. The best way is to treat the case purely 
symptomatically, seeking to keep up the patient's strength and mitigate his suf- 
fering until, if we are very fortunate, we have a chance for operative interference. 
When once the other symptoms are re-enforced by the discovery on palpation of 
a fluctuating tumor, the diagnosis is established, and the pus should be evacuated 
and the cavity drained. Particulars about the operation should be sought in 
works on surgery. More than one case of the large tropical abscess has been 
cured in this way ; but the cases which are most common among us — namely, 
embolic abscesses and those excited by gall-stones— hardly ever afford any oppor- 
tunity for surgical interference. 



CHAPTER IV. 

CIRRHOSIS OF THE LIVER. 

( Chronic Diffuse Interstitial Hepatitis. LaenneJs Cirrhosis. Gin-drinkers' 1 Liver.) 

^Etiology and Pathology. — Cirrhosis of the liver is usually defined as a diffuse 
interstitial inflammation, chronic in duration, and resulting in a secondary atro- 
phy of the true hepatic parenchyma. This conception makes the disease perfectly 
analogous to " chronic interstitial inflammation "of the kidney and many other 
organs. Weigert's careful study of the processes of " chronic interstitial nephritis " 
has shown that at least a large part of the changes which take place in the con- 
nective tissue are not primary, but secondary, and the consequence of a primary 
destruction of the genuine renal parenchyma. The question naturally suggests 
itself, whether the same may not be true of the apparently closely allied phenom- 
ena of hepatic cirrhosis. It must be confessed that as yet no special investigation 
has been made with the object of settling this doubt ; but still we believe that there 
is much which gives probability to the new view. 

We are inclined, therefore, to believe that the primary lesion is in the cells of 
the parenchyma, some of which are thereby destroyed, and are replaced by a sec- 
ondary hyperplasia of connective tissue, which eventually contracts. A primary 
lesion of the parenchyma of the kidneys, heart, or spinal cord, has the same effect 
upon the connective tissue in them. 

Such a conception would be extremely compatible with one fact about the aeti- 
ology of the disease, namely, that chronic alcoholism is universally regarded as a 
potent predisposing cause. Hence the English name, " gin-drinkers' liver. " The 
harmful influence of alcohol can be appreciated if we remember that on being 
absorbed it is carried directly by the blood-vessels to the liver. The stronger 
liquors are more potent for evil in this direction ; wine and beer are not harmless, 
however. According to the usual view of the disease, the poison excites a chronic 
inflammation of the connective tissue ; while, according to the new view, the alco- 
hol exerts a specific injurious influence upon the hepatic cells proper, impairing 
their nutrition, and finally causing their destruction. That the disease attacks the 
periphery of the lobules and the interlobular connective tissue is equally conso- 



CIEEHOSIS OF THE LIVER. 



449 



nant with, either theory. It is well known that the capillary anastomoses of the 
portal vein are situated between the lobules. 

The abuse of alcohol is by no means the only cause of cirrhosis, for quite often 
the disease attacks persons in whose case no such aetiology is possible. In such 
instances we are seldom able to demonstrate the real cause. The excessive use of 
spices, and other analogous substances, has sometimes been regarded as causative. 
It is also said that sometimes malaria, and the acute infectious diseases, leave 
behind them a tendency to cirrhosis. The form of cirrhosis which follows dis- 
eases of the bile-ducts, and also " syphilitic cirrhosis," will receive separate consid- 
eration. 

Cirrhosis of the liver is seen much oftener in men than in women, and usually 
occurs in middle life. 

The anatomical changes are usually divided, without regard to the way in 
which they are brought about, into two stages. In the first stage the liver is 
uniformly enlarged, resistant, with its edge blunt, and its surface at first per- 
fectly smooth, but later presenting little dimples. On section, the increased con- 
sistency, or " interstitial induration "of the liver, can be readily perceived. The 
acini are separated from one another by a relatively thick band of grayish-red 
interstitial tissue, and are at first readily distinguishable. Later on, the interstitial 
hyperplasia invades the acini themselves, and they cease to be discernible. The 
microscope shows that the cause of this increase in size and firmness of the organ 
is due exclusively to the abundant cellular infiltration and the new formation of 
connective tissue between the individual lobules. The neighboring cells of the 
parenchyma exhibit signs of disintegration, undergoing either simple atrophy or 
else fatty degeneration. 

The second stage corresponds with the process of contraction of the newly 
formed connective tissue, but in this stage the destruction of the proper hepatic 
tissue has already assumed grave proportions. On the old theory, the parenchyma 
perishes because of the great disturbance of circulation in the portal capillaries, 
great numbers of which are obliterated by the shrinking of the connective tissue. 
Under this process of contraction the liver undergoes progressive atrophy, and its 
surface becomes mammillated. The size of the nodules varies. The size of the 
whole organ may be reduced one half, or even more. Frequently its general con- 
tour is considerably modified. Upon microscopic examination, we now find 
merely vestiges of parenchyma, embracing which are wide, firm bands of con- 
nective tissue. Even within the acini there is decided interstitial hyperplasia 
along the blood-vessels. Brown masses of pigment are often found here and 
there, which have been left behind by the hepatic cells now destroyed. Regenera- 
tive changes can also be detected quite frequently. The most common of these is 
the formation of small biliary passages in the broad bands of interstitial tissue. 

The division of hepatic cirrhosis into two stages is somewhat diagrammatic, for 
there is really no sharp dividing line between them. The same liver may in dif- 
ferent places illustrate both stages simultaneously. Thus, the surface is often dis- 
tinctly granular, while the liver as a whole remains hypertrophic. 

Clinical History. — The onset of the disease is usually insidious. At autopsies, 
quite an advanced stage of cirrhosis is sometimes found, to which not a single 
clinical symptom had pointed ; and it is often observed that the duration of 
unambiguous symptoms is much shorter than the degree of anatomical change 
discovered post mortem would have led us to expect. 

It is, however, true that certain prodromata may appear long before the 
genuine cirrhotic symptoms ; but there is generally room for doubt whether 
these prodromata are excited by the incipient hepatic disease or whether they 
are not due to other coincident affections, such as the chronic gastric or intestinal 
29 



450 



DISEASES OF THE DIGESTIVE OKGANS. 



catarrh which, drunkards so often have. There are anorexia, nausea, epigastric 
uneasiness, eructations, constipation, and sometimes vomiting. There is evident 
constitutional disturbance in many cases, but in others the strength is unimpaired. 
The severer symptoms usually date from the time when disturbance of the portal 
circulation arises. We have already stated that the diseased process is most active 
in the interlobular connective tissue — that is, where the portal capillaries are situ- 
ated. When the contraction of the connective tissue has resulted in the destruc- 
tion of a large number of these portal capillaries and the minute veins from which 
they spring, the portal circulation is inevitably impeded and there arises a passive 
congestion of the whole portal system. The signs of this are soon manifest. 

The stasis in the veins of the peritoneum is, as a rule, the first to attract atten- 
tion, from the ascites which it occasions. The distention of the abdomen and the 
sensation of weight and pressure, due to this effusion, are often the first things 
which excite the patient's attention and lead him to seek medical advice. Later 
on, the ascites sometimes becomes enormous, causing immense swelling and 
extreme tension of the abdominal walls, and, of course, proportionate discomfort. 
Proper nursing and internal treatment may diminish the ascitic effusion, but 
they will seldom wholly remove it. It quite often remains nearly uniform, 
until finally, for some reason, there is a change for the worse. 

Next to ascites, the most important symptom of portal obstruction is enlarge- 
ment of the spleen, which is due both to the increased amount of blood in the 
organ and to a diffuse hyperplasia of its tissues. As a rule, the increase in size is 
considerable, amounting sometimes to two or three times the normal dimensions. 
The demonstration of splenic tumor is of great diagnostic importance, but is often 
a difficult matter. Percussion and even palpation are greatly interfered with by 
the co-existing ascites. On the whole, however, palpation is the more reliable. 
Pain or other subjective symptoms are rarely observed. Exceptionally, there is 
no splenic enlargement. This may be due to the firmness and thickness of its 
capsule, or to the general marantic condition of the patient. 

The venous congestion of the stomach and intestine excites catarrh, which is 
evinced by anorexia, nausea, and irregularity of the bowels. Usually there is quite 
obstinate constipation, but there may be persistent diarrhoea. None of these symp- 
toms occupy the foreground of the clinical picture, however, both because they are 
frequent in all grave chronic diseases and because many patients have had digest- 
ive derangements long before these severer troubles began. A more significant 
symptom, if it occurs, is haemorrhage. This is now and then occasioned by the 
extreme gastro-intestinal congestion. The bleeding may be either from the 
stomach or the intestine, and is sometimes a relatively early phenomenon. Some- 
times there is a capillary oozing sufficient to tinge the stools day after day for 
some time. Very rarely there is haemorrhage from the oesophagus. 

The patient may be moderately jaundiced even in the common form of cirrho- 
sis. This is sometimes due to duodenal catarrh. Often there is no jaundice what- 
ever; or there may be a slight yellowish tinge of the skin, in addition to the 
dirty, grayish, earthen color which not infrequently characterizes the cirrhotic. 
Perhaps the jaundice is due in many cases to stenosis of the intra-hepatic bile- 
ducts, involving biliary retention. 

The above signs of portal obstruction will often render the diagnosis of hepatic 
disease extremely probable, but we should always endeavor to confirm our opin- 
ion by physical examination of the liver. In the later stages of the disease, and 
particularly if there be great ascites, our efforts may be fruitless ; but at first, or 
after paracentesis has been performed, percussion and palpation may yield valua- 
ble information. In the earliest stages the liver is large. Hepatic dullness 
reaches some ways below the edge of the ribs, and we can often feel the anterior 



CIRRHOSIS OF THE LIVER. 



451 



edge and upper surface of the organ. Later on we find the upper surface irregu- 
lar and rough. If we can feel these little nodules or prominences through the 
abdominal walls, as we sometimes can, of course the diagnosis of cirrhosis of the 
liver is nearly certain. As already mentioned, it often happens that irregulari- 
ties are already to be felt upon the surface of the organ while it still remains 
hypertrophic. The demonstration of atrophy by percussion in the later stages of 
the disease is less reliable. The ascites often interferes with such an attempt. We 
may also be misled by coils of intestine distended with gas and perhaps lying in 
front of the liver. If, however, after guarding against error, we constantly find 
the area of hepatic dullness diminished, the sign has some value. 

General nutrition is usually much impaired in the later stages of the disease. 
At first the patient may retain vestiges of his former corpulence, but finally he 
grows emaciated. Anasarca may exceptionally occur toward the close ; but there 
is frequently considerable oedema of the lower extremities, and even of the scro- 
tum and the dependent portions of the abdominal walls. The cause of this is a 
purely local one — the pressure of the ascites impedes the return of blood from the 
lower limbs to the heart. 

Occasionally there are ecchymoses into the skin, the mucous membranes, the 
retina, and other parts. These are probably due to malnutrition of the vascular walls. 

Unless there are complications, there is no fever. Respiration may be impeded 
and accelerated on account of the upward displacement of the diaphragm. The 
pulse is usually small, and often somewhat more rapid than normal. 

At first the urine presents no characteristic changes. When the ascites has 
become considerable and there is oedema, the urine grows scanty, dark, and con- 
centrated, and often has an abundant sediment of urates. It should be mentioned 
that earlier observers found a diminished excretion of urea. This is perhaps due 
to a disturbance of the urea-generating function of the liver, about which both 
earlier and more recent investigators agree. In a few instances the urine has been 
found to contain a trace of sugar. 

It remains for us to describe briefly the collateral circulation which may be 
developed in cirrhosis, so as to enable the blood of the portal system to reach the 
systemic veins. The clinical history of the disease does not indicate that this 
attempt at compensation is very successful. We may have : 1. Communications 
between the veins of the mesentery and of the abdominal walls. 2. Communica- 
tions between the coronary vein of the stomach and the veins of Glisson's capsule 
on the one hand, and the phrenic veins on the other. 3. Anastomoses between 
the internal hemorrhoidal and the hypogastric veins. 4. As pointed out by 
Baumgarten, enlargement of the not yet completely obliterated umbilical vein in 
the ligamentum teres. Through all these the blood may flow from the portal 
system into the veins of the abdominal walls — that is, in the reverse of the normal 
direction. In cases of portal obstruction the veins of the abdominal walls are 
often much enlarged, and this may be partly due to the changes just enumerated. 
In some instances the veins around the umbilicus have been strikingly tortuous 
and swollen; this condition has been termed "caput Medusae." 

The complications which sometimes occur are probably in part due to the same 
injurious influences as the cirrhosis. This is apparently true, for example, of the 
cardiac hypertrophy, the contracted kidney, and the chronic pachymeningitis. An 
interesting combination is the simultaneous occurrence of cirrhosis and chronic 
tubercular peritonitis. Various observers as well as ourselves have observed this 
with comparative frequency. The explanation is unknown. Probably cirrhosis is 
the primary lesion, and it in some way predisposes the system to the other disease. 

As to the general course of the disease, its duration can not easily be deter- 
mined because the onset is usually insidious. As a rule, the disease lasts one to 



452 



DISEASES OF THE DIGESTIVE ORGANS. 



three years, or rarely longer. In many cases the symptoms are insignificant for 
the first six to eighteen months. Then the disorder takes on a severer form, per- 
haps rather suddenly. Ascites appears, for example. These graver symptoms 
persist, till after a few months the patient dies. The course of the disease reminds 
one of cardiac cases, where for a long while the compensatory changes avert any 
distress, till on a sudden the circulatory disturbances become pronounced and per- 
sist to the end. 

The prognosis is always unfavorable, at least when the symptoms have once 
become well marked. It may be that in the earlier stages the disease can be 
checked or even permanently cured ; but even this is open to doubt. No case 
recovers in which the diagnosis of cirrhosis is certain. 

Death is due either to intercurrent disease, or more often to gradually increas- 
ing exhaustion. In some few cases severe cerebral symptoms suddenly appear : 
there are coma, general convulsions, and delirium; and these usually are soon 
fatal. Just how these nervous phenomena originate we do not certainly know 
(see the chapter on acute yellow atrophy of the liver). 

Diagnosis. — The diagnosis is seldom very easily made. It becomes extremely 
probable if a patient who is known to have been addicted to alcohol gradually 
develops ascites and splenic tumor, and has a liver which presents distinct evi- 
dences of disease, such as an irregular surface. Often, however, we are left in 
doubt, because one or another of these more characteristic symptoms can not 
be clearly made out. Often a patient does not come under observation till a con- 
siderable ascitic effusion has already taken place, so that physical examination of 
the liver and spleen is rendered very difficult. Then we must first exclude any 
general disturbance of circulation as a cause of the ascites. If the heart, lungs, 
and kidneys are found to be normal, and if there is no oedema in the upper half of 
the body, it is very probable that there is a local derangement of the portal circu- 
lation ; but we have still to determine whether the cause of this derangement is 
cirrhosis of the liver. This may be assumed to be the case if the whole course of 
the disease warrants the assumption, and if the history furnishes that most frequent 
of all ^etiological factors, chronic alcoholism. Otherwise we must be cautious, 
for portal obstruction with precisely similar results may be due to other causes — 
like the external pressure of tumors or portal thrombosis. Many forms of hepatic 
syphilis (q. v.) can not be differentiated from cirrhosis by mere clinical observation 
of the hepatic disorder. Here it is only the aetiology and the demonstration of 
other signs of syphilis that can justify the assumption that the disease in hand is 
of specific origin. 

It is also very difficult in many instances to exclude chronic peritonitis. The 
aetiology may aid us. Other points are, that in chronic peritonitis there may be 
tenderness on pressure, the abdominal distention is less uniform, and there is no 
enlargement of the spleen. The combination of cirrhosis and chronic tubercular 
peritonitis can not be diagnosticated with any approach to certainty unless we find 
both the symptoms of cirrhosis and pronounced indications of a tubercular affec- 
tion. In such a case coincident pleurisy is significant of tuberculosis. 

Treatment. — As we kuow the causes which sometimes excite cirrhosis of the 
liver, an obvious prophylaxis consists in avoiding them ; and, even after the early 
symptoms of the disease have appeared, alcohol should be forbidden, as well as 
spices and other similar articles, in the hope that we may thus do something to 
prevent the extension of the abnormal process. 

If the disease has already made considerable progress, treatment becomes 
purely symptomatic. Iodide of potassium is said to exert a favorable influence 
upon cirrhosis of the liver, but its powers are doubtful. Probably it does good 
only in syphilitic hepatitis. Of the individual symptoms the results of portal con- 



BILIARY AND HYPERTROPHIC CIRRHOSES OF THE LIVER. 453 



gestion deserve the most consideration. It is important that the patient should 
enjoy complete physical rest, and that his bodily vigor should be promoted in 
every way possible. Even by these means we are sometimes able to diminish, or 
at least prevent the increase of, the ascites and other effects of portal obstruction. 

Further remedies are given with the purpose (1) to deplete the congested por- 
tal system, and (2) by promoting the watery excretions to cause reabsorption of 
the ascitic effusion. Depletion is usually attempted with purgatives, the action of 
which is expected to diminish the high tension existing in the portal vein. The 
custom is an old one. In the milder cases, just developing, salines are recom- 
mended, usually in the form of mineral- waters ; but if the ascites is already great, 
it is claimed that drastic remedies sometimes prove beneficial. Gamboge is 
reputed to be particularly appropriate in cirrhosis. We should not persist in the 
use of such drugs, however, if they disturb digestion. 

The second indication of promoting watery discharges is fulfilled by diuretics. 
Beside the usual remedies of this class, like potassic acetate and squills, copaiba 
and its resin have been especially recommended for the various forms of ascites 
by English authors. The dose [of the resin] is about fifteen grains (grm. 1) 
daily, best given in capsules. In some cases this remedy has caused a rapid 
increase in the amount of urine and an accompanying diminution of the ascites. 
The improvement is not permanent, however. 

If the ascites is so excessive as to occasion much local discomfort and to impede 
respiration, the removal of the fluid by paracentesis may afford relief. The 
details of this proceeding were given in the last section. Many physicians recom- 
mended tapping as early as possible, before it is absolutely necessary. The relief 
is said to be more lasting in that case ; but, as a rule, the abdomen generally is 
quickly filled again. Possibly the application of an elastic bandage after the fluid 
is removed may retard its reaccumulation by the pressure thus exerted upon the 
abdominal cavity. 

Special symptoms may sometimes demand attention. They are to be treated 
according to general principles. 



CHAPTER V. 

BILIARY AND HYPERTROPHIC CIRRHOSES OP THE LIVER. 

There are two forms of cirrhosis which differ in many respects from the dis- 
ease just described : they are called biliary cirrhosis and hypertrophic cirrhosis of 
the liver. Charcot and other French investigators were the first to call attention 
to them. Since then the literature of the subject has become quite considerable, 
but all doubts and differences of opinion are not yet settled. We shall try to state 
the most important points in what follows. 

Whenever there is retention of bile in the liver for any length of time, no 
matter what causes it, certain changes result. The small and the medium-sized 
bile-ducts become distended, and granules of pigment are deposited, both in the 
interlobular connective tissue and within the acini themselves. Beside this, how- 
ever, and undoubtedly because of the noxious influence of the retained bile, the 
hepatic cells undergo destructive changes. In accordance with the general rule, 
connective tissue gradually fills the gaps thus left in the parenchyma, and, more 
than this, the interstitial hyperplasia is so great as to increase the size of the organ. 
If r therefore, there is persistent obstruction of the common duct by a gall-stone, or 
a cicatricial stenosis, or a tumor pressing from without upon the duct, the liver 



454 



DISEASES OF THE DIGESTIVE ORGANS. 



will, in all such cases, be fouud to be larger, firmer, and richer in fibrous tissue 
than normal — in a word, " cirrhotic." Hence this condition does not represent an 
independent disease, but is a result of chronic biliary retention, in whatever way 
occasioned. It is appropriately termed (secondary) biliary cirrhosis. That reten- 
tion is really the cause of this change has been proved by experiments, for it has 
been shown that ligature of the common duct in animals causes well-marked bili- 
ary cirrhosis. 

This secondary cirrhosis is due to occlusion of the large bile-ducts. There is 
also a rare primary form of the biliary cirrhosis, usually known as hypertrophic 
cirrhosis. French authors have given it the name of " cirrhose hypertrophique 
avec ictere" out of regard to its most important clinical symptom. That there is 
an essential difference between this form and the ordinary " atrophic " cirrhosis 
of Laennec is manifested by the clinical behavior of the disease. 

Often this disorder attacks hard drinkers, but they are not its only victims. 
While, in the common form of cirrhosis, ascites is usually the earliest grave symp- 
tom of disease, in hypertrophic cirrhosis a slight jaundice generally appears simul- 
taneously with the first indefinite symptoms of pressure in the region of the liver, 
languor, and anorexia. This jaundice rapidly increases, and persists throughout 
the illness. In ordinary cirrhosis there may be, as we have said, hardly any jaun- 
dice, or, at any rate, it is a rather late symptom, and even then it is seldom extreme. 
On the other hand, ascites may be slight or absent in hypertrophic cirrhosis. It 
is true that there have been cases with great ascitic effusion, but it never comes 
till the disease is quite far advanced. 

On physical examination the liver is usually found to be considerably enlarged, 
and its surface is smooth, as a rule, or rarely rough. In general there is said to 
be this important difference between the ordinary and the hypertrophic forms, 
that in the latter the newly formed connective tissue evinces little tendency to 
contraction, so that the liver remains large, even late in the course of the disease, 
and does not shrink. Somewhat too much stress has been laid upon this point. 
If, in many cases of hypertrophic cirrhosis, the liver has remained large to the 
end, this is probably in part due to an early death, before there was opportunity 
for much shrinkage. Cases that lasted longer have presented a contracted liver. 

It must be said that the pathological appearance of the liver, particularly in 
the later stages of the disease, affords no certain evidence as to whether the cir- 
rhosis was of the ordinary or of the " primary biliary " variety. Clinically, how- 
ever, the two forms present such important diversities as to justify the distinction 
made. Of course, the clinical peculiarities of primary biliary cirrhosis must be 
due to some anatomical lesion. The most noticeable peculiarity of this sort is, 
that the development of connective tissue in hypertrophic cirrhosis is more active 
within the lobules than is the case in ordinary cirrhosis. Probably the hyper- 
plasia in hypertrophic cirrhosis is most vigorous at first around the small biliary 
ducts, and thus leads to a retention of bile within the minutest biliary passages, 
with consequent jaundice, while the ramifications of the portal vein are not 
encroached upon till the process is far advanced. Whether these two forms of 
cirrhosis are merely modifications of one disease, or whether they are two inde- 
pendent disorders, is as yet unsettled. Certainly there are transitional forms. 

As to the other clinical symptoms of primary biliary, or hypertrophic, cirrhosis 
we need say little. The most noticeable symptoms beside the hepatic enlarge- 
ment and the jaundice are the effects of the jaundice itself — namely, digestive dis- 
turbances, slowness of the pulse, and nervous disorders. Of the occasional dis- 
turbances in the portal system, we have mentioned the ascites already. Still 
more frequent, and usually earlier in the time of its appearance, is chronic passive 
congestion of the spleen, with enlargement. 



ACUTE YELLOW ATROPHY OF THE LIVER. 



455 



The entire duration of the disease is about one or two years ; but it may last 
much longer. The prognosis is almost always bad. Occasionally a case will 
exhibit marked temporary improvement or an apparent arrest of the disease. 
Death comes as a result of gradual exhaustion, or is suddenly ushered in by coma, 
convulsions, and other grave nervous symptoms, usually ascribed to cholsemia 
(vide infra). 

The diagnosis of hypertrophic cirrhosis can sometimes be made with consider- 
able positiveness, and sometimes can merely be regarded as probable. The gradual 
development and persistence of jaundice and the presence of an enlarged liver 
would suggest the disease strongly ; but in some cases it is often impossible to 
exclude the existence of some mechanical obstruction in the larger biliary passages, 
such as gall-stones or new growths. 

The treatment should conform to the principles laid down in the chapters on 
jaundice and ordinary cirrhosis of the liver. 



CHAPTER VI. 
ACUTE YELLOW ATROPHY OP THE LIVER. 

JEtiology. — Acute fatty degeneration of the liver occurs both as a primary dis- 
ease and as secondary to other hepatic disorders, or as a symptom of constitu- 
tional diseases. Secondary acute fatty degeneration in rare instances accompanies 
severe acute infectious diseases, like typhoid fever, recurrent fever, septicaemia, and 
puerperal disease. It also appears, with equal rarity, in the course of cirrhosis of 
the liver or of persistent biliary retention ; and it is a constant phenomenon in 
acute phosphorus poisoning. Indeed, the effects of phosphorus resemble the 
symptoms of primary acute yellow atrophy in many ways so closely, even post 
mortem, that formerly the two were often confounded. 

Primary acute yellow atrophy of the liver is an extremely severe disease which 
almost invariably leads to speedy death. There is generally no determinable 
cause, and its victims are struck down in blooming health. It is so rare that not 
much over two hundred cases have thus far been reported. It is most common in 
young adult life, say between the fifteenth and thirty-fifth year. Children and 
elderly people have been occasionally attacked. Females are much more liable 
to the disease than males ; and pregnancy increases the predisposition to it. 

As we have said, we can not as a rule find any exciting cause. It is stated that 
sometimes the onset has been preceded by some violent emotional excitement, or 
excess in alcohol, or the like ; but how important these factors may be is not at 
all clear. 

It is an interesting fact that sometimes the disease becomes rather more fre- 
quent than usual, and endemic. For instance, several members of one family 
will be attacked. This favors a view as to the nature of acute yellow atrophy 
which a majority of the present investigators seem inclined to adopt. The view 
referred to is suggested not only by the whole course of the disease, but by the 
pathological appearances, and places it in the category of acute infectious diseases. 
It must be confessed that as yet we know nothing about the intimate nature of 
the infection. Klebs maintains that he has discovered micrococci in the hepatic 
blood-vessels ; but thus far the observation lacks confirmation. 

Pathology. — The chief change found post mortem is in the liver, and has 
determined the name given to the disease. 

The liver is much atrophied, sometimes being only one half or one third its 



456 



DISEASES OF THE DIGESTIVE OKGANS. 



normal size. This makes its capsule often seem contracted and wrinkled. The 
organ is usually soft and flabby, so that in some places it seems as if the finger 
could be pressed into it. The color of the surface, and for the most part of the 
cross-section also, is yellow, like ochre or saffron ; but the cut surface may be parti- 
colored, having red and yellow spots interspersed. Hence the names u red atro- 
phy" and "yellow atrophy." The arrangement and relative extent of these 
patches may vary indefinitely. The red places look as if they had collapsed, and 
seem tougher than the yellow. They correspond, as we shall soon see, to the 
more advanced stages of the affection, while the yellow spots have undergone 
less change. The lobules are, as a rule, no longer distinguishable by the naked 
eye. Such lobules as can still be made out seem abnormally small and have a 
gray periphery. 

On microscopic examination, we find that the essential change is an intense 
and uniform fatty degeneration of the hepatic cells, affecting the entire paren- 
chyma. But few cells still retain their normal condition. The others are filled 
with large and small fat-globules, and many are already suffering evident disin- 
tegration and absorption. Where the degeneration is furthest advanced, fat, 
detritus, and pigment alone remain. Inasmuch as the lymphatics rapidly absorb 
and remove the fatty and albuminoid granules, there is finally little left except blood- 
vessels and connective tissue. The blood-vessels are frequently quite congested, 
and thus occasion that red color which the naked eye detects in the more 
advanced, broken-down portions. Frerichs made an interesting discovery, which 
deserves mention, of the existence of leucine and tyrosine crystals both in the paren- 
chyma and in the blood-vessels. Bilirubin crystals also are sometimes found in 
the detritus, and more rarely in the interior of the hepatic cells. 

Not only the liver, but many other organs present fatty degeneration : the 
heart in particular, the kidneys, and rarely the muscles ; but the process is always 
most intense in the liver. The skin {vide infra) and most of the viscera are evi- 
dently tinged with jaundice. 

Acute splenic tumor is invariably present. This suggests that the disease may 
be infectious. That the disease is a constitutional one is also to be inferred from 
the numerous ecchymoses in the skin and the interior of the body, especially in 
the mucous membrane of the stomach and intestines, in the serous membranes, 
in the pelvis of the kidneys, and the kidneys themselves, and more rarely in the 
brain and heart. This, again, is like the grave septic diseases. The blood itself is 
dark, with few clots. Leucine and tyrosine have repeatedly been detected in it. 
The peritoneum and other serous cavities sometimes contain a considerable amount 
of serum. 

Clinical History. — The disease is usually divided into two stages, the first of 
which corresponds to the milder prodromal symptoms, the second to those severe 
symptoms which are alone characteristic. In many instances, however, the first 
period is wanting, or is so brief that the patient is plunged almost without warn- 
ing into the gravest condition. 

The prodromata in most cases consist of constitutional disturbances and mild 
gastro-intestinal symptoms. The patient is languid, without appetite, and disin- 
clined to exertion. There are headache, nausea, vomiting, and sometimes moderate 
fever. After a few days jaundice usually appears. This is almost invariably 
taken for an ordinary catarrhal attack. 

After a few days, or it may be weeks, the second stage begins. The chief 
characteristic of this is the occurrence of grave nervous symptoms. First there 
is violent headache, with sleeplessness and marked restlessness. The intellect is 
usually somewhat dulled even now, and articulation is slow and clumsy. The 
mental confusion usually advances very rapidly to a noisy and violent delirium. 



ACUTE YELLOW ATROPHY OF THE LIVER. 



457 



The excitement becomes at times maniacal. The patient screams and storms, and 
can hardly be kept in bed. Often there are convulsive twitchings of individual 
muscles ; and there may be typical epileptiform attacks, but this is not common. 
After one or two days, or rarely longer, the excitement abates, and is followed by 
sopor, which soon passes into deep coma. At death the patient is usually per- 
fectly unconscious. It is exceptional for the excited stage to be wanting ; in such 
cases the first nervous symptom is sopor. 

The cause of the nervous symptoms has not yet been explained in a way to 
silence discussion. The same theories which have been set up to account for the 
grave form of jaundice in general (see appendix to this chapter) have also been 
employed to elucidate the nervous phenomena of acute yellow atrophy. Thus, 
some refer them to cholaeruia, some to acholia, and still others to acute cerebral 
ansemia. It seems to us worth considering whether the cerebral disturbance in 
acute yellow atrophy of the liver may not be due to the constitutional infection 
which we have seen to be so probable. 

The jaundice, which is present even in the first stage, afterward usually deep- 
ens. The urine contains bile-pigment, and many investigators have also found 
bile-acids in it. If these latter are present, it suggests that the jaundice is not 
haematogenous — that is, the result of a destruction of red blood-corpuscles and the 
transformation of their pigment into biliary coloring matter — but is rather due to 
a retention of bile. Just how this retention arises we do not yet know for certain. 
The obstruction can not be in the large bile-ducts, for the gall-bladder is usually 
found empty. Hence the cause of the retention of bile and of the jaundice is prob- 
ably a derangement of the smaller biliary passages within the liver. We should 
add that in a few rare cases there has been little or no jaundice. 

On physical examination of the liver during the last stage of the disease, there 
is usually a striking diminution of hepatic dullness, corresponding to the atrophy 
of the organ. Generally the first change to be detected is a contraction of the 
left lobe, as shown by the development of tympanitic resonance in the epigastrium. 
At the commencement of the illness, the hepatic dulness is normal or slightly 
increased in area. If the disease proves very rapidly fatal, the organ may never 
become very small. In most cases, though by no means in all, there are pain and 
tenderness in the hepatic region, but these are seldom so great as in phosphorus 
poisoning. 

The enlargement of the spleen has been already mentioned as an almost con- 
stant symptom of the disease. Even during life some increase of the area of 
splenic dullness can usually be made out, and sometimes the spleen can be felt 
under the edge of the ribs. 

The occurrence of the haemorrhages, which have already been referred to 
under the pathological lesions, can often be demonstrated during life. The cuta- 
neous ecchymoses can, of course, be seen, and the haemorrhages in the mucous 
membranes may give rise to haematemesis, bloody stools, bleeding from the 
female genitals, or epistaxis. The haemorrhages are probably due to the impaired 
nutrition and diminished resisting power of the vascular walls occasioned by the 
grave constitutional disturbance. 

The condition of the urine in acute yellow atrophy is very interesting. The 
amount is either normal or slightly diminished, and the specific gravity is some- 
what increased. Often there is a trace of albumen. We have already mentioned 
the presence of bile-pigment. The point of chief interest, however, is one that 
Frerichs discovered and various others have since confirmed, and is the great 
diminution of urea and the appearance in its place of several other substances, 
which are likewise the products of the decomposition of albuminoid matter, and 
represent in all probability the first steps in the formation of urea. Of these sub- 



458 



DISEASES OF THE DIGESTIVE ORGANS. 




stances, the most important are leucine and tyrosine. Their characteristic crys- 
tals can often be detected by the microscope in the urinary sediment (see Fig. 51). 
The crystals may also be obtained by allowing a drop of the fresh mine to evapo- 
rate slowly upon an object-glass. There is a chemical test for them which we can 
not here describe. There are some other abnormal constituents to be found in the 
urine beside leucine and tyrosine ; but what their significance is we do not know. 
Among these are sarcolactic acid, oxymandel acid, peptonoid substances, and large 
amounts of kreatine. 

It at once suggests itself that this disappearance of urea and appearance of 
leucine and tyrosine, which are regarded as preparatory stages in the formation 

of urea, gives valuable support to Meissner's and 
Von Schroder's idea that this substance is manufac- 
tured in the liver. 

As to the other organs little need be said. Vomit- 
ing is very frequent in the second stage, as well as 
in the first. It usually ushers in the severe cerebral 
symptoms. The stools are, as a rule, clay-colored, 
as is usual in jaundice. There is generally consti- 
pation. The pulse is rapid, often reaching 140 to 
160 beats per minute, and is also small and com- 
pressible. It is this acceleration of the pulse, con- 
trasting with its usual slowness during the first stage, 
Fl6 '& 51 S?os^ne cr5 e st2s. StalS ' which, along with the vomiting, announces the onset 
of dangerous symptoms. The pulmonary signs are 
seldom marked, although there may be bronchitis or a pneumonia due to the 
inhalation of foreign substances. During the coma which precedes death respira- 
tion is usually hurried, and often deep and noisy. Sometimes it is irregular. 

The temperature is generally approximately normal. Toward the fatal termi- 
nation there may be a subnormal temperature. Still more frequently the tem- 
perature rises before death, and even sometimes grows higher after death, reach- 
ing 107-5° (42° C.) or more. 

In case the disease attacks a pregnant woman, abortion or premature delivery 
is almost certain to occur. 

The entire duration of the disease depends mainly upon the length of the first 
stage. This may be entirely absent, or may be brief, or may occupy several 
weeks. The duration of the second stage, reckoning from the occurrence of grave 
cerebral symptoms, is generally only a few days (two to four), rarely a week. 
The termination is invariably fatal. In the few cases of recovery reported there 
is doubt about the correctness of the diagnosis. 

The diagnosis can not be made till the second stage. The symptoms of the 
first stage are indistinguishable from those of simple catarrhal jaundice. "With 
the development of the grave symptoms all doubt usually vanishes. The general 
course of the disease, the deep jaundice, the cerebral disturbances, the cutaneous 
ecchymoses, and the character of the urine, form a clinical picture resembling no 
other disease. The only cases where there can be any uncertainty about the diag- 
nosis are the exceptional ones in which there is no jaundice. Acute phosphorus 
poisoning (q. v.) is in many respects very similar in its phenomena, but can gen- 
erally be differentiated, even if the history of the case is not conclusive. The 
chief points are that in phosphorus poisoning the liver remains of large size for 
some time, and is very painful ; that the nervous symptoms much less frequently 
assume the form of maniacal excitement ; and that in but few cases is there any 
large amount of leucine and tyrosine in the urine. 

After what has been said, we need hardly add that treatment is unavailing. 



PERNICIOUS JAUNDICE. CHOLiEMIA AND ACHOLIA. 459 



Usually laxatives are employed, e. g. , calomel. The nervous symptoms are com- 
bated by au ice-cap and baths and narcotics ; the vomiting, by opium and bits of 
ice ; and the cardiac weakness, by stimulants. 

APPENDIX. 

PERNICIOUS JAUNDICE. CHOL^MIA AND ACHOLIA. 

Reference has been repeatedly made in the preceding chapters to the possibil- 
ity of the sudden supervention of grave nervous derangements in the course of 
various hepatic diseases. These nervous symptoms resemble each other so much 
in the different instances of their occurrence that we are forced to believe them 
always due to the same cause. 

These symptoms are relatively most frequent where there is chronic biliary 
retention. Whether this retention be the result of obstruction of the common or 
the hepatic duct, or of stenosis of the biliary passages from a carcinoma involving 
the opening of the common duct into the duodenum, or that duct itself, the patient 
may quite suddenly fall into a condition which in many respects corresponds to 
the second stage of acute yellow atrophy just described. Grave cerebral disturb- 
ances declare themselves, with delirium, convulsions, and coma. There are haem- 
orrhages into the skin and into the mucous membranes, and in a few days the 
patient dies. Usually the end is attended with high fever. We have ourselves 
seen a temperature of 107*4° (41*9° C.) in a case of cancer at the duodenal 
extremity of the common duct. It is this group of symptoms which is usually 
termed pernicious jaundice ; but almost precisely similar phenomena may sud- 
denly appear in hepatic cirrhosis, when there is no great degree of jaundice, 
if any. 

Just what produces these grave results in acute yellow atrophy and the other 
disorders just enumerated, we are not certain. Three theories have been pro- 
pounded in explanation. The first theory, the latest champion of which is Ley- 
den, attributes pernicious jaundice to cholsemia — that is, to the accumulation in 
the blood of the constituents of bile, and in particular of the biliary acids, as a 
result of absorption. This accumulation, it is said, is promoted by the paralyzing 
effect of the jaundice upon the activity of the kidneys. Opposed to this theory is 
the fact that these same symptoms may occur where there is no marked hepa- 
togenous jaundice. 

Traube has suggested that as a result of the great impairment of nutrition 
there is a cerebral anaemia, which in its turn brings on the nervous attacks. 
Cohnheim also advocated this view, with some modifications. 

The view which we are most inclined to accept is that of Frerichs. He has 
given to the group of symptoms under discussion the name of acholia. These 
symptoms he ascribes to the pernicious influence of those substances which under 
normal conditions are manufactured by the liver into bile, but which in such cases 
accumulate in the blood and the tissues. As Frerichs himself has said, and we 
believe very justly, this view should be extended to include all other transforming 
functions of the liver, and especially the production of urea. It is also very pos- 
sible that, in addition to the acholia, cholaemic poisoning may sometimes exert a 
simultaneous influence. 

The termination of cholaemia or acholia is almost always as unfavorable as 
that of acute yellow atrophy. In cases of this kind there is usually marked fatty 
degeneration of the hepatic parenchyma to be found post mortem. 



460 



DISEASES OF THE DIGESTIVE ORGANS. 



CHAPTER VII. 

ICTERUS NEONATORUM. 

{Jaundice of the New-bom.) 

Frequently the normal red color of the skin in children changes on the 
second, third, or fourth day after birth to a distinctly yellow, jaundiced hue. The 
yellow tinge is deeper on the face and trunk than on the extremities. There are 
no special digestive or constitutional disturbances. Still it may be taken for the 
rule that weaklings more often present this jaundice than do vigorous babes. 
The abnormal hue is almost certain to vanish in a week or two, and leave no 
sequelae. The termination is unfavorable in those instances alone where there is 
some special complication, not directly connected with the jaundice as such. 

The aetiology is a disputed matter. A large number of all sorts of theories have 
been set up, no one of which to this day has gained universal acceptance. For- 
merly there was considerable tendency to regard the jaundice as haematogenous— 
that is, due to the transformation of the pigment of broken-down blood-corpuscles 
into bile-pigment. Points which seemed to support this view are the light (not 
jaundiced) color of the urine and the yellow co]or of the stools (from bile). But 
more accurate examination has shown that the urine does contain biliary pig- 
ment, as do also the kidneys of such infants as happen to die during the existence 
of the jaundice ; and the biliary acids have been clearly shown to be present in 
the serous transudations. It may therefore be considered certain that icterus 
neonatorum is hepatogenous ; but how the biliary retention and consequent 
absorption are caused we do not know. Perhaps at first the bile is not ejected 
properly, from weakness, or the ducts may be narrow, or temporarily plugged by 
desquamated epithelium. We should also consider, as Hofmeier points out, that 
probably during the first few days of extra-uterine life there is a comparatively 
large amount of bile secreted, occasioned by the destruction in considerable num- 
bers of the red blood-globules. 

It is well to mention in conclusion that in very rare instances there is complete 
congenital stenosis, or even entire absence, of the larger bile-ducts. Then deep 
jaundice comes on soon after birth, and is persistent. The children become 
extremely emaciated, and, after a few weeks, inevitably perish. 



CHAPTER VIII. 
SYPHILIS OF THE LIVER, 

iEtiology and Pathology. — Syphilitic disease of the liver occurs both when the 
syphilis is acquired and when it is congenital. Congenital syphilitic disease of 
the liver may be diffuse or localized, and causes a cellular infiltration in either 
case. If the changes are extensive, the organ is hard and considerably enlarged; 
or, if the newly formed connective tissue has undergone contraction, the liver is 
smaller than normal, and its surface is uneven. In some cases of hereditary 
syphilis, distinct gummata of considerable size have been observed. 

In acquired syphilis, hepatic disease is one of the so-called tertiary symptoms, 
and does not usually develop, at least to any great extent, until several years after 
infection. Indeed, it may be a very late result. It may take the form either of 
a diffuse syphilitic hepatitis, or of circumscribed gummata or syphilomata. The 



SYPHILIS OF THE LIVER. 



461 



diffuse hepatitis does not present essentially different anatomical appearances from 
those of ordinary cirrhosis. The gummata are the most characteristic, and the 
most important clinically. They may form separate tumors the size of an apple 
or even larger. The convex surface of the organ, particularly that portion near 
the suspensory ligament, seems to be a favorite location for the new growth. The 
same is true of the porta hepatis, where Glisson's capsule enters the liver. At the 
autopsy the gummata have in most cases already begun to undergo contraction. 
If so, the liver is usually smaller than normal, and traversed in various directions 
by deep furrows, which divide it into lobes. These furrows are due to firm cica- 
tricial bands, among the fibers of which we may sometimes find necrotic and 
cheesy vestiges of the gumma proper. Often there is evident syphilitic endarteri- 
tis in the smaller and sometimes also in the larger branches of the hepatic artery 
and portal vein. 

Clinical History. — Circumscribed syphilitic changes in the liver often give rise 
to no symptoms whatever. It is only when the disease comes to disturb the portal 
circulation that a series of symptoms result, which, for evident reasons, may be 
analogous in all essential points to the effects of ordinary cirrhosis. "Whenever 
the syphilitic growths contract so as to obliterate a large number of branches of 
the portal vein, or whenever a gumma happens to be so situated as to compress 
the trunk of the portal vein itself, then the well-known results of portal obstruc- 
tion are inevitable, the chief being ascites and enlargement of the spleen. The 
disturbance of circulation often gives rise also to anorexia and digestive disorders. 
Experience shows jaundice to be rare in hepatic syphilis, but it may appear 
when the lesions involve the larger bile-ducts or a considerable number of the 
smaller biliary passages. 

On physical examination, the results vary according to the form and the stage 
of the disorder. Sometimes the larger gummata may be plainly felt through the 
abdominal walls, usually as flattened hemispheres. Frequently, also, we can feel 
the edge of the enlarged organ, and can detect that the edge is less sharp than 
normal. In other instances the separate elevations and prominences can be made 
out. The area of dullness on percussion of course varies in different cases. 

It deserves mention that hepatic syphilis quite often causes severe pain, some- 
times over the entire region of the liver and sometimes in just one spot. Pain is 
by no means felt in every case. With the pain there may be great tenderness on 
pressure. 

The course of the disease is usually tedious, and may occupy many years. 
Probably, too, lesions exist in many cases long before there are any symptoms. 
Just as in cirrhosis, ascites is usually the first thing to attract the patient's atten- 
tion. Improvement and temporary arrest of the disease are more frequent than 
in ordinary cirrhosis. Still, in most cases, where the lesion's are at all extensive, 
the termination is unfavorable. 

The diagnosis is not always easy. Usually the objective changes in the liver, 
the ascites, and the enlarged spleen, indicate hepatic trouble, but we are often 
unable to determine just what the trouble is. Naturally, the setiological factors 
are of great importance. In a toper we would think rather of the common form 
of cirrhosis. If there is a syphilitic history, or if we find scars in the throat, irregu- 
larities in the surface of the bones, or other signs of a specific dyscrasia, we would 
naturally ascribe the hepatic disorder to the same cause. As to special signs, if 
the prominences on the liver are rather large in contrast to the smaller granula- 
tions of common cirrhosis, syphilis is somewhat more probable. Severe pain in 
the right hypochondrium also suggests syphilis rather than cirrhosis. 

Treatment— Whether we feel certain that syphilitic hepatitis exists, or merely 
suspect it, specific treatment should be tried. Mercury and potassic iodide should 



462 



DISEASES OF THE DIGESTIVE ORGANS. 



both be given, but probably the iodide is the more valuable of the two. But these 
remedies can be successful only when the gummata are still in process of forma- 
tion. Our therapeutic efforts produce no impression upon the cicatricial bands, 
the contraction of which is the main cause of derangement. Hence we see why 
the results of treatment in advanced cases are seldom very favorable. 

For symptomatic treatment, the reader is referred to cirrhosis of the liver. 



CHAPTEE IX. 
CANCER OF THE LIVER AND BILE-DUCTS. 

iEtiology and Pathology. — Primary cancer of the liver is very rare, but sec- 
ondary or metastatic cancer of this organ is met with comparatively often. The 
chief explanation of this latter fact is the slowness of the blood-current in the 
liver, which favors the deposition of the cancerous germs suspended in the blood. 

Secondary hepatic cancer may be a sequel to primary cancer of any organ. 
It is most often seen, however, when the primary growth lies within the portal 
system, in the stomach, intestines, rectum, oesophagus, or pancreas. In some in- 
stances the projection of the primary growth into the lumen of a branch of the 
portal vein has been directly demonstrated, thus furnishing an obvious source for 
metastasis. The secondary cancers in the liver may be very numerous. They are 
found both within the organ and upon its surface. If superficial, they form flat- 
tened protuberances, which are often dimpled in the middle. If the new growth 
is extensive, the liver may be greatly enlarged, so as to occupy a great part of the 
abdominal cavity. 

As we have said, primary cancer of the liver is very unusual. It may occur 
either in the form of separate large nodules, or as a more diffuse cancerous infil- 
tration pervading the greater part of the organ. Histologically considered, the 
primary growths are of cylindrical-cell carcinoma, apparently originating from 
the epithelium of the minute bile-ducts, but also, according to some authors, 
sometimes starting from the cells of the parenchyma. 

Primary cancer of the larger bile-ducts is of more frequent occurrence than 
genuine primary hepatic cancer, and therefore it is of more importance clinically. 
The gall-bladder may also be the seat of primary carcinoma. From these sources 
may proceed abundant metastatic growths in the liver itself. 

As to the aetiology of hepatic cancer we can be brief. The disease is most fre- 
quent in advanced life, from forty to sixty, following in this the general rule for 
cancer. Special causes are not known. It sometimes seems possible to trace a 
hereditary predisposition to it. 

Clinical History— Diagnosis— Many small nodules of cancer, as well as large 
masses which are favorably situated, may exist in the liver without exciting any 
symptoms. If there is an undoubted primary cancer in another organ, such as 
the stomach, we must always remember the possibility of metastatic growths in 
the liver ; but they can not be proved to exist, unless they alter appreciably the 
size or shape of the organ. Sometimes they may be inferred, when we observe 
either ascites and enlargement of the spleen from pressure on the portal vein, or 
jaundice from pressure on the bile-ducts. 

On palpation, we are often able to make out one or more tumors plainly in 
hepatic cancer. These tumors are in the region of the liver, and they are directly 
connected with it, as we can prove by marking out its limits by percussion and 
palpation. Another characteristic sign is that almost all hepatic tumors can be 



CANCER OF THE LIVER AND BILE-DUCTS. 



463 



felt to move with respiration, on account of the inspiratory depression of the dia- 
phragm pushing down the liver and all that is joined to it. Percussion over a 
hepatic tumor almost invariably gives flatness, in contrast to the muffled tym- 
panitic resonance of many gastric tumors. 

The most characteristic condition is not a very rare one ; in it the liver is the 
seat of a very large number of cancerous nodules. In such cases the organ is 
usually much enlarged. Often we can detect by mere inspection a great, irregular 
prominence in the hepatic region, pressing forward the flabby, atrophied walls of 
the abdomen, and reaching down to the level of the umbilicus, or even lower. 
On palpation, we can feel most of the anterior surface of the liver, and the sepa- 
rate cancerous nodules scattered over it. These usually are as large as walnuts, 
or even apples. The lower or anterior margin of the liver can often be made out 
plainly, and it also is often the seat of nodules ; and we can sometimes feel nodules 
on the lower surface of the organ. 

The other clinical phenomena in hepatic cancer have several causes : (1) The 
primary disease, such as cancer of the stomach ; (2) the general cancerous cachexia, 
as shown by languor, emaciation, and possibly a slight oedema of the ankles ; and 
(3) the possible compression of the blood-vessels or bile-ducts. This compression is 
not infrequent, and produces a moderate or even a large ascitic effusion. Even in 
these instances the spleen is seldom much enlarged as a result of the passive con- 
gestion, because the universal emaciation and anaemia counteract the tendency to 
increase in size. Jaundice is relatively more frequent in cancer of the liver than 
is ascites. It is caused by compression either of the hepatic duct or of the minuter 
bile-ducts. On the other hand, however, we can easily see that hepatic cancer 
may exist without producing either icterus or ascites. 

The differential diagnosis of hepatic cancer from cancer in other organs is 
sometimes extremely difficult. This is particularly true of pyloric cancer, and 
especially so when the pylorus has become adherent to the liver, which often is the 
case. Cancers of the omentum and of the colon sometimes simulate hepatic cancer, 
but they seldom move so decidedly in respiration as do hepatic tumors. Given a 
new growth in the liver, it is usually comparatively easy to distinguish between 
carcinoma and other tumors. The benign growths, like adenoma, are so rarely 
found in the liver that they can actually be almost disregarded. If there are 
syphilitic growths, we may be aided by the history of the case and other signs of 
syphilis, or by the eventual contraction and atrophy of the organ. Echinococci 
have, as a rule, a much more regular shape, like a flattened sphere. Large 
abscesses are rare in our latitudes; and if they occur, usually the astiology is 
significant. They also frequently cause fever and rigors, which cancer does 
not. 

When we have decided that cancer of the liver is present, the question arises, 
Is it primary or secondary ? In the first place, primary cancer here is so rare that 
the probabilities are in favor of a secondary growth. Not infrequently the 
primary tumor can not be detected during life. Thus a small cancer of the 
stomach, or a flat oesophageal cancer, or carcinoma of the pancreas, are all easily 
overlooked. If we find many nodules in the liver and no primary trouble else- 
where, then there comes the possibility that there is primary cancer in the gall- 
bladder or the bile-ducts. In rare instances palpation may discover the gall- 
bladder in a state of cancerous degeneration close underneath the liver ; but 
usually the viscus will be small and contracted, and the flat and ulcerating growth 
is not noticeable, except from the inside. It is particularly in those cases of hepatic 
cancer where there is great and persistent icterus, and no evidence of carcinoma in 
any other organ, that we should be most apt to think of primary cancer of the bile- 
ducts. 



464 DISEASES OF THE DIGESTIVE OEGANS. 



The duration of hepatic cancer is usually not prolonged. The first decided evi- 
dences of its existence no sooner present themselves than marasmus and cachexia 
rapidly develop. The fatal end comes in a few months, or at latest within a year. 

The prognosis is hopeless. Treatment can avail only to alleviate somewhat 
the patient's sufferings. 



CHAPTER X. 



ECHINOOOOOUS OF THE LIVER. 



Natural History and Pathology. — Inasmuch as it is the liver which suffers 
most frequently from invasions of the echinococcus, we will here state the main 
general points relative to the troubles produced by this parasite. 

The taenia echinococcus (see Fig. 52) is a small tape-worm about four milli- 
metres long, and composed of three or four joints. It inhabits the intestinal 
canal of the dog. Man becomes infected by the ingestion of the eggs of this tape- 
worm into the stomach. The striking prevalence of the disease in Iceland is 
explained by the fact that the inhabitants live in constant 
contact with their numerous canine friends. Among us 
the echinococcus is comparatively rare. 

If a human being has become infected, the blood-current 
carries the embryo into some organ. In a great majority 
of cases it passes through a branch of the portal vein into 
the liver and there fastens itself ; but the echinococcus may 
be developed in other organs — like the lungs {vide page 
234), the bones, the brain and the kidneys. A hydatid cyst 
develops from the embryo, and is filled with a non-albu- 
minous fluid. The cyst is composed of an external cuticle 
of lamellated structure, and au inner, parenchymatous 
layer, which contains muscular fibers and blood-vessels. 
Surrounding the cyst, as it lies in the infested organ, there 
is gradually developed a thick capsule of connective tissue. 

After the cyst has continued its growth for some four to 
six months, being now about the size of a walnut, there 
are generated upon the inner surface of the capsule, from 
the parenchymatous layer, so-called breeding capsules, 
containing numbers of echinococcus-heads, or " scolices." 
Each scolex has four suckers and a circlet of hooks. It 
can draw itself into the breeding capsule and produce a 
prominence upon the outer surface of the latter (see Figs. 
53, 54, and 55). 

Usually the primary cyst gives rise to secondary " daugh- 
ter vesicles," and these to " granddaughter vesicles." Some 
of these are formed in the cuticle, others from the breeding 
capsules. In man they generally grow inward — that is, 
are endogenous (echinococcus hydatidosus^, and finally 
become detached. Hundreds of them may sometimes be found free in the liquid 
contents of the cyst. In animals the daughter vesicles are more often exogenous 
(echinococcus veterinorum seu granidosus). A peculiar kind of echinococcus, 
which was formerly regarded as a kind of new growth, is that called by Virchow 
echinococcus multilocularis. This gives rise to a hard tumor, which is composed 



I 



Fig 



. 52.— (From Heller.) 
Taenia echinococcus, 
enlarged. Above, at 
the right, echinococ- 
cus, of natural size. 



ECHINOCOCCUS OF THE LIVER. 



465 



of vesicles the size of a pea, and which seems to grow along the lymph- vessels, and 
possibly in the blood-vessels also. 

The growth of a hydatid cyst is slow, and may continue for years. It may 
finally attain the size of a child's head. At last, however, the echinococcus dies. 





Figs. 53 and 54.— (From Heller.) Echinococcus scolices, 
free, drawn in and turned outward. 



f 



Fig. 55. — Echinococcus 
hooklets. 



The cyst then undergoes considerable though gradual contraction, and both walls 
and contents become calcified. 

Clinical Phenomena. — As long as the cyst in the liver retains moderate dimen- 
sions, there is usually no discomfort. Frequently the cysts perish and become 
calcified, without having ever attracted attention, and are found post mortem 
merely by accident. 

If the cyst becomes very large, it causes a sensation of pressure and pain in the 
hepatic region. In rare instances, unusually large cysts, if situated on the convex 
surface of the liver, may crowd up the diaphragm so as to compress the lower 
portions of the lung and induce dyspnoea. Again, the cyst may be so situated as 
to compress the portal vein or a large bile-duct. Then appear ascites and enlarge- 
ment of the spleen, or jaundice, as the case may be. 

It is an important fact that sometimes the cyst ruptures and discharges its 
contents into neighboring parts. Thus in repeated instances the pleural cavity 
has been invaded ■ also the lungs, as evidenced by the expectoration of vesicles ; 
the intestinal canal, with the appearance of vesicles in the stools ; the bile-ducts, 
followed by jaundice and the eventual appearance of vesicles in the intestine ; the 
vena cava inferior, causing sudden death from pulmonary embolism ; and some- 
times it perforates outward through the abdominal walls, and terminates in 
recovery. Exceptionally, the echinococcus-sac undergoes purulent inflammation, 
with all the symptoms of a hepatic abscess. 

A multilocular echinococcus usually excites grave disturbance. The liver is 
decidedly enlarged, and generally is firm and smooth, not uneven, to the touch. 
As a rule, there are jaundice, swelling of the spleen, and ascites, and accompany- 
ing these a gradual loss of flesh and strength, ending fatally. 

A diagnosis is sometimes easily reached if the cysts can be felt upon the surface 
of the liver. Usually the tumors are flat or globular, and of firm consistence, 
though often evidently elastic. A peculiarly characteristic sign, though one which 
is seldom obtainable, is the "hydatid thrill." It is felt upon giving the tumor a 
quick, short blow with the flat of the hand. The diagnosis is certain if, in any 
way, echinococcus vesicles are discharged. Aspiration for purposes of diagnosis 
has been repeatedly performed. The fluid thus evacuated is light-yellow, almost 
always non-albuminous, and, upon microscopic examination, sometimes presents 
fragments of the lamellated membrane, or some of the hooklets. But if we do 
not find these morphological elements, we are by no means warranted in exclud- 
ing echinococcus. Chemically, the fluid should yield sugar and succinic acid. 
This fact may perhaps aid diagnosis. 
30 



466 



DISEASES OF THE DIGESTIVE OEGANS. 



Frequently it is difficult to distinguish between an echinococcus of the liver 
and other hepatic disorders. We may need to consider all the circumstances — 
causation, age, fever, shape of the tumor, or perhaps the results of an exploratory 
puncture. Large cysts, which crowd themselves upward into the pleural cavity 
may simulate a pleuritic effusion. 

Treatment. — The administration of internal remedies is extremely unreliable. 
Iodide of potassium and mercury are especially recommended. It is, however, 
operative interference alone that holds out any promise of success ; but this has 
its dangers, and should, therefore, be held in reserve till the symptoms become 
grave or very distressing. For details of the numberless methods of operation 
which have been proposed, we would refer to works on surgery ; but we may 
mention here that simple aspiration of the contents of the cyst sometimes affords 
permanent relief ; the cyst becomes obliterated, and there is complete recovery. 
In a few cases, after the sac has been emptied, tincture of iodine has been injected. 
Most of the other methods aim (1) to bring about adhesion of the sac to the abdomi- 
nal walls, and (2) to lay it open and evacuate the contents. At the surgical clinique 
in Leipsic the favorite and a very satisfactory method is to employ a caustic paste, 
made with chloride of zinc, which slowly effects an opening of the cyst, and, by 
the adhesive inflammation it excites previously, fixes the cyst to the abdominal 
walls. Simon's method is to thrust in several trocars, at intervals from one another, 
and allow them to remain till adhesions are formed. Then the points of puncture 
are united by an incision, the sac emptied, syringed out, disinfected, and allowed 
to heal gradually. 



CHAPTEE XI. 
CIRCULATORY DISTURBANCES IN THE LIVER. 

1. Hepatic anaemia is seldom extreme except in cases of profound general 
anaemia, and has no clinical importance, as far as we are aware. 

2. Passive congestion of the liver is of frequent occurrence and is of importance. 
It may arise in any disorder which disturbs the systemic circulation. It is 
oftenest seen in connection with heart disease, particularly mitral disease. It 
also follows pulmonary emphysema and chronic processes which result in con- 
traction of the lungs. The liver is enlarged and engorged. The hepatic veins 
being situated in the center of the lobules, this central portion becomes darkly 
pigmented, while the periphery of the lobules seems lighter colored. The periph- 
eral cells may even appear distinctly yellow, from a fatty infiltration which is not 
infrequent. In this way the cut surface comes to present that variegated appear- 
ance which has led to the name of " nutmeg liver. 1 ' If the venous stasis be persist- 
ent, there is considerable atrophy of the hepatic parenchyma, involving especially 
the cells near the center of each lobule. Thus the liver atrophies, and its surface 
may become slightly granular. This is the " atrophic nutmeg liver." 

The clinical phenomena are chiefly those due to the hepatic enlargement. If 
chronic cardiac disease, emphysema, or some analogous trouble has occasioned 
congestion of the liver, the area of hepatic dullness is increased, and frequently 
we can feel the edge or even a portion of the anterior surface. In pronounced 
cases the organ may extend almost a hand's breadth below the ribs. Often there 
is a slight jaundice. Sometimes it is quite marked. It is probably due to the dis- 
tended blood-vessels compressing the smaller bile-ducts. We have already men- 
tioned how characteristic, in many cardiac cases, is a complexion presenting both 
cyanosis and jaundice. 



ATROPHY OF THE LIVER. 



467 



Quite often the congestion, if great, produces subjective disturbances. There is 
a feeling of pressure and weight in the hepatic region ; and if the capsule of the 
organ is tightly stretched, there may be actual pain. 

The prognosis and treatment depend, of course, upon the primary disorder. 

3. About active hyperemia of the liver we have little definite information. 
Formerly there was a great deal said about it, as one of the conditions in 
"abdominal plethora." Active hyperemia is most frequently assumed to exist 
in case of those who are good livers and of sedentary habit. In such, we are 
told, the temporary physiological hyperemia which attends digestion passes on 
into a permanent congestion of the liver. Thereby the organ is enlarged, there 
are painful sensations in the right hypochondrium, digestive disturbances, and 
occasional slight jaundice. The abnormal condition just described is certainly 
often met with in practice, but it would seem hardly possible to draw a clear 
dividing-line between active hyperemia of the liver and other disturbances 
which give rise to similar symptoms. Such are chronic gastric and intestinal 
catarrhs ; cardiac hypertrophy and functional cardiac derangement, with passive 
congestion of the liver ; fatty liver ; and incipient cirrhosis. 

A prominent factor in the production of active hyperemia of the liver is also 
ascribed to the ingestion of such matters as are said to " irritate the liver, like 
the various spices, coffee, and, above all, alcohol. 

It should also be noted that the liver may be much engorged in many acute 
infectious diseases, particularly in pernicious malarial diseases and in typhus or 
typhoid fever. 

It is also maintained that the hypersemia may result from the cessation of 
haemorrhages elsewhere, such as the catamenia or bleeding from haemorrhoids. 
The facts that have been brought forward to sustain this view are none of them 
conclusive. We will mention that the " menstrual jaundice " which occasionally 
appears when the menses are scanty or absent has been referred to a vicarious 
hyperemia of the liver. 

It is, of course, impossible to make general statements about the course and 
duration of active hyperemia of the liver. The treatment of the first variety 
mentioned — namely, that arising from an improper mode of life — demands careful 
regulation of the diet, abundant exercise in the open air, like horseback-riding, 
and laxatives. We may give rhubarb, aloes, or a course of the waters at Carlsbad, 
Marienbad, or Kissingen. 



CHAPTER XII. 

ATROPHY, HYPERTROPHY, AND DEGENERATIONS OF THE LIVER. 

1. Simple Atrophy of the Liver.— Simple atrophy is not of rare occurrence, 
being seen in senile marasmus, and in malnutrition from almost any cause. The 
degree of atrophy varies. The borders of the organ are much wrinkled. The 
lobules seem decidedly smaller than normal, and even the individual cells that 
still remain are atrophied and also usually deeply pigmented. 

The condition does not of itself give rise to any special symptoms. The area 
of hepatic dullness is usually lessened, but this sign is too ambiguous ever to 
justify us in making from it a diagnosis of hepatic atrophy. Perhaps there is 
some value in the alleged lighter color of the stools, as indicating a diminished 
secretion of bile. 



468 



DISEASES OF THE DIGESTIVE OKGANS. 



2. Hypertrophy of the Liver. — Even under normal circumstances the liver 
undergoes quite marked alterations in size. The exact point, therefore, where an 
abnormal hypertrophy begins can not be set. Sometimes the autopsy reveals an 
unusually large liver, of which there had been no indications during life, and for 
which no cause can be made out. 

There are certain diseases in which enlargement of the liver is found with 
comparative frequency : diabetes mellitus, chronic malarial poisoning, leukaemia, 
and sometimes rachitis. Topers quite often have enlarged livers, which as a rule 
present simple hypertrophic changes. Occasionally a liver has been reported as 
showing spots of localized hyperplasia, which may form flattened prominences 
upon the surface of the organ. 

Hypertrophy is to be diagnosticated only when palpation and percussion give 
proof of an enlargement, and yet amyloid, hypertrophic cirrhosis, and other dis- 
eases which cause an increase in the size of the liver, can be excluded. The aeti- 
ology of the case should also be considered. 

3. Fatty Liver. — This name is applied to excessive, diffuse, fatty infiltration of 
the hepatic cells. The size of the organ is increased. It is firm, anaemic, and of a 
uniform yellow color, both externally and upon section. The microscope shows 
that the cells of the parenchyma are filled with large and small globules of fat. 
The fat is most abundant toward the periphery of the lobules. 

The causes of fatty liver are by no means clear. Sometimes it is found in 
cases of general obesity, where we may assume that the amount of fat which the 
liver receives as nourishment is abnormally great ; but often we find a liver that 
contains comparatively little fat in those who have a well-developed panniculus 
adiposus and much fat in other organs. Topers may have a decidedly fatty liver. 
The occurrence of fatty liver in the cachectic, and particularly in the consumptive, 
is remarkable ; and individuals suffering from cancer, or marantic children, may 
also exhibit the same change. We have no intimate knowledge of the conditions 
that prevent, in such cases, the oxygenation of the fat which comes to the liver 
from the ingesta or from other organs. 

We do not know that the fatty liver is in any way functionally impaired. The 
only clinical indication, therefore, of its existence is the increased bulk of the 
organ. In phthisis we may sometimes feel pretty certain that the liver is fatty, if 
an increase in bulk can be demonstrated, and if other causes for this enlargement, 
like amyloid, appear improbable. If the anterior edge of a fatty liver can be felt, 
it is usually found to be noticeably thick and blunt. 

The treatment of fatty liver is to combat the original disease. 

4. Amyloid Liver (Waxy Liver). — Amyloid degeneration of the liver is almost 
invariably a part of extensive amyloid disease, involving also the spleen, kidneys, 
intestine, and other organs. The disease occurs chiefly in certain cachectic condi- 
tions, such as chronic suppuration, as in caries and persistent empyema, and also 
in chronic pulmonary tuberculosis, and constitutional syphilis. 

The amyloid liver is usually increased in bulk. The organ may even become 
almost double its normal size. It feels very firm and hard, its surface is perfectly 
smooth, and its edge is slightly thickened. The cut surface presents a character- 
istic grayish-brown u waxy " appearance. 

The microscope shows that the degenerative process attacks chiefly the walls of 
the hepatic capillaries, the hepatic cells proper showing infrequent and slight 
amyloid changes. Very often the cells of the parenchyma are atrophied and 
somewhat infiltrated with fat. 

The diagnosis of amyloid liver requires (1) the demonstration by palpation and 
percussion of hepatic enlargement. We can often feel a large part of the anterior 
surface and the margin of the hard and firm organ. The liver may reach as low 



ANOMALIES IN THE SHAPE AND POSITION OF THE LIVER. 469 



as the level of the umbilicus. The diagnosis further demands (2) that some dis- 
ease which predisposes to amyloid be present, and (3) that there be evidence of the 
degenerative process in other organs : the spleen should be enlarged, and the kid- 
neys secrete albuminous urine. 

The other symptoms, as well as both prognosis and treatment, are determined 
mainly by the nature of the causative affection. About amyloid disease in general 
see the chapter on amyloid kidney (page 812). 



CHAPTER XIII. 

ANOMALIES IN THE SHAPE AND POSITION OF THE LIVER. 

1. Corset Liver. — The constant pressure of the lower ribs against the liver, as a 
result of tight lacing, often produces an atrophy of the hepatic parenchyma from 
pressure, as shown by a deep furrow crossing transversely the anterior surface of 
the organ. This " corset furrow " lies chiefly in the right lobe. Its usual situation 
corresponds to the margin of the ribs, and the atrophy may be so extreme that the 
liver is divided into a large upper part and a small, usually roundish, lower portion, 
connected by a narrow isthmus of tissue. At the atrophic place, the connective- 
tissue capsule of the liver is almost always much thickened. Often the lower sec- 
tion can be bent upward as if attached by a hinge. 

This deformity of the liver is found quite often in elderly females, and rarely 
in men, as in soldiers. Unless extreme, it can not be detected during life, and 
causes no discomfort. The bad cases even do not, as a rule, occasion any special 
symptoms ; but they can be clearly made out if the abdominal walls are lax. The 
deep transverse furrow can be felt, and also the lower section, with its usually 
blunt edge. Particularly in the case of old women we must bear this condition 
in mind, else we might easily confound it with some enlargement of the liver, like 
amyloid or passive congestion, or even new growths. 

In rare instances there are clinical symptoms. A constant sensation of press- 
ure and pulling is felt in the hepatic region ; and sometimes, as a result of venous 
stasis, there is a temporary but decided swelling of the isolated portion, and pos- 
sibly violent pain and indications of irritation of the peritoneum, such as vomit- 
ing and an approach to collapse. Usually rest in bed and cold applications give 
speedy relief ; but relapses are possible. 

2. Movable Liver. — A movable or "wandering" liver is of very rare occur- 
rence, and has thus far been seen only in women. Its cause is not perfectly deter- 
mined. Probably the suspensory ligament is abnormally long. The liver does 
not occupy its usual position, but lies deep in the lower part of the abdomen. 
Here it can be plainly felt, and, by external pressure, it can generally be brought 
back into its normal place with considerable ease. It is always abnormally mov- 
able, and can be shown to change its position when the patient changes from one 
side to the other. 

In most cases a movable liver causes considerable discomfort, particularly pain 
and digestive disturbances. The only way of affording relief is by applying a 
bandage which may maintain the organ in its proper position. 



4:70 



DISEASES OF THE DIGESTIVE ORGANS. 



CHAPTER XIV. 

SUPPURATIVE PYLEPHLEBITIS. 

{Purulent Inflammation of the Portal Vein and Us Branches.) 

^Etiology.— Purulent pylephlebitis is seldom a primary, idiopathic disease. In 
most instances it is due to the propagation of a suppurative inflammation of 
neighboring tissues to the walls of the vein. The main trunk of the portal vein 
is rarely directly attacked. Usually the process originates in the hepatic branches 
of the vein or in the veins of the portal system, and thence extends to the larger 
vessel. 

Perityphlic abscess is the most frequent source of suppurative pylephlebitis. 
The inflammation involves a mesenteric vein, and thence extends upward. Other 
causes are gastric ulcer, intestinal ulcers, as in dysentery, splenic abscess, and 
purulent inflammation at the porta hepatis or within the liver itself, as in abscess 
due to gall-stones. The mode of production in these cases is precisely analogous 
to that in perityphlitic abscess ; but they are rare. 

A special form of pylephlebitis is observed in the new-born. Here the inflam- 
mation originates in the umbilical vein, and we need hardly say that the cause is 
a septic infection through the navel. 

In rare instances it has been found that pylephlebitis has resulted from the 
penetration into a vein of some foreign body that had been swallowed, such as a 
pin. Here, too, the true factors in producing the inflammation are, of course, 
the bacteria which adhere to the foreign body. 

Pathology. — Where the inflammation has attacked the vascular walls, the vein 
is thickened, and often the surrounding connective tissue is infiltrated with pus- 
cells and mottled with minute ecchymoses. If the vein is cut open, the intima 
is seen to be opaque and often superficially ulcerated. The lumen of the vessel 
is filled with a thrombus, which is usually to a great extent in a state of purulent 
softening, so that offensive purulent or sanious fluid flows out. The course of 
events is as follows : First, the wall of the vein becomes inflamed. As a conse- 
quence of this, a thrombus forms at the same place. The bacteria penetrate this 
thrombus and occasion its purulent softening. 

The extent of a pylephlebitis naturally varies in different cases. As a rule, 
little fragments become detached from the thrombus and enter the liver, produc- 
ing metastatic abscesses. Secondary suppuration may also occur in the lungs, 
kidneys, brain, and joints, so that we have all the anatomical characteristics of a 
general pyaemia. 

Clinical History. — Inasmuch as the primary, causative disease may be very 
different in different cases, it is impossible to delineate the disease comprehen- 
sively. It is, however, frequently ushered in by a number of symptoms, which 
render a diagnosis possible, at least in some cases, if the original disease has 
been recognized. 

The symptoms of suppurative pylephlebitis are in part due directly to the local 
disease itself, and in part are occasioned by the general pyaemia. One of the local 
symptoms is pain in the epigastrium. This is rare. It may radiate downward or 
laterally, according to the starting-place and extent of the inflammation. An 
inevitable result of the portal thrombosis is portal obstruction. The spleen 
becomes considerably swollen, and, if the disease be not too quickly fatal, there 
is an evident effusion into the peritoneal cavity. The splenic enlargement 
can not be regarded as due merely to venous stasis, but is in part the " acute 
splenic tumor " of constitutional septic conditions. If the inflammation spreads 



THROMBOSIS OF THE PORTAL VEIN. 



471 



from the branches of the portal vein to the neighboring bile-ducts, jaundice results. 
This is seen quite often. Sometimes it is also due to the hepatic abscesses, or to a 
gall-stone which happens to cause trouble simultaneously. Now and then there 
is no jaundice whatever. 

Of the pyaemic symptoms, hepatic abscesses come first. They are due, as we 
have said, to the conveyance of septic matter directly into the liver by emboli. 
The one almost constant sign of their occurrence is a decided enlargement of the 
liver. Where there are no hepatic abscesses, the organ usually retains its normal 
bulk. 

The course of the fever is very characteristic. As in other pysemic conditions, 
there are almost invariably great elevations, to 106° (41° C), or higher, accom- 
panied by rigors, and followed by marked remissions, with profuse perspiration. 
These onsets of fever occur at irregular intervals, either daily, or every two or 
three days. 

There are at the same time indications of constitutional septic infection, which 
keep increasing in severity. The pulse grows rapid and small. Intelligence is 
impaired. Somnolence and delirium come on, and the strength rapidly fails. 

There are other symptoms. Vomiting is frequently seen. The bowels are sel- 
dom constipated, but usually relaxed. The dejections may contain blood, because 
of the venous stasis. In some cases the inflammation extends so as to produce a 
fatal general peritonitis. It is noticeable that the urine is generally scanty, and 
the amount of urea is strikingly diminished. 

The disease usually runs a rather acute course. On the average, it lasts about 
two weeks, but may occupy three or four weeks, or even a longer period. It is 
invariably fatal. At least, no cases of recovery are known. 

The diagnosis can sometimes be made with considerable positiveness. In other 
instances it is impossible to exclude other pysemic conditions, or abscess due to 
gall-stones, etc. Important factors are the origin of the trouble — if it can be made 
out— the pysemic rigors, the enlargement of the spleen and liver, jaundice, epi- 
gastric pain, and the evidences of general sepsis. 

Treatment is unfortunately almost entirely useless. The fever is not affected 
even by large doses of quinine. All we can aim at is to support and relieve the 
sufferer as far as possible. 



CHAPTER XY. 

THROMBOSIS OF THE PORTAL VEIN. 

(Chronic Adhesive Pylephlebitis. Pylethrombosis.) 

iEtiology and Pathology. — Like suppurative pylephlebitis, chronic portal throm- 
bosis is not an independent disease, but is the sequel of a great variety of pathologi- 
cal conditions. Marantic thrombosis is of rare occurrence, and is usually formed 
toward the close of life, so as not to be of practical interest. Apart from this, 
almost all cases of thrombosis of the portal vein are due to a compression of the 
trunk of that vessel or one of its main branches. This most often occurs in cer- 
tain chronic hepatic diseases which involve a mechanical stenosis, either of the 
smaller branches of the portal vein within the liver, or of the vein itself, with 
resulting coagulation of the blood within it. Chief among these diseases are cirrho- 
sis and syphilis of the liver, which have repeatedly been observed to entail portal 
thrombosis ; but other diseases in the neighborhood of the vein may produce a 
similar effect. New growths of various kinds may press upon the vessel, or chronic 



4Y2 



DISEASES OF THE DIGESTIVE OKGANS. 



inflammatory hyperplasia of the connective tissue at the porta hepatis may act in 
the same way. This is illustrated in chronic peritonitis, whether circumscribed or 
diffuse, an example of the former being sometimes seen as an effect of duodenal 
ulcer. 

It was formerly held that many forms of so-called " lobulated liver " were due 
to a primary adhesive pylephlebitis. This is erroneous. These cases are probably 
all due to some primary hepatic disease, usually syphilitic. The size of the liver 
is little influenced by obstruction of the portal vein, even if long- continued, for 
the hepatic artery suffices to supply all the blood required by the organ. 

The anatomical changes in pylethrombosis do not differ essentially from those 
seen in thrombosis of any other vein. If fresh, the thrombus is still red ; later 
it grows harder, paler, and more friable. If the thrombosis has existed a long 
while, the clot becomes completely organized. We have observed this even in the 
main trunk of the portal vein. 

Clinical History. — The symptoms of portal thrombosis are those occasioned by 
the obstruction, and therefore such as we have already repeatedly met with, in 
connection with various hepatic diseases. The intensity and extent of these results, 
as well as the time occupied in their development, depend, of course, upon the 
place and size of the clot. If it is the portal vein itself which is attacked, and if 
the thrombus is extensive enough to obstruct the flow of blood, then the signs of 
venous stasis are evident throughout the portal system. The spleen becomes 
much enlarged, as can be easily demonstrated by percussion and palpation. Soon 
ascites appears, as a result of the passive congestion of the peritoneal veins ; and 
from a similar condition of the gastro-intestinal veins arise catarrhal disorders, 
like diarrhoea ; or, not so very exceptionally, there is repeated gastric and intesti- 
nal haemorrhage. 

As we have seen, a collateral circulation may be developed {vide page 451), by 
which the venous blood of the portal system is enabled to reach the systemic 
veins. This explains why some of the symptoms of venous stasis may tempora- 
rily (perhaps permanently) vanish. We saw one case of portal thrombosis, the 
sequel to what was apparently a syphilitic disease of the liver, where a quite large 
ascitic effusion appeared some six or seven times at intervals of three to six months, 
and under proper treatment as often abated. The patient did not die till the ill- 
ness had lasted six years, and tapping had been demanded some fifteen times. At 
the autopsy the trunk of the portal vein was found to be converted into a fibrous 
cord, with a lumen which barely admitted a knitting-needle. It is the develop- 
ment of a collateral circulation which causes the frequent distention of the veins 
in the abdominal walls. Sometimes these enlarged veins take the form of the 
" caput Medusa " mentioned above. 

In simple pylethrombosis there are no local symptoms such as pain. The con- 
dition of the liver depends upon the primary disease. It is possible that a moder- 
ate atrophy of the entire organ might at length ensue if the portal blood were 
permanently cut off from it. But, as we have said, any cirrhotic changes, or any 
" lobulation," are not to be regarded as the result, but as the cause of the throm- 
bosis, or at least related to the cause. 

The course and duration of the trouble are according to the nature of the 
original, causative trouble. No general statements can be made. 

The diagnosis of thrombosis of the portal vein is usually extremely difficult, 
and can really hardly ever be made with absolute certainty. We may, indeed, 
recognize readily that there is some decided obstruction to the portal circulation ; 
but whether this be due to a thrombus, or to compression of the portal vein, or to 
the obliteration of a large number of the smaller branches of that vein within the 
liver, we can very seldom determine. Pylethrombosis may be regarded as prob- 



DISEASES OF THE PANCREAS. 



473 



able, if no other possible cause of the portal obstruction seems likely, and if 
we are able to discover a cause for thrombosis, like a former attack of circum- 
scribed peritonitis. 

The prognosis is always unfavorable, although there may be, as we have said, 
great temporary improvement. Treatment must be symptomatic, and follows in 
the main the principles set forth under cirrhosis of the liver. 



APPENDIX. 

DISEASES OF THE PANCREAS. 

The few facts of clinical importance that are known about the pathology of 
the pancreas are given below. 

1. Haemorrhages into the Pancreas of small size occur as one symptom of a 
general haemorrhagic diathesis, or as the result of excessive passive congestion. 
They are of no special importance. Klebs and Zenker have described a few cases, 
however, where there was extensive haemorrhage into this organ, and where this 
was the only discoverable cause of death. The patients had been previously well 
and vigorous, although decidedly obese, and had died suddenly. Perhaps the 
speedy termination was caused by the influence of the haemorrhage upon the 
semilunar ganglion or solar plexus. The cause of the haemorrhage could not be 
determined. 

2. Atrophy of the Pancreas. — The organ may share in a general marasmus. 
There is also extreme atrophy of the pancreas in those who have died of diabetes 
mellitus (q. v.). What relation this change bears to the diabetes is not known. 

3. Pancreatitis. — A few cases have been reported of what would seem to be a 
primary acute pancreatitis. The disease is certainly very rare. It begins with 
violent colicky pains in the epigastrium. Vomiting and collapse soon follow. 
The pulse grows small, the extremities become cool, and death is speedy. At the 
autopsy the pancreas is found to be much enlarged, and mottled with ecchy- 
moses, or even presents scattered foci of suppuration. The aetiology is unknown. 
Secondary abscesses of the pancreas are not infrequent in pyaemia. 

Chronic interstitial pancreatitis sometimes results from the extension of chronic 
inflammatory processes affecting neighboring parts. Friedreich states that it 
sometimes is a primary disease in topers. Syphilitic lesions of the pancreas have 
been observed, occasioning contraction and induration. None of these changes 
give rise to special clinical symptoms; or, if there were a single distinctive 
symptom, it would be one common to all sorts of grave pancreatic disorder — 
namely, the appearance of a large amount of fat in the stools. As we know, the 
pancreatic juice is an important factor in the digestion of fat, so that it is very 
natural for any great derangement of the organ to have this result ; and yet the 
bile alone may render the ingested fat capable of absorption, so that in repeated 
instances there have been no fatty stools when the pancreas has been completely 
atrophied or degenerated. 

4. Cancer of the Pancreas. — Primary cancer is the most frequent, and, there- 
fore, clinically the most important disease of this organ. As a rule, the new 
growth is situated in the head of the pancreas. It is usually of the medullary 
variety, though occasionally colloid. It may involve neighboring parts by direct 
extension, and a great many organs by metastasis ; for example, the liver, peri- 
toneum, and lymph-glands. 



DISEASES OF THE DIGESTIVE OEGANS. 



The clinical symptoms of cancer of the pancreas are very seldom so decided as 
to justify a positive diagnosis. Sometimes the secondary nodules can be detected 
in the liver, peritoneum, and elsewhere. Then we are left in doubt about the seat 
of the primary growth. Or the primary tumor may be plainly felt through the 
abdominal walls ; but then we can hardly ever exclude cancer of the stomach or 
of the omentum, and neighboring parts. 

The symptoms of pancreatic cancer, as a whole, resemble closely those occa- 
sioned by most cancers of abdominal organs. Usually the patient is elderly. The 
first symptoms are loss of flesh and strength, or are the result of compression. 
Often there is complaint of a persistent dull pain in the epigastrium. If the portal 
vein is pressed upon by the tumor, ascites appears. If the common duct is com- 
pressed, there is jaundice. Marasmus increases, and usually at the end of six 
months or a year the patient dies. 

The diagnosis can be said to be somewhat probable in those cases only where 
there are fatty stools, where a tumor can be felt in a position corresponding to the 
pancreas, and where primary cancer of any other organ is unlikely ; but usually, 
as we have said, the symptoms are very ambiguous. There have been no fatty 
stools in a number of cases, even where the cancer was extensive. 

The prognosis is absolutely bad. The treatment is merely symptomatic, with 
the aim of lessening the patient's suffering. 



DISEASES OP THE NERYOUS SYSTEM. 



I. — The Diseases of the Peripheral Nerves. 

SECTION I. 
Diseases of the Sensory Nerves. 

CHAPTER I. 

GENERAL REMARKS UPON THE DISTURBANCES OF SENSIBILITY. 

The disturbances of sensibility, like all other functions of tbe nerves, are mani- 
fested in two directions. Under pathological conditions we observe either an 
abnormal diminution or a complete absence of sensibility — anaesthesia — or a morbid 
increase — hyperesthesia. While in anaesthesia the ordinary, or even the strong- 
est irritations which excite the sensory nerves, produce only a weak and insignifi- 
cant sensation, or even no corresponding sensation at all, in hyperaesthesia very 
severe and painful sensations are caused by weak irritations. The " symptoms of 
sensory irritation " are to be distinguished from hyperaesthesia, although they are 
often present along with it. By this term we mean sensations which cause inter- 
nal irritation, not from without, but from certain abnormal morbid conditions in 
the nerve itself. In the region of cutaneous sensibility, with which we shall 
chiefly concern ourselves in what follows, these symptoms of sensory irritation 
show themselves partly as actual pain and partly as the so-called paraesthesia — 
that is, abnormal sensations in the skin, which are termed " formication " (the 
crawling of ants), " prickling," " numbness," " a funny feeling," etc. 

The Different Varieties of Cutaneous Sensibility and the Methods of testing 
them. — As is known from physiology, the irritation of the sensory cutaneous 
nerves produces in us a number of sensations, differing in quality according to 
the manner of action of the irritation. If, therefore, we would obtain an accurate 
estimate of the condition of the patient's cutaneous sensibility, we must make a 
special test of all the different forms of sensation, for we often see that the disturb- 
ances of sensibility do not involve all the forms mentioned alike, but that one 
kind of irritation is followed by perfectly normal sensations, while there is more 
or less complete anaesthesia for another kind. We term such partial anaesthesias 
of the skin, which are manifest toward only one form of irritation, " partial paraly- 
ses of sensation." Such partial paralyses will be much more easily understood if 
the remarkable statements of Blix, Goldschneider, and others are confirmed. 
According to these statements, the different qualities of cutaneous sensation are 
transmitted to the consciousness by special nerve-fibers, so that there are in the 
skin special nerves for the tactile sense, for the sense of cold, for the sense of heat, 



476 



DISEASES OF THE SENSORY NEBVES. 



etc. Such a condition is analogous to the well-known specific energy of the 
different fibers of the optic nerve to colors, assumed by many physiologists. The 
separate varieties of cutaneous sensibility, and the methods of testing them, are as 
follows : 

1. Tactile Sensibility.— The examination of the tactile sensibility — that is, of 
the sensibility of the skin to simple contact — is usually performed by repeatedly 
touching the part of the skin to be tested with the finger or some other blunt 
object (not of metal, in order to exclude sensations of cold) while the patient's eyes 
are shut, and making the patient say whether he has felt the touch or not. When 
it is necessary to call the patient's attention to the investigation, it is always best 
to do so afresh by asking " Now ? " and then either really touching the skin or else 
asking the question when only pretending to do so. In this way we are safest 
from error, which is otherwise easily produced by a lack of attention or of practice 
on the part of the patient. All accurate tests of sensibility must be repeatedly per- 
formed and controlled in order to obtain sure objective results. 

If , as in most cases, we have to do with disturbances of sensibility which affect 
only a part of the skin, we must make comparative tests of sensibility on the 
healthy and, if possible, symmetrical portions of the skin. Slight disturbances of 
sensibility are then often shown in this way, that the patient feels almost every 
touch on the affected part ; but the sensation always seems to him more indefinite, 
blunter — in short, " different " from that on the corresponding normal portion of 
the body. 

Beside simply touching the skin, we also try how far the patient is able to dis- 
tinguish the form and certain external peculiarities of objects by the aid of his 
tactile sense. We touch the skin with smooth and rough (woolly) or round and 
angular objects, and see whether the patient can distinguish them respectively 
with his eyes shut, and also whether he can distinguish between the head and the 
point of a pin, etc. If we are testing the sensibility of the fingers, we may put 
different well-known objects — like coins, rings, or keys — into his hands, and let 
him name them with his eyes shut. We may also try the last method of testing 
by the aid of a number of wooden geometrical objects, cubes, octahedra, or cones. 

2. Sense of Locality. — Under normal conditions, as we know, not only do we 
feel the touch of an object, but we can tell with a good deal of accuracy the place 
on our skin which was touched. This power we term the ability to localize our 
sensation. In nervous patients we often see that, while cutaneous sensibility is 
still present (we refer not only to tactile sensibility but also to the other forms), it 
is localized more poorly and with less accuracy than is the case under normal con- 
ditions. 

In the simple test of the tactile sense we may also examine, at least roughly, 
the power of localization if we make the patient also state where the touch is felt, 
or if we ask him to designate with his hand as carefully as possible the part of the 
skin touched. A more accurate method, much used in nervous pathology, was 
proposed by E. H. Weber. It consists in determining the smallest distance which 
must separate two simultaneous cutaneous irritants from each other, in order that 
they may be perceived as two locally distinct sensations. Weber has found that 
this distance differs very much in different parts of the body, and from this he has 
divided the whole surface of the skin into so-called tactile circles. As data for the 
examination of patients, some of the figures obtained by Weber in healthy indi- 
viduals may here be given : The smallest distance at which the two points of a 
pair of compasses * applied at the same time to the skin may plainly be distin- 
guished from each other is 11 to 15 millimetres on the cheeks, 6 mm. at the tip of 



* There are special " tactile compasses" with blunt ivory points and graduated quadrants. 



REMARKS UPON THE DISTURBANCES OF SENSIBILITY. 477 



the nose, 22 mm. on the forehead, 1*2 mm. at the tip of the tongue, 4 to 5 mm. at 
the back of the tongue and on the lips, 34 mm. on the neck, 77 mm. on the upper 
arm, 40 mm. on the forearm, 31 mm. on the backs of the hands, 11 to 16 mm. on 
the backs of the fingers, 2 to 3 mm. at the tips of the fingers, 55 to 77 mm. on the 
back, 45 mm. on the chest, 77 mm. on the thigh, 40 mm. on the leg, 40 mm. on 
the instep ; but these figures show certain variations in different individuals, so 
that they are to be regarded as only average values. 

Testing the sense of locality according to Weber's method takes a great deal of 
time, and demands much patience and good will on the part of the patient. The 
influence of practice is manifested in a very remarkable way, since the perceptible 
difference becomes considerably less if the examinations are repeated often. On the 
other hand, a single examination, as in testing any form of sensibility, must not be 
too long protracted, for otherwise the patient may easily become fatigued, and the 
data obtained will be entirely contradictory. If we test the sense of locality by 
bringing down the two points not at the same time but one after the other, and 
vary it by touching the same place twice, or a different place each time, we obtain 
from the outset, as we have repeatedly proved, smaller numbers than if we touch 
the skin with the two points of the compasses at the same time. We also obtain 
some different values for the fineness of the sense of locality if we test the so- 
called sensations of motion (Leube) — that is, the distinction between simple cir- 
cumscribed touch of the skin, and a very short line drawn with a stick on the 
skin. In this way we can also determine whether the patient can distinguish 
accurately the direction of transverse and longitudinal lines. 

We may also mention here the peculiar symptom termed by Fischer poly- 
aasthesia, which is that certain patients, especially ataxics, when the skin is touched 
with only one point of the compasses, have a sensation as if they felt two or even 
more points. The cause of this remarkable anomaly of sensation is not yet 
adequately explained. 

3. Sense of Pressure. — Since E. H. Weber's investigations we know that we 
estimate the difference in the intensity of our sensations of pressure, not according 
to the absolute, but according to the relative increase in the pressure. If, for 
instance, a place in the skin has a weight of nineteen grammes on it, and we 
perceive the first manifest increase in our sensation of pressure when a weight of 
one gramme is added to it ; when the skin has a weight of one hundred and ninety 
grammes on it, we first perceive the increase of pressure not when one gramme is 
added, but when we add ten grammes. If this law, on more accurate testing, is 
not as simply proved as it seems according to the results of Weber's first investi- 
gations; still it is generally a fact that under normal conditions an increase of 
pressure of about one twentieth to one thirtieth of the original pressure may be 
plainly perceived in the different parts of the body. 

Different methods and instruments, like Eulenburg's "baraesthesiometer," have 
been devised for accurately testing the sense of pressure in patients, but they have 
entered but little into practice on account of their elaborate character. We 
usually content ourselves with testing the sense of pressure by applying different 
weights, or coins. We must mention here that the part of the body to be tested 
must be fully supported, that we must also exclude sensations of temperature at the 
same time by putting something beneath the weights, and that we must apply the 
separate weights to the same place on the skin at equal intervals of time, which must 
not be too long after one another. There are cases where the patient does not feel 
even the doubling or tripling of the weights. We can easily confirm a consid- 
erable loss of the sense of pressure by means of pressure with the hand or any 
object. 

Partial paralyses of the sense of pressure are by no means rare. We find quite 



478 



DISEASES OF THE SENSORY NERVES. 



often, especially in spinal diseases, like locomotor ataxia, that the patient feels a 
light touch on the skin, but that he can not distinguish a marked pressure at all, 
or only obscurely. 

4. Sense of Temperature. — The same general rule obtains for the sense of 
temperature as for the sense of pressure — that we can not employ the absolute, but 
only the relative differences of temperature in estimating the intensity of the 
sensation. Within the moderate degrees of temperature, 80° to 100° (25°-35° C), 
differences of a degree Fahrenheit (0*5° C.) are plainly distinguished under normal 
conditions, and even half a degree (0*2° C.) on the face and fingers, but only about 
two degrees (1° C.) on the back. 

The test of the sense of temperature is performed most simply by bringing test- 
tubes, or, better still, little wooden cylinders with metallic bottoms (Nothnagel), 
containing water at different temperatures, in contact with the skin, and having 
the patient give the differences in temperature. Eulenburg has described a special 
" thermaesthesiometer," which, on account of its rather complicated arrangement, 
has met with little favor in practice. This consists of two thermometers movable 
on a standard, with flat vessels for the mercury, in order to apply them to the 
skin. The mercury vessel of one of the two thermometers is surrounded by an 
isolated platinum wire, and may be warmed at pleasure by a galvanic current run- 
ning through this wire. As we set the two thermometers, brought to different 
temperatures, on the same part of the skin, one soon after the other, we can test 
the sensibility of the skin for the given difference in temperature. A simple 
method, which is useful in practice, is to try whether the patient can distinguish 
the cool blowing on the skin from some distance from the warm breathing on it 
from the immediate vicinity. In this way we can easily confirm rough anomalies 
in the sense of temperature. Sometimes, most frequently in ataxics, we find an 
almost complete paralysis of the sense of temperature in certain parts, where sen- 
sibility for other forms of irritation is quite well preserved; but, on the other 
hand, it also happens that patients, who are almost completely anaesthetic to other 
forms of irritation, are still sensitive to marked thermal irritants, especially to cold. 

A peculiar and rare symptom is that termed by us a perverse sensation of tem- 
perature, which is when the patient feels cold irritants, like cold water and ice, as 
decidedly warm. We have found this symptom most distinct in a case of disease 
of the medulla oblongata. It also occurs in rare cases in patients with locomotor 
ataxia. 

5. Sensation of Pain. — The fact is of great theoretical interest that the cuta- 
neous sensibility for touch and pain do not always, under pathological conditions, 
run parallel with each other. We sometimes see that a patient does not feel a 
simple touch on the skin, when sticking a needle into it is immediately painful ; 
while, on the other hand, we often find that a patient feels quite a light touch on 
the skin, but that the most marked irritation, like pinching or pricking it, does not 
excite the slightest pain, but is felt only as a simple touch, or at most as a slight 
pressure on it. This latter condition of sensibility, the loss of cutaneous sensibility 
to pain with retained tactile sensibility, is termed analgesia. Both in peripheral 
and in central nervous diseases analgesia is a symptom that may be quite fre- 
quently observed. 

The test of sensibility to pain may be made most simply by the point of a pin, 
and also by pinching or severe pressure on the skin, by painful thermal irritants, 
by strong electrical currents, etc. 

6. Electro-cutaneous Sensibility. — The test of cutaneous sensibility by 
means of the electric current has been proposed from various quarters. The 
advantage of it is that in this way the intensity of the irritation can be very 
easily and accurately graded and expressed in numbers, by the position of the 



EEMAEKS UPON THE DISTURBANCES OF SENSIBILITY. 479 



cylinder in using the faradic current, or by the galvanometer in using the con- 
stant current. The faradic current is usually sufficient in testing the sensibility, 
and we designate it by the position of the cylinder when the first sensation is felt 
and the position when the first pain is felt. In general, the differences of the 
farado-cutaneous sensibility are not very marked. Pathological deviations are 
given by comparison with normal portions of the skin, testing, if possible, sym- 
metrical parts, or with healthy people. For practical purposes the test of electro- 
cutaneous sensibility is unnecessary, since its results are the same as in testing the 
sensibility to touch, and especially to pain. 

7. Delayed Conduction of Sensation and After-sensations. — In diseases of 
the spinal cord, especially in locomotor ataxia (q. v.), we quite frequently see a 
marked delay in sensation after the action of an irritant ; this is also seen, but 
more rarely, in peripheral lesions. This delay of conduction affects chiefly the 
sensibility to pain. If in such a case we stick a pin into the sole of a patient's 
foot, several seconds elapse, even ten or twenty it is said, before the pain is felt. 
As was first observed by Naunyn and E. Remak in ataxics, and as has often been 
confirmed since, after sticking a pin into the foot there is first a sensation of 
touch, and some seconds later the peculiar sensation of pain, so that the patient at 
once responds to the prick with " Now," and a little later with " Ow ! " as an expres- 
sion of pain. 

This latter phenomenon has a certain relation to the abnormal after-sensations 
which are often observed under pathological conditions. After a simple pin-prick 
a feeling of burning lasts for an extraordinary long time, or else the first pain 
disappears quite soon, and then a new sudden sense of pain appears several times 
in the same part of the skin, just as if the patient were pricked again. There is 
also a delayed conduction of the sensations of touch and temperature, but it is 
rarer, and can be made out only by the aid of more accurate methods of measur- 
ing time. 

The Sensibility of the Muscles and Joints— A number of sensations are classed 
together under the names of "muscular sense" or "muscular sensibility." They 
are not all wholly of the same value, and, under pathological conditions, they 
must be tested separately. 

Ordinarily we call our power to be informed of the position of any of our 
limbs without the help of our eyes, and of the extent of any motion made by 
them, the " muscular sense." In nervous patients this power is often in great 
measure lost. If the patient closes his eyes he at once loses his power of judging 
of the position of the affected extremities. The extent and direction of passive 
motions made by them are stated with complete uncertainty, and incorrectly ; 
but this symptom does not depend exclusively on a loss of muscular sensibility, 
but probably the sensibility of the joints, the ligaments, and, in part, the different 
degrees of tension in the skin drawn over the joints, play an important part here. 

We also include in the muscular sense the power of estimating the amount 
of work done by muscular contraction. This is the so-called "sense of power." 
In raising weights we can distinguish with considerable accuracy the lighter from 
the heavier, when the pressure on the skin is excluded as far as possible. In such 
cases, also, we do not deal with the absolute, but with the relative differences in 
weight ; we can usually tell quite plainly when one fortieth of the original 
weight has been added or taken away. The sense of power, then, is somewhat 
finer than the sense of pressure. In order to exclude the latter in the test we 
have the patient lift the weight, suspended in a towel, with his hand or foot, but 
in the lower extremities it is scarcely possible to exclude entirely the co-existing 
sensations of pressure. 

We must mention, in conclusion, that muscular contraction is in itself accom- 



480 



DISEASES OF THE SENSORY NERVES. 



panied by a sensation, as may be proved, for example, in irritating the muscles by 
faradism — electro-muscular sensibility; but we have not yet found any real prac- 
tical value in testing the feeling of contraction in muscles. We must state, how- 
ever, that in certain forms of spasm the muscular contraction becomes so strong 
that it causes a decided pain, which is probably due to irritation of the sensory 
muscular nerves discovered by C. Sachs. 

Anomalies of muscular sensation are seen chiefly in locomotor ataxia, and 
sometimes in paralysis of cerebral origin, and quite frequently in severe hyster- 
ical affections. 



CHAPTER II. 
ANESTHESIA OP THE SKIN. 

JEtiology and Pathogenesis.— In every tract of the conducting path, which 
runs from the terminal apparatus of the sensory cutaneous nerves to the centers 
for the perception of sensation in the cerebral cortex, we may have, under patho- 
logical conditions, a break in the conduction, and, as a result of it, a complete or 
partial anaesthesia of the corresponding part of the skin. We speak of a periph- 
eral, spinal, or cerebral anaesthesia, according to the place where this break in the 
conduction occurs. The precise anatomical course of the sensory fibers is, how- 
ever, very imperfectly known, so that we can only approximately determine the 
location of the sensory fibers in the different portions of the nervous system. 

We know this, however, of the mixed peripheral nerves before their entrance 
into the spinal cord, that all their sensory fibers enter the cord through the 
posterior roots. A part of the posterior root-fibers pass directly into the sub- 
stance of the posterior gray cornua, while another part enter toward the median 
line into the external (in the lumbar cord, more correctly the median) portion of 
the posterior columns — that is, into the region of the " root-zones," or the so-called 
"elementary bandies of the posterior columns." Since new fibers from the 
posterior roots constantly enter the posterior columns of the cord, going upward 
from the lumbar region, the fibers which have entered in the lower portions must 
gradually be more and more crowded inward toward the median line. Hence it 
follows that the fibers entering the lumbar region, belonging to the sciatic, the 
crural, etc., must in the upper dorsal and cervical region occupy that internal 
portion of the posterior columns which is called the " columns of Goll " (Fig. 85, 
G). We can not, however, state definitely at present which of the different pro- 
longations of the posterior roots is the special path for sensory conduction. We 
are ourselves very much inclined to the opinion that the special sensory fibers of 
the posterior roots for the most part enter directly into the gray matter of the 
posterior cornua, and that the elementary bundles of the posterior columns — the 
continuation of the fibers which enter directly into the posterior columns — accord- 
ingly serve chiefly for other functions. We are led to this opinion especially by 
observations of quite severe disease of the columns of Goll, which occasioned no 
perceptible disturbance of sensation in the lower extremities during the patients' 
life. Disease of the posterior cornua of the gray matter, however, is always asso- 
ciated with disturbances of sensibility. It is not probable, according to our 
present experience, that there is a sensory tract in the lateral columns also in 
man. The fact is certainly proved, and is of importance, that all, or at least the 
greater part, of the sensory fibers undergo a decussation after their entrance into 



ANAESTHESIA OF THE SKIN. 



481 



the spinal cord, so that the fibers from the right half of the body pass upward in 
the left half of the cord, and vice versa. We know absolutely nothing definite as 
to the further course of the sensory fibers through the medulla oblongata and the 
pons, or as to their relations to the gray matter there, but it seems to be certain 
that the sensory tract passes on farther to the cerebral hemispheres, not through 
the crusta, but through the tegmentum. From this point the sensory fibers pass 
to the internal capsule, and a number of experiments show that they lie in the 
posterior third of the posterior limb of the internal capsule behind the pyramidal 
tracts (see Fig. 63), a place where the cutaneous and muscular sensory fibers are 
probably near the fibers for the impressions for the special senses, like the eye, 
the ear, etc. Nothing certain is known as to the central termination of the 
sensory fibers. Perhaps the posterior central convolution and the portions of the 
parietal lobe behind it may be regarded as the special place of termination for the 
sensory tract. We do not know whether tracts of conduction go to the brain 
which are distinguished from one another according to the different forms of 
cutaneous sensibility. 

Regarding the separate causes of anaesthesia, we see, in the first place, periph- 
eral anaesthesia under conditions where the terminal organs of the sensory cutane- 
ous nerves have lost their direct irritability. After chilling the skin, after the 
local action of ether and similar substances, from the corrosive action of acids and 
alkalies, carbolic acid, etc., as well as from the use of certain narcotics, like cocaine, 
morphine, or atropine, we see an anaesthesia of the skin, which is due to injury of 
the terminal sensory organs. We may probably put the frequent anaesthesia of 
washerwomen in this class, for their hands and forearms are exposed all day to the 
action of cold, lye, etc. The anaesthesias which develop in circulatory disturbances 
of the skin also have the same peripheral origin, especially the " spastic anaemia " 
which sometimes comes in the hands and is due to a spasm of the small arteries. 

We distinguish the peripheral anaesthesia of conduction, which may be pro- 
duced by all forms of lesion of the nerve-trunks, from the peripheral anaesthesia 
in the strict sense of the term. Traumatic influences, compression from new 
growths, and inflammation and degeneration of the peripheral nerves, as in neuri- 
tis, are the most frequent causes of this form of anaesthesia, which is often limited 
to the region of distribution of one or more definite nerves. 

Spinal anaesthesia is very often seen in the different diseases of the spinal cord, 
most frequently in locomotor ataxia, because this, as we shall see later, attacks 
chiefly the posterior roots, the posterior columns, and the posterior cornua of the 
cord ; but spinal anaesthesia is not infrequent in diffuse acute and chronic inflam- 
mation of the cord and in compression and new growths. As a rule, it is bilateral, 
para-anaesthesia. The hypothesis advanced by Schiff is quite wide-spread, but is 
by no means certainly proved, that the gray matter of the cord conducts chiefly 
the impressions of pain, and the white matter of the posterior columns the sensa- 
tions of touch. According to this, in a spinal analgesia we must assume chiefly 
an impairment of the gray matter. 

Cerebral anaesthesia is seen especially in haemorrhages, foci of softening, and 
tumors, which affect the posterior portion of the internal capsule ; but of course 
the break may occur in any other part of the tract of sensory conduction in the 
brain. If the cerebral anaesthesia, as is often the case, affects the half of the body 
opposite the lesion in the brain, we term it hemianaesthesia. Very extensive 
cerebral anaesthesia of a marked degree is quite frequently found in severe cases of 
hysteria. We also know that the anaesthetic action of the remedies termed anaes- 
thetics and narcotics, like chloroform, morphine, ether, alcohol, bromide of potas- 
sium, etc., must be explained by their influence on the central nervous system. 

Among other aetiological factors we must also mention that we sometimes see 
31 



482 



DISEASES OF THE SENSORY NERVES. 



more or less extensive anaesthesia as a result of acute diseases, like typhoid, diph- 
theria, and other acute infectious diseases, the origin of the anaesthesia, whether 
peripheral or spinal, being as yet uncertain. Peculiar insular and, rarely, diffuse 
anaesthesia, showing itself chiefly on the backs of the hands and the chest, is found 
in the secondary stages of syphilis, according to Fournier ; but there has been no 
further confirmation of this statement as far as we know. 

Symptoms. — In many cases the patient himself notices the existence of anaes- 
thesia. He finds that in certain parts of the body he no longer feels the pressure 
of his clothing or the bed-clothes in the usual way. Anaesthesia of the hands 
is soonest noticed, because this can affect the patient's occupation in diverse ways, 
so that, for example, he readily lets fine objects, like needles, drop from his hands. 
In other cases, of course, the anaesthesia is first found on a physical examination, 
which alone can give definite disclosures as to the extent and intensity of the 
affection. For this purpose the skin must be carefully examined by the methods 
given in the preceding chapter. It is worthy of note that hysterical anaesthesia 
especially, even if it is very marked and extensive, may often be wholly over- 
looked by the patients themselves. 

Anaesthesia is very often combined with abnormal subjective sensations, paraes- 
thesiae, in the affected portions of the skin. The patient has a feeling there of 
" numbness," or a " furry feeling," or complains of prickling or formication. The 
anaesthetic parts may even be the seat of very decided pain (anoesthesia dolorosa), 
if there is abnormal irritation of the sensory nerves from the break in the con- 
duction toward the center. The most diverse forms of anomalies of motility and 
of the reflexes, and vaso-motor disturbances, may of course be present in addition 
to the anaesthesia. Special mention must be made of trophic disturbances which 
are often seen in anaesthetic regions. We shall return to the peculiar characteris- 
tics of this repeatedly in subsequent chapters ; therefore we need state here only 
that the trophic disturbances have nothing to do with the anaesthesia itself. They 
depend either upon a co-existing lesion of special trophic or vaso-motor nerves, or 
upon the fact that external irritants, which act upon any anaesthetic portion of 
the skin, are not felt normally by the patient, and hence are often not avoided. In 
anaesthetic regions we often find large external wounds, burns, bed-sores, inflam- 
mations, etc., which were not noticed by the patient in time to prevent them, and 
hence they often attain an unusual extent. 

Voluntary motion is not disturbed by anaesthesia in itself, of however great a 
degree, as long as the motions may be controlled by the eyes ; but with the' eyes 
shut the motions of the anaesthetic parts become very uncertain, both in anaesthesia 
of the skin and of the deeper parts, the muscles and joints, since then the patient 
loses, to a great degree, his power of judging of the extent and of the precise 
direction of his movements. Very extensive anaesthesia of the skin, associated at 
the same time with anaesthesia of the organs of special sense, is sometimes not 
without influence upon consciousness. We have for several years had under 
observation a very remarkable case of total anaesthesia of the whole body asso- 
ciated with unilateral blindness and deafness. If we entirely exclude this patient 
from all external impressions of sense by closing his still serviceable eye and ear, 
we can at once in this way put him into a deep sleep ! 

We can not here go into the details of the different forms and distributions of 
anaesthesia, since they will be spoken of under the different diseases which lie at 
the basis of the anaesthesia. The course, the duration, and the prognosis of the 
affection depend, in the first place, of course, upon the form of the primary dis- 
ease. We will add here merely a few remarks upon anaesthesia of one nerve, 
namely, anaesthesia in the distribution of the trigeminus. 

Anaesthesia of the trigeminus is observed in tumors, syphilitic new growths, 



ANESTHESIA OF THE SKIN. 



483 



chronic inflammations, and analogous processes at the base of the skull, which 
compress the trunk, the Gasserian ganglion, or one of the three branches of the 
trigeminus, or directly involve the nerves. Traumatic lesions of the trigeminus 
are also not very uncommon. The distribution of the anaesthesia, according as 
the affection involves the whole trigeminus, or only one branch of it, may be seen 
in Figs. 56 and 57. In total anaesthesia of the trigeminus the conjunctiva and 
cornea, the mucous membrane of the nose, the cavity of the mouth, and the tongue 
are anaesthetic on the affected side. Hence we often find ulcers on the tongue 
and the mucous membrane, which come from being bitten. The " neuroparalytic 
ophthalmia," not infrequently seen in anaesthesia of the trigeminus, is of special 
"iterest, and has been much studied by physicians and physiologists. This is an 




Figs. 56 and 57.— Distribution of the sensory cutaneous nerves in the head : oma and omi. Occipitalis 
major and minor, am. Auricularis magnus. cs. Superficial cervical. F x , F 2 , V % . First, second, 
and third branches of the fifth (V). so. Supraorbital, st. Supratrochlear, it. Infratrochlear. 
e. Ethmoidal. I. Lachrymal, sm. Subcutaneus malae, or zygomatic, at. Auriculo - temporal. 
b. Buccinator, m. Mental. B. Posterior branches of the third cervical. 

ulcerative keratitis, almost always beginning in the lower segment of the cornea, 
and sometimes passing over into a purulent inflammation of the whole eyeball. 
This affection is regarded in many quarters as an immediate result of the disturb- 
ance of special "trophic" functions, but, after careful experiments (Senftleben), it 
seems most probable that external traumatic influences always occasion the first 
trouble, and render the intrusion of inflammatory agents j)ossible. It is still 
uncertain whether we must also assume a specially diminished power of resistance 
on the part of the tissues as a result of the nervous lesion. 

The skin of the face is often somewhat bloated in anaesthesia of the trigeminus, 
and it is cyanotic and feels cool. The reflexes are lost in peripheral anaesthesia, 
and the lachrymal secretion is diminished. The taste is almost always decidedly 
diminished on the anterior two thirds of the tongue on the affected side, the terri- 
tory supplied by the lingual nerve. 

Treatment, — Since anaesthesia, in most cases, is only a symptom, treatment, of 
course, must always first be directed against the underlying disease. Therefore 
we will mention here only those measures which are to be used symptomatically 
against anaesthesia, and which must be tried when the special cause can not be 
discovered, or when it is inaccessible to treatment. 

The chief remedy is, without doubt, the electric current. We treat the anaes- 



484 



DISEASES OF THE SENSOEY NERVES. 



thetic part of the skin with the f aradic current, using ordinary electrodes, or, bet- 
ter still, the wire brush, or with the galvanic current, stroking the skin slowly 
back and forth with the kathode for three or four minutes. Sometimes we can 
see a result immediately after the sitting. Hysterical anaesthesia may often be 
removed in this way in a very short time. 

Beside electricity we usually prescribe embrocations to irritate the skin, like 
spirits of camphor, spirits of mustard, formic acid, spirits of thyme, etc., and also 
baths, and cold or hot local douches, combined with rubbing the skin. The action 
of internal remedies is extremely doubtful. Nux vomica or stiychnine, tincture 
of valerian, etc., have been recommended. 

It is very important to protect the anaesthetic part against external injuries. 
In anaesthesia of the trigeminus, particularly, we guard the eye as far as possible 
from the development of a neuro-paralytic keratitis, by a carefully applied occlu- 
sive bandage. 



As an appendix, we will add here some illustrations (Figs. 58 to 62) to represent, 
in a diagrammatic fashion, the distribution of the sensory cutaneous nerves. These 




Figs. 58 and 59.*— Distribution of the sensory cutaneous nerves in the trunk and upper extremities : 
Fig. 58. Posterior aspect. Fig. 59. Anterior aspect. The shaded portion in Fig. 58 designates the 
territory supplied by the radial nerve. (From Henle.) sc. Supraclavicular nerves (from the cervi- 
cal plexus), ax. Cutaneous branch of the axillary nerve, cps and cpi. Superior and inferior pos- 
terior cutaneous nerves from the radial (ra). cmd, cm, and cl. Median cutaneous, median, and 
lateral nerves, vie. Median nerve, u. Ulnar nerve, dn. Second dorsal nerve, dxn. Twelfth dorsal 
nerve, ih. Ileo-hypogastric nerve, ii. Ileo-inguinal nerve, il. Lateral perforating branches, and 
ia. Anterior perforating branches of the intercostal nerves. 

diagrams will be of service, both in the consideration of anaesthesia and in the 
diagnosis of the neuralgias to be described in the following chapters. 



* Henle's nomenclature of the peripheral nerves has been adopted. — Trans. 



NEURALGIA IN GENERAL. 



485 



CHAPTER III. 



NEURALGIA IN GENERAL. 



li 



top 



ALTHOUGH every pain is, of course, excited by abnormal irritation of the nerves, 
still we are justified in giving a certain special variety of pain the name of neu- 
ralgia. The characteristics of this particular " nervous pain " are as follows : 1. It 
is felt exactly in the course or in the distribution of one or more special nervous 
trunks or nervous branches ; 2. It 
is usually of very considerable in- 
tensity ; and 3. As a rule, it is not 
present continuously, but shows 
manifest remissions and intermis- 
sions. It often comes on in single 
pronounced paroxysms of pain, 
which are either due to definite 
causes, or which can not be re- 
ferred to any evident external 
irritation. 

Pathogenesis and iEtiology — 
In many cases the cause of neu- 
ralgia is entirely unknown, but in 
other cases we can discover factors 
which may be regarded either as 
more or less direct exciting causes, 
or at least as predisposing causes, 
for the appearance of neuralgia ; 
but in all these cases the precise 



cl 



cr 



cjjm 
















m 








L2k\ 




TU 


J U \ 


ii 



\cpen sa,i 



Fig. 60.— Detailed distribution of the nerves 
to the dorsal surface of the fingers. 
(From Krause.) r. Radial nerve, m. 
Median nerve, u. Ulnar nerve. 



cti) 



Figs. 61 and 62.— Distribution of the sensory cutaneous 
nerves to the lower extremities. Fig. 61. Posterior 
aspect. Fig. 62. Anterior aspect. (From Henle.) 
ii. Heo-inguinal nerve. li. Lumbo-inguinal nerve. 
se. External spermatic, cp. Posterior cutaneous, cl. 
Lateral cutaneous, cr. Crural, obt. Obturator, sa. 
Saphenous, cpe. Peroneal communicating nerve. 
cti. Tibial communicating nerve, per'. Superficial 
branch of the peroneal nerve, per". Deep peroneal 
nerve, cpm. Posterior median cutaneous nerve. 
cpp. Cutaneous plantar nerve. 



form of action, and the peculiar nature of the disturbance produced in the nerves, 
are almost wholly unknown to us. At best we may suspect that perhaps some- 
times we have to do with slight inflammatory changes in the nerve-trunks, with 
hyperaemia, exudation, cedema, etc. , 

We may mention the following as predisposing factors, which clinical observa- 
tion has taught us : 1. Age. Neuralgia comes on most frequently in middle life, 



486 



DISEASES OF THE SENSORY NERVES. 



but it is also found in older people, and more rarely in children. 2. Sex exerts an 
influence so far that certain forms, like trigeminal neuralgia, are seen more fre- 
quently in women, and other forms, like sciatica and brachial neuralgia, are more 
common in men. Certain phases of sexual life, too, like puberty, pregnancy, 
child-bed, and the climacteric, favor the disposition to neuralgia. 3. The general 
neuropathic predisposition, which is hereditary in the majority of cases, is of great 
significance. Neuralgia often appears in people who suffer from other neuroses, 
or in whose families other nervous diseases, like the psychoses, epilepsy, hysteria, 
or neurasthenia have repeatedly occurred. 4. The physical constitution also 
seems to be of influence. We often see neuralgia in anaemic people, or in those 
whose constitution has been impaired by physical and mental strain, by imprudent 
living, or by mental excitement. 

We may mention, as exciting causes of neuralgia : 1. Cold, the action of 
draughts, wind, or wet — the so-called "rheumatic neuralgias." It is not per- 
fectly clear how the cold acts in such cases. We usually assume that by its action 
slight anatomical (inflammatory ?) changes arise directly or in a reflex manner in 
the nerves themselves. 2. Mechanical and traumatic action. Among these are, 
first, wounds and contusions which directly involve the nerves. Thus, for exam- 
ple, extremely severe neuralgia sometimes arises from the pressure of foreign 
bodies, like splinters of wood or of bones in wounds, on the branch of a nerve. 
We may also mention here the very severe neuralgia sometimes met with after 
amputations, which develops as a result of the so-called amputation neuromata. 
To this class, too, belong diseases in the neighborhood of nerves which act as 
mechanical irritants. Diseases of the bones or periosteum often lead to neuralgia 
in those nerves which run through bony canals or grooves. Lastly, tumors, 
aneurisms, hernias, or the gravid uterus, may lead to neuralgia by pressure on the 
neighboring nerves ; but we must call fo mind that every pressure on a nerve 
dees not lead to neuralgia in the same way, so that we must assume a special con- 
sequent change in the nerve in " neuralgia from compression." 

The relation which certain infections and poisons have to the development of 
neuralgia is very important. In the first place, it is not impossible that many of 
the apparently " idiopathic " neuralgias are to be referred to infectious causes — an 
assumption which may be made, for instance, in intercostal neuralgia associated 
with an eruption of zoster {q. v.), or in many acute trigeminal neuralgias. Many 
neuralgias, however, also have a definite relation to other infectious diseases. We 
may mention in particular the malarial neuralgias, which are directly dependent 
upon the malarial infection, often come on at regular intervals, and are cured by 
specific treatment — namely, quinine. Neuralgia is often seen during the course, 
or as a result, of typhoid, small-pox, and similar acute infectious diseases ; and in 
the secondary stage of syphilis. Among toxic substances we may mention espe- 
cially lead, copper, mercury, and also alcohol and nicotine, as those which have a 
special relation to the development of neuralgia. 

Neuralgia is also found in many constitutional diseases, in gout, and quite often 
in diabetes mellitus, and seems to bear a direct relation to the general disease ; 
and hence, like many of the other neuralgias mentioned as symptomatic, it may 
be contrasted with the idiopathic neuralgia due to some direct affection of the 
nerves themselves. Finally, neuralgia is met with sometimes in distant nerves in 
diseases of other than nervous organs, like the sexual organs, and is termed "reflex 
neuralgia." 

General Symptomatology of Neuralgia.— The neuralgic paroxysm begins either 
quite suddenly, or, more frequently, after certain prodromata, like cold feelings, 
prickling, slight painful sensations, etc., have preceded it for some time. The 
pain during the attack is usually of the greatest severity, and is described as either 



NEUKALGIA IN GENERAL. 



487 



burning and boring, or as shooting and tearing like lightning. There are fre- 
quently short temporary remissions of the pain. The location of the pain usually 
corresponds precisely to the distribution of the affected nerve, so that the patient 
can often point out quite definitely the anatomical course of the nerve. At the 
height of the attack there is often an " irradiation " or shooting of the pain into 
the territory of neighboring nerves. External irritants, like cold air, and espe- 
cially movements of the affected part, often produce an increase of the pain. 

On physical examination, we notice, first, certain disturbances of sensibility. 
The skin in the neuralgic part often shows more or less anaesthesia, which may be 
made out especially in the intervals between the separate attacks and immediately 
after them. Much more frequently, however, both during the attack and during 
the time when the patient is free from pain, there is hyperesthesia of the skin 
and the parts beneath. There are certain definite points which are often very 
sensitive and tender even to light pressure. These are called painful points 
(points douloureux). They were first fully described by Valleix, in 1841, for the 
different forms of neuralgia, and they have quite a great diagnostic importance, 
since they may often be found, not only during the attack itself, but also during 
the free intervals, although in a ]esser degree. The painful points always corre- 
spond to certain places in the course of the trunk or the larger branches of the 
affected nerve, and are found especially where, in marked and deep pressure on 
the nerve, we can press on some firm part beneath. They are probably always 
due to an abnormal sensitiveness to pressure in the affected nerve itself. In many 
cases of neuralgia they may of course be wholly wanting. 

Motor symptoms as well as sensory are not infrequent in neuralgia. Co-exist- 
ing symptoms of paralysis must always be regarded as a complication caused by 
some coarse lesion of the motor nerves ; hence in ordinary idiopathic neuralgia 
they are entirely absent. The co-existing symptoms of motor irritation, which 
are often seen, are usually directly dependent upon the neuralgia, however, and 
hence are to be regarded as reflex contractions, set up in the muscles by the great 
irritation of the sensory nerves. 

Yaso-motor symptoms are often seen in neuralgia. In the face especially, in 
trigeminal neuralgia, we often see a marked pallor or a decided reddening of the 
skin and conjunctiva. Abnormal secretions, of tears or sweat, may also be seen 
during the attack or at the end of it. We do not know whether all these symp- 
toms arise from direct or reflex nervous irritation. Trophic disturbances are 
noticed in various ways. During the attack we see eruptions of urticaria, or still 
more frequently of herpes vesicles, along the course of the affected nerves, as in 
herpes zoster. In severe and protracted neuralgias permanent changes in the 
tissues have been repeatedly seen in the parts supplied by the affected nerves. 
Among these are a falling out or a whitening of the hair, or more rarely an 
abnormally great growth of hair, thickening or atrophy of the skin, staining or 
pigmentation of the skin, etc. Lastly we may mention that during the neuralgic 
attack we sometimes find a diminished frequency of the pulse. 

The general nutrition of the body often does not suffer at all in neuralgia, but 
in many cases, especially when sleeping and eating are constantly disturbed by 
the attacks of pain, the disease gradually has a noticeable action on the whole 
constitution. The patient becomes pale and emaciated, and often the persistent 
and distressing pain is not without influence on his mental condition. He becomes 
irritable and inclined to melancholy. Patients have, in repeated instances, even 
committed suicide as a result of severe and incurable neuralgia. 

The whole course of neuralgia shows the greatest diversity. As has been said 
repeatedly, the onset of the disease in separate attacks is the chief characteristic 
feature. The precise pathogenesis of these attacks is, of course, entirely unknown 



488 



DISEASES OF THE SENSOEY NERVES. 



to us. These attacks usually come on every day or several times a day, or some- 
times at greater regular or irregular intervals. They may last only a few minutes 
or several hours. During the period between the attacks many patients feel quite 
well, but some have still a certain sensitiveness of the skin. The disease as a whole 
sometimes lasts only a few days or weeks, but sometimes it persists with manifold 
variations for years and years, and, in a word, is not capable of improvement; 
although, on the other hand, there are recoveries after the disease has lasted for 
years. In many cases, of course, the whole course of the disease depends upon 
the presence of some definite anatomical cause, like a tumor, a disease of the bone, 
or an aneurism. 

Many details as to prognosis and also as to the diagnosis of neuralgia will be 
spoken of in the following chapter. 

General Treatment of Neuralgia. — Prophylaxis of neuralgia is possible in this 
way, that certain constitutional anomalies, like anaemia or a general nervous predis- 
position, favor its appearance, as we have seen ; and in attacking these conditions, 
we may perceive a factor which can prevent to a certain degree any subsequent 
development of neuralgia. It is still more important, in people who have already 
suffered from neuralgia, to prevent the return of the affection if we can. For this 
object we must first consider the strengthening of the whole body, in order to 
make it better resist the action of any causes of disease. The measures to be 
chiefly employed for this purpose are proper food, good air, baths, sea-bathing, 
cold bathing, gymnastics, etc. Of course, we must also particularly guard the 
part of the body that has once been attacked from any irritation, like cold, me- 
chanical irritants, or over-exertion. 

In treating neuralgia itself we must always look first with great care for some 
causal factor, which may be accessible to treatment. This fulfillment of the 
causal indication is often possible in neuralgias which are due to mechanical 
causes. The extirpation of tumors, the excision of cicatrices, the removal of for- 
eign bodies, the treatment of inflammatory new growths, of syphilitic affections, 
of aneurisms, etc., is in many cases attended by brilliant success, but, of course, in 
many other cases the underlying disease is unfortunately not amenable to success- 
ful treatment. We should also carry out a causal treatment in the neuralgias 
which are to be referred to general anaemia, to a general neuropathic constitution, 
to hysteria, etc. In such cases we must always ascribe great value to the general 
treatment, such as diet, manner of life, baths, iron, and nervines, as well as to the 
special treatment directed against the neuralgia, and the same holds true, of 
course, in the neuralgias occurring in diabetes, gout, and syphilis. Lastly, we may 
fulfill the causal indication in the malarial neuralgias. If neuralgia comes on at 
approximately regular intervals in persons who come from a malarial district, and 
who perhaps have already suffered from other malarial affections, the exhibition 
of quinine in large doses, twenty to forty-five grains (grm. l'S-S'O) at once, will 
usually speedily cut short the attack. In obstinate cases in which quinine does no 
good, we should try arsenic, as Fowler's solution. In many toxic neuralgias, too, 
from lead, mercury, or alcohol, our first endeavor in treatment should be to remove 
the cause of the disease. 

In all cases where the causal treatment can not be carried out, or where it 
alone is not sufficient, we must consider those numerous remedies and methods of 
treatment which correspond to the indicatio morbi and to the symptomatic indica- 
tions. Starting with the hypothesis of an inflammatory condition of the nerve, we 
have often tried to exert a favorable influence on the disease by local derivations, 
mustard plasters, irritating embrocations, like spirits of mustard, veratrine oint- 
ment (two and a half per cent.), or tincture of iodine, or by blisters, or even by the 
hot iron. The remedies first mentioned are used only in mild cases. Vesicatories, 



NEURALGIA IN GENERAL. 



489 



placed along the course of the affected nerve, or behind the ear in facial neu- 
ralgia, sometimes act very well in fresh cases, especially those of a " rheumatic " 
character. We resort to the hot iron chiefly in old and very severe cases, in 
which, indeed, especially in sciatica, some very favorable results have been thus 
obtained. 

The local electrical treatment of neuralgia is more important and more efficient 
than the remedies mentioned. Although we do not know certainly how electricity 
acts, still it is unquestionably often attended with great success in the treatment of 
neuralgia. We many times secure an improvement in the symptoms, which is of 
course temporary, even in those cases where the special cause of the disease is not 
influenced by the electricity, although in idiopathic neuralgias in fresh, and some- 
times even in old cases, we can often obtain a complete cure. There are no gen- 
eral rules with regard to the methods to be employed, since different specialists have 
their own favorite methods. The following methods of application are most in 
use and are most to be recommended : 1. Stabile action of the anode of a constant 
current on the affected nerve-trunk over as great an extent as possible, especially 
on any painful points. We must entirely avoid any great variations in the current 
or interruptions of it. We gradually increase the intensity of the current up to 
medium strength. The sittings should last three to six minutes, and sometimes 
even longer, and must be repeated daily. 2. In neuralgia of the larger nerves we 
should use a stabile descending (sometimes ascending) constant current, in which 
the anode is placed on the most central point of the nerve-trunk available, or on 
the vertebral column, and the kathode on different peripheral points. 3. The 
faradic current also frequently acts very well. We faradize the nerve either with 
a moderately strong " increasing " current, or we apply the wire brush to the skin 
over the affected nerves. The latter method is very painful, but it is often attended 
with excellent results. 4. Some electro-therapeutists, like Moritz Meyer, lay stress 
upon the stabile application of the anode of the constant current to any painful 
points on the vertebral column, such as have been described in many neuralgias 
by Trousseau. 

As a general rule, it is always well to begin with a mild and very cautious use 
of electricity, and not to go on to the stronger currents until later. Electricity 
often acts brilliantly at once, during the attack of pain, but sometimes no improve- 
ment is seen until after several sittings. If, after two or three weeks, we obtain 
no result at all, after employing different methods of applying electricity, it is the 
best plan to give up electrical treatment entirely as not suited to the case. 

In the treatment of neuralgia we must consider a number of internal remedies, 
as well as electricity, some of which act symptomatically, like the narcotics, while 
others have obtained the reputation of having a specific action. Among the 
latter, quinine has decidedly the greatest value. In severe cases quinine may 
do excellent service, not only in malarial neuralgias, although most surely in 
these, but also in " idiopathic " neuralgias. It is in these cases that the remedy is 
given in large doses. We begin with fifteen to thirty grains (grm. 1-2) a day, 
best given in one dose, and in severe cases we may increase to sixty or seventy-five 
grains (grm. 4-5) or more. We see the best results from quinine in trigeminal 
neuralgia, while in other forms, like sciatica, it is much less efficient. Some cures 
have been obtained by salicylate of sodium. Next in rank come arsenic and 
bromide of potassium. The former is given in pill form or as Fowler's solu- 
tion, five drops three times a day, increasing gradually. Bromide of potassium 
acts only in large doses, forty-five to seventy-five to a hundred and fifty grains a 
day (grm. 3-5-10). Among the many other remedies which have been recom- 
mended, we may mention here ergotine, internally and subcutaneously, oil of 
turpentine, oxide of zinc, valerianate of zinc, tincture of gelsemium, aconitia, 



490 



DISEASES OF THE SENSOKY NERVES. 



phosphorus, iodide of potassium, subcutaneous injections of osniic acid, ten to 
fifteen minims (grm. 0*5-1) of a one-per-cent. solution, etc. 

In all severe neuralgias the use of narcotics, especially of morphine, is unavoid- 
able. Morphine is used almost exclusively during the attack, and is best given as 
a subcutaneous injection of one twelfth to one sixth of a grain (grm. 0 '005-0 "01) in 
the vicinity of the painful part. The anodyne effect almost invariably follows, but 
in obstinate and protracted cases the patient gradually becomes accustomed to the 
remedy. We must then resort to still larger doses, and these, too, finally fail in 
their effect. Among the victims of the morphine habit we find many patients 
who have suffered or who still suffer from severe neuralgia, so that we must 
always be very cautious and conservative in the protracted use of morphine. 
We should be especially cautious before deciding to put the hypodermic syringe 
into the patient's own hand. Many physicians ascribe not only a palliative but a 
permanent benefit to injections of morphine in neuralgia. We sometimes see, in 
fact, that mild neuralgias recover under the exclusive use of morphine injections ; 
but these are probably cases of spontaneous recovery. The internal use of mor- 
phine and opium preparations is decidedly inferior to the subcutaneous adminis- 
tration in certainty and rapidity of action. The external application of narcotic 
ointments, or embrocations, is much employed in practice, but it appears to be 
of advantage only in milder cases. We prescribe ointments with extract of opium 
(one to ten), extract of belladonna (two to ten), extract of opium and veratrine 
(one part of each to twenty of simple ointment), etc. We may also use chloroform 
(equal parts of chloroform and oil of hyoscyamus) and ether. Chloral and also 
paraldehyde are often prescribed in chronic neuralgias for their hypnotic effect. 
Croton chloral has been especially recommended in neuralgia. Finally, we must 
add that some physicians have praised the anodyne effect of subcutaneous injec- 
tions of atropine, gr. Vi 80 to 1 Uo to 1 / 99 l at aldose (grm. 0 "0005-0 -001-0-003 !), 
sometimes even in cases where morphine does not act. 

In severe cases the surgical treatment of neuralgia is often of great importance 
— the section of nerves, neurotomy, or the excision of a portion of the nerve, neu- 
rectomy— in order to prevent the union of the divided nerve. Without doubt this 
operation is often attended with success ; but in some cases, of course, it has no 
effect at all on the disease, or else the neuralgia returns with its old severity after 
a temporary improvement. We can understand the success of neurotomy in cases 
where we can assume that the cause of the abnormal sensory irritation is peripheral 
to the point of section ; but observations are reported in literature where the opera- 
tion has had a favorable influence even on central neuralgias. The operation is 
to be proposed only in severe cases, where all other remedies have been tried in 
vain, and the patient can always be promised the possibility, or even the proba- 
bility, of success, but never the certainty of it. Beside section of the nerves, nerve 
stretching has lately been frequently tried in neuralgia — sometimes with distinctly 
good results. 

The chief question as to the use of baths arises only in the treatment of 
neuralgias in the domain of the nerves of the extremities, especially in sciatica, 
and therefore these and massage will be spoken of more in detail in connection 
with the. separate forms of neuralgia. 

We see, then, that a large number of remedies are at our command in the treat- 
ment of neuralgia, and that the choice among them is not always easy. In any 
given case we look for the causal indication, and try to fulfill it if possible. In 
the many cases, however, where we fail to find this, we must first of all try to 
alleviate the pain, for which purpose, if external derivatives do not suffice, our 
most effective remedy is morphine. We must then lay out a special plan of treat- 
ment. We try electricity, or, if this be not practicable, one of the other remedies 



THE INDIVIDUAL FORMS OF NEURALGIA. 



491 



mentioned above. We put most trust in quinine, especially in fresh cases ; among 
other remedies, in anaemic persons, arsenic, and, in more robust persons, bromide 
of potassium are of service. If all these and similar remedies give no aid, in 
proper cases we may still hope for success from operative interference, or else we 
must confine ourselves simply to a purely symptomatic treatment with narcotics. 



CHAPTER IV. 
THE INDIVIDUAL FORMS OF NEURALGIA. 

1. Neuralgia of the Trigeminus. 

{Prosopalgia. Tic douloureux. FothergiW s Face-ache.) 

iEtiology. — Trigeminal neuralgia is one of the commonest and most impor- 
tant neuralgias. In its origin many causes and predisposing factors of all 
sorts play a part, as we have learned in the preceding chapter. Many cases, 
especially the milder ones, come from taking cold. Sometimes we can not find 
any definite cause. Malarial neuralgias are very often localized in the region of 
the trigeminus. The other especial causes which may give rise to trigeminal neu- 
ralgia are diseases of the cranial bones and periosteum, very often diseases of the 
teeth, caries, exostoses, and anomalies in development and position; and also dis- 
eases of the nasal and frontal cavities as well as of the middle ear. Romberg 
found an aneurism of the internal carotid, pressing on the Gasserian ganglion, 
as a cause of a severe and incurable case. We have since seen a precisely analo- 
gous case. Lastly, excessive use of the eyes is not infrequently related to the 
development of trigeminal neuralgia. 

Symptoms and Course. — The attacks of pain in neuralgia of the fifth pair are 
usually quite intense, and in severe cases may attain a most distressing and terrible 
severity. They arise either entirely without cause, or from some slight influ- 
ence, like washing, taking bodily exercise, or mental irritation. The pain is limited 
to the distribution of the different branches of the trigeminus, but it sometimes 
shoots into the occiput, the back of the neck, the shoulders, etc. We can often 
perceive reflex twitchings in the face, especially blepharospasm, and twitching 
of the corners of the mouth. The vaso-motor disturbances are noticed at first as 
abnormal pallor, but later usually as quite an abnormal redness of the face and 
conjunctiva. In neuralgia of the upper two branches we often see, during the 
attack, an unusually great secretion of tears. An excessive flow of saliva and 
an increased secretion from the nasal mucous membrane are more rare. Some- 
times, but still quite rarely, we see herpetic eruptions in the course of the affected 
nerve, zoster frontalis, herpes of the conjunctiva, etc. In some cases, too, more 
severe diseases of the eyes, belonging to the category of neuroparalytic ophthal- 
mia, have been observed. In neuralgias that have lasted longer, we often see still 
further trophic disturbances : changes in the skin and subcutaneous cellular tis- 
sue, the hair turning gray or falling out in the frontal region, etc. 

Most trigeminal neuralgias are situated, not in the whole distribution of the 
nerve, but only in one or more of its branches (see Fig. 56, page 483). We accord- 
ingly distinguish: 1. Neuralgia of the first branch {ophthalmic neuralgia), which 
is especially frequent as supra-orbital or frontal neuralgia. In this we find, as a 
rule, that pressure on the point of exit of the nerve at the supra-orbital foramen is 
more or less painful. More rarely we find painful points also on the nose, at the 
inner angle of the eye, or the parietal eminence, etc. 2. Neuralgia of the second 



492 



DISEASES OF THE SENSORY NERVES. 



branch (supra-maxillary neuralgia), is most frequent in the distribution of the 
infra-orbital nerve, infra-orbital neuralgia, with the chief painful point at the 
infra-orbital foramen, and others on the zygoma, on the upper lip, etc. 3. Neu- 
ralgia of the third branch (infra-maxillary neuralgia), whose most frequent seat 
is in the territory of the inferior alveolar nerve ; but neuralgia also occurs in the 
temporal region, in the auriculo-temporal nerve, and in the tongue, in the lingual 
nerve. The chief painful point is at the mental foramen. 

The general course of neuralgia of the fifth pair differs very much in different 
cases. We see all forms, from the mildest, which rapidly passes off, to the sever- 
est and incurable types, which may drive the patient to despair and even to sui- 
cide. In general, neuralgia of the first branch usually belongs to the relatively 
milder forms ; neuralgia of the second, and especially of the third branch to the 
severer forms. Trousseau has termed a particularly severe form " epileptiform 
neuralgia," although we can find no definite relation between this disease and gen- 
uine epilepsy. We can find no cause for epileptiform neuralgia ; the attacks of it 
come on with the greatest intensity either after brief pauses or after intervals of 
weeks and months, and they defy all attempts at cure with the greatest obstinacy. 
It is worthy of note that this form appears in individuals with the neuropathic 
taint. 

Diagnosis. — In all pronounced cases the diagnosis of trigeminal neuralgia is 
easy. We must regard accurately the distribution of the pain, its paroxysmal 
onset, and the points of pressure. Otherwise in a superficial examination we 
may of course confuse it with inflammatory affections of the bones and perios- 
teum, with genuine toothache, with migraine, and with other forms of headache 
and face-ache. 

Prognosis. — The prognosis is never to be made with complete certainty. It is 
most favorable in fresh cases which have a manifest cause, which may be removed, 
as a basis ; but if the affection is due to a coarse anatomical cause which can not 
be removed, or if we are dealing with old cases " which have become habitual," 
the prognosis, unfortunately, is often utterly unfavorable. 

Treatment. — The treatment of trigeminal neuralgia rests entirely upon the 
principles given in the preceding chapter. In searching for the causal indications 
we must look chiefly, in neuralgia of the second and third branches, for diseased 
teeth, and also in all cases for any affections of the nose, of the frontal sinuses, or 
of the middle ear. Carious teeth, which are painful and which seem to have any 
relation to the neuralgia, should always be removed, and any of the other affec- 
tions mentioned are to be treated on special principles. 

Of other remedies we use first of all electricity, the anode to the painful points, 
with the kathode on the back of the neck, or the wire brush, etc. ; we also use qui- 
nine, Fowler's solution, and in severe cases narcotics. In cases where the neu- 
ralgic attacks come on with approximate regularity, quinine especially often does 
excellent service ; we give fifteen to twenty grains (grm. 1-1 '5) at first, two or 
three hours before the expected attack. If quinine does no good, we try arsenic 
in not too small doses, and if these remedies are unsuccessful we may try one of 
the other drugs recommended : butyl chloral (croton chloral) in two-to-five-grain 
capsules (grm. O^l-O^), or, according to Liebreich's formula : 

^ Croton chloral gr. lxxv- 3 ijss. (grm. 5-10) ; 



S. One or more tablespoonfuls every five or ten minutes. 

We may also give tincture of gelsemium sempervirens, five to twenty drops several 
times a day; aconitia in pills of V200 to 1 / 12o °f a grain (grm. 0*0003-0 '0005), three 



Glycerine . . . 
Aquse destill 



3 vj. (grm. 20) ; - 
I iv. (grm. 120). M. 



THE INDIVIDUAL FORMS OF NEURALGIA. 493 



to five times a day ; nitrite of amyl, ammoniated copper, in powders of one or two 
thirds of a grain (grm. 0*02-0 04), oil of turpentine, etc. Special indications for 
all these remedies can not be given, so that we are recommended simply to test of 
them. In desperate cases Trousseau has tried very large doses of opium, which he 
has gradually increased until he gave two to three drachms ( !) (grm. 8-12) a day. 
Sometimes an attack may be diminished or shortened by compression of the 
carotid. 

If a severe neuralgia persists in spite of rational treatment by electricity or 
drugs, we should not delay too long in proposing to the patient operative treatment 
if possible. In frontal and infra-orbital neuralgia especially the section of the 
nerve is a comparatively slight operation, which — of course with many failures — 
has many excellent results to show. The full description of the technicalities of 
the operation, as well as the description of nerve-stretching and of the ligature of 
one carotid, which has been done in some desperate cases, must be left to the text- 
books on surgery. 

2. Occipital Neuralgia. 

Of the neuralgias involving the sensory region of the upper four cervical 
nerves, neuralgia of the occipitalis major is the most frequent and practically the 
most important. Beside the factors to be considered in all neuralgias, we must 
pay particular attention, in regard to aetiology, to diseases of the upper cervical 
vertebrae — caries and new growths. The painful paroxysms may attain the great- 
est severity. They are usually located in the two occipital nerves at once, being 
accordingly bilateral, although often more severe on one side than on the other. 
Painful points are most frequently found midway between the mastoid process 
and the upper cervical vertebrae. Vaso-motor disturbances, falling out of the hair 
etc., have been often observed. 

The prognosis is comparatively favorable in cases which have no severe ana- 
tomical disease, like spondylitis, as a basis. The most efficient remedies are 
strong cutaneous irritants to the back of the neck, vesicatories in fresh cases, the 
constant current, and injections of morphine. 

Other neuralgias in the distribution of the cervical plexus are rare. They 
occur in the distribution of the occipitalis minor, which, according to Seeligmul- 
ler, is quite frequently due to syphilis, and then is easily cured by iodide of potas- 
sium, and in the distribution of the great auricular and the supra-clavicular 
nerves. A phrenic neuralgia even has been described, in which the pain extends 
along the course of the phrenic nerve to the insertion of the diaphragm ; but this 
is at all events very rare. 

3. Neuralgia in the Region of the Brachial Plexus. 

(Cervico-brachial Neuralgia.) 

Brachial neuralgia is, on the whole, rare, and it is hardly ever strictly 
limited to the distribution of a single nerve. In general, the radial and ulnar 
nerves are rather more frequently affected than the median. We also see at times 
neuralgia of the internal cutaneous nerve. In regard to aetiology, we have to 
mention first wounds and contusions of the nerves, and also cicatrices and foreign 
bodies. The amputation neuralgias also belong to this class. It is worthy of note 
that sometimes we see severe brachial neuralgia after wounds of the fingers, which 
perhaps depends upon an ascending neuritis. Bilateral brachial neuralgia must 
always direct our suspicions toward some spinal affection, especially toward 
spondylitis of the lower cervical vertebrae. 

We have little to add concerning the special symptomatology of brachial neu- 
ralgia. The pain is usually ascribed to the whole course of the nerves without 



494 



DISEASES OF THE SENSORY NERVES. 



being very exactly localized, as we have stated. Painful points are sometimes 
found over the brachial plexus, over the radial on the external surface of the 
upper arm, over the ulnar in the sulcus at the internal condyle, over the median 
at the inner border of the biceps, and where the cutaneous nerves emerge from 
the fasciae. Vaso-motor and trophic disturbances have sometimes been seen, as 
" glossy fingers," a peculiar, shiny, atrophic condition of the skin of the fingers. 
In severe neuralgia a pronounced atrophy of the whole arm has also been 
observed. The diagnosis is usually easy ; we must bear in mind only the risk of 
confusion with articular affections. 

In regard to treatment, we must consider electricity, beside fulfilling any 
causal indications and trying the ordinary remedies, narcotics, derivatives, and 
salicylate of sodium in rheumatic cases. In some severe cases good results have 
been obtained by nerve-stretching. 

4. Intercostal Neuralgia. 

{Dor so-intercostal Neuralgia.) 

The neuralgias of this class are almost always pure intercostal neuralgias, since 
the posterior dorsal branches of the thoracic nerves are only exceptionally affected. 
The middle intercostal nerves, from the fifth to the ninth, are usually affected, 
one or more of them being attacked at the same time. The affection is much 
more frequent on the left side than on the right. 

In regard to aetiology, it is important to remember that obstinate intercostal 
neuralgias are often a symptom, and for a long time the only symptom, of severe 
organic disease, especially affections of the ribs ; diseases of the vertebrae, Hke 
caries and carcinoma ; diseases of the cord, like locomotor ataxia, spinal meningitis, 
and tumors ; and aneurism of the aorta. Genuine idiopathic intercostal neuralgia, 
however, is often met with, as well as these symptomatic forms, especially in 
anaemic and nervous women and girls in youth and middle life. Traumatic 
lesions of the intercostal nerves and taking cold also play a part in the aetiology, 
and, lastly, "reflex" intercostal neuralgia is not infrequent m diseases of the 
female sexual organs. 

The pain in intercostal neuralgia may attain a remarkable severity, and is 
usually increased by any considerable movement of the thorax. Hence the 
patient avoids deep inspirations, coughing, loud talking, etc., as much as possible. 
We usually find three painful points — one near the vertebral column, one some- 
where in the middle of the nerve, and a third near the sternum or over the rectus 
abdominis. "We may mention, among the trophic disturbances, the comparatively 
frequent occurrence of herpes zoster. In such cases we probably always have an 
actual neuritis of one or more nerves. The pam precedes the eruption of zoster, 
or comes on at the same time with it. It often lasts for a long time after the 
cutaneous affection has healed. The formation of zoster has usually been con- 
sidered until the present time a " trophic disturbance," but recent careful anatom- 
ical investigations (A. Dubler) favor the hypothesis that the formation of vesicles 
arises simply from a direct extension of the inflammatory process from the ter- 
minal branches of the nerves to the skin. It is worthy of note that the attacks of 
zoster often exhibit a certain epidemic, and sometimes even an endemic distribu- 
tion, so as to suggest an infectious agency. The almost constant swelling of the 
neighboring lymph-glands, in the axillae, at the lower border of the pectoral mus- 
cle, etc., perhaps supports this view. 

The course of intercostal neuralgia depends chiefly upon the aetiology of the 
affection. Primary neuralgias are often quite obstinate, but on the whole they 
usually give a favorable prognosis. The differential diagnosis between genuine 
intercostal neuralgia and rheumatic affections of the muscles, incipient pleurisy, 



THE INDIVIDUAL FORMS OF NEURALGIA. 495 



etc., is not always easy. In these cases a careful physical examination, a con- 
sideration of the localization of the pain, of the presence of painful points, and of 
the whole course of the disease, are needed to protect us from errors. 

The treatment is governed by the general rules given in the previous chapter. 
Blisters often act very well in fresh cases. Electricity is given by the faradic 
brush or the constant current ; with the latter, the kathode is placed on the verte- 
bral column, and the anode on the lateral and anterior painful points, using quite 
a strong stabile current. In severe cases we can not avoid injections of morphine. 
Herpes zoster heals by simple treatment with salves or by dusting on powders, like 
one part of zinc oxide to two of starch. 

Mastodynia {Neuralgia of the Mammary Gland). — Mastodynia (/' irritable 
breast " of Astley Cooper) is to be considered as a special neuralgia in the distribu- 
tion of the intercostal nerves. It occurs almost solely in women, after the age of 
puberty, and is a very painful, distressing, and obstinate affection. The pain is 
either continuous, or it comes on in separate paroxysms, sometimes accompanied 
by vomiting. The whole breast is extremely sensitive to the touch. We know 
little that is certain as to its aetiology. Anaemia, hysteria, and traumatic action 
seem to have some influence on it. We sometimes feel little nodules in the breast, 
which are very painful {tuber eula dolorosa, neuromata ?), and which may some- 
times give rise to the suspicion of the development of carcinoma. 

The disease may last for years. Treatment is difficult. Warm packs to the 
breast, bandaging the breast, and especially narcotics, may afford relief. Elec- 
tricity may be of distinct service. In the worst cases operative interference has 
been attempted — amputation of the breast, or extirpation of the painful nodules — 
but its results are uncertain. 

5. Neuralgia in the Region oe the Lumbar Plexus. 

As the neuralgias of this class are rare, and show few peculiarities, we will 
content ourselves with a brief account of the most important forms. 

Lumbo-abdominal neuralgia causes pain in the lumbar region, which shoots 
into the buttocks, the hypogastrium, and the genitals. Crural neuralgia is seated, 
in part, in the region of the external anterior cutaneous nerve of the thigh, and in 
part in the region of the cutaneous branches of the crural nerve, the internal and 
middle cutaneous. Its distribution over the cutaneous distribution of the great 
saphenous nerve, the inner portion of the calves, and the inner border of the foot, 
is especially characteristic. In obturator neuralgia the pain extends along the 
inside of the thigh, down to the vicinity of the knee-joint (see Figs. 61 and 62, 
page 485). 

In their individual characteristics, all these neuralgias agree with what has been 
said in the previous chapter. The diagnosis is not always easy, and we must pay 
special attention to avoid confusing them with affections of the bones and joints, 
with lumbago, renal colic, etc. 

6. Sciatica. 

{Ischiatic Neuralgia. Malum Coiunnii.) 

iEtiology. — Next to trigeminal neuralgia, neuralgia of the sciatic nerve is by 
far the most frequent, and practically the most important form of neuralgia. In 
contrast to most of the other neuralgias, it is more frequent in men than in 
women. Cold, wet, and over-exertion of the leg are found to be the most frequent 
aetiological factors. More rarely venous stasis in the pelvic veins (haemorrhoids) 
and habitual constipation give rise to the development of sciatica. We see symp- 
tomatic neuralgia in the region of the sciatic nerve in pelvic tumors, caries of the 



496 



DISEASES OF THE SENSOEY NERVES. 



sacrum, and analogous affections. Other traumatic influences, and compression 
of the nerve, as in constant, uncomfortable sitting, are sometimes evident causes 
of the disease. Pressure of the gravid uterus on the sciatic plexus may sometimes 
excite sciatica, and in women it has been seen as a result of delivery by forceps. 

Symptoms and Course. — The pain, coming on usually with mild prodromata 
and gradually increasing to severe paroxysms, generally begins at the posterior 
surface of the thigh, in the vicinity of the sciatic notch. From this point the 
lightning-like pains shoot down, usually into the peroneal region, the outer part 
of the leg, and the outer border and top of the foot, or more rarely into the tibial 
region, the sole of the foot. They either come on in characteristic neuralgic 
paroxysms, or they are more continuous, and are then described by the patient as 
" burning," " boring," and the like. They are often worse at night. In severe 
cases the leg can scarcely be moved, owing to the pain, so that walking becomes 
very difficult or almost impossible, and the affected leg is kept quiet in a slightly 
flexed position. Very often the pain comes on after long standing or sitting. 
Painful points are often found along the course of the sciatic, over the gluteus 
maximus, or at its lower border, in the popliteal space (tibial nerve), at the head 
of the fibula (peroneal nerve), at the malleoli, on the top of the foot, etc. 

Beside the pain, we often find other disturbances of sensibility in the affected 
leg, like paresthesia, hyperesthesia, or slight anaesthesia. Reflex muscular ten- 
sion, tremors, and even complete clonic spasms have been repeatedly observed in 
severe cases. A slight stiffness and weakness of the leg are very often found. A 
slight atrophy of the muscles often develops, but the higher degrees of atrophy 
indicate that there are serious anatomical changes in the nerve. Eruptions of 
zoster have been repeatedly observed, but, ou the whole, it is rare. 

The disease lasts several weeks, although sometimes, in many obstinate cases, it 
continues for months and even years ; but, except in cases which have an incurable 
anatomical lesion as an underlying cause, the termination is at last usually favor- 
able. Relapses are, of course, quite frequent. 

Diagnosis. — The diagnosis of sciatica is easy in the majority of typical cases, but 
it may sometimes be quite difficult. It is chiefly confused with lumbago, an acute 
coxitis, nervous coxalgia {vide infra), and psoas abscess. We must also bear in 
mind the occurrence of sciatic pain in the beginning of locomotor ataxia. In 
doubtful cases we can decide only after the most careful physical examination, 
embracing every part and function, and by considering the localization of the pain 
and of the painful points. 

Treatment. — Sometimes we can obtain favorable results by fulfilling the causal 
indication. In regard to this we may mention especially the improvement of 
many cases of obstinate sciatica, associated with habitual constipation, by method- 
ical treatment with laxatives, especially by the springs at Marienbad, or Kissingen, 
and also improvement after any possible removal of tumors, foreign bodies, etc. 

In regard to the treatment of ordinary sciatica, we must first take care, in 
all severe cases, to keep the leg perfectly quiet and in a good position during the 
painful paroxysm. Usually the local application of warmth, warm poultices, or 
bandages, is grateful to the patient. Sometimes a vapor bath gives real relief. 
More energetic local derivatives, blisters, or even local blood-letting, are of especial 
use in cases of "rheumatic origin." If the pain be very severe, a subcutaneous 
injection of morphine is the only certain remedy, and is sometimes indispensable. 
Embrocations of narcotics are also frequently prescribed in practice. 

Of the other remedies to be considered we may mention, in the first place, elec- 
tricity and massage. In electrical treatment we usually employ quite strong 
descending currents with large electrodes, which we let act on the nerve for five 
or ten minutes a day, while we include one portion of the nerve after another in 



THE INDIVIDUAL FOEMS OF NEURALGIA. 



497 



the current. Where there is much stiffness in the leg, we opeu and close the cur- 
rent a few times, in order to excite muscular contraction. Many cases are suitable 
for the use of the faradic current, especially for the wire brush. Beside electricity, 
massage has often given excellent results in sciatica. Details of the technique to 
be employed may be found in the special treatises on this important method of 
treatment.* 

Beside electricity and massage, baths deserve special consideration in tedious 
cases. Good results are often obtained from the indifferent thermal baths, like 
Teplitz, Wildbad, and Wiesbaden. We would also recommend warm local 
douches and hot sand baths, like Kostritz, as particularly efficient. 

In general, we can promise but slight results from the very many internal 
remedies recommended against sciatica, but, if there is a suspicion of syphilis, we 
must try iodide of potassium. Quinine has usually no effect in sciatica. Salicy- 
late of sodium should be tried only in fresh " rheumatic " cases. We have also 
very rarely seen any definite action from oil of turpentine, which is much used, 
especially in England. Some good results have lately been obtained by injections 
of osmic acid (see page 490). 

In very severe and obstinate cases, in which all other remedies have been tried 
in vain, we are justified in proposing to the patient to try nerve-stretching. This 
operation has been attended with very good results in some cases — but unfortu- 
nately, of course, not in all. Some favorable action in old cases has been ascribed 
to the use of the hot iron, and finally it may be mentioned as a curiosity that 
different observers claim to have obtained a recovery from sciatica by cauteriza- 
tion of the lobe of the ear ! 

7. Neuralgia of the Genitals and the Eectal Region. 

Neuralgic affections of the parts named are not frequent, but still a number of 
cases have been described by different observers. The pain has its seat either in the 
external genitals, or in the urethra, or in the anal and perineal region. The most 
frequent form is spermatic neuralgia ("irritable testis" of Astley Cooper), in 
which there is the most intense pain in the spermatic cord and the testicles, which 
is almost always associated with an extreme hyperesthesia of the affected parts. 
The treatment of this form of neuralgia by narcotics and electricity is often unsuc- 
cessful, so that in severe cases resort has sometimes been had even to castration. 
In women genuine uterine and ovarian neuralgias seem to occur, especially as 
one symptom of hysteria. 

Coccyodynia is the name of a form of severe pain in the coccygeal region, seen 
usually in women, which is much increased by walking, defecation, etc. The 
affection is so distressing that operations have been repeatedly performed on 
account of it to remove or to cut around the coccyx. We have twice seen this 
same symptom as a complication of locomotor ataxia. 

* Busch, "Allgeraeine Orthopadie, Gymnastik u. Massage," Leipsic, Vogel, 1882; Schreiber, 
" Praktische Anleitung zur Behandlung durch Massage," Vienna, 1883; Eeibmayr, "Die Massage 
und ihre Verwerthung in der prakt. Medicin," Vienna, 1883, etc. 



32 



498 



DISEASES OF THE SENSOEY NERVES. 



CHAPTEE V. 

NEURALGIA OF THE JOINTS. 

{Articular Neuroses.) 

Neuralgia of the joints, first described by the English physician Brodie, was 
first generally known in Germany after Esmarch proved, by publishing many 
observations, that apparently severe and very painful diseases of the joints are 
often found, at the basis of which there is no discoverable anatomical disease of 
the joint, and which we are therefore justified in regarding as nervous affec- 
tions. Since the localized pain in the joint is the chief symptom in most of the 
cases of this class, the term of " neuralgia of the joints " has been quite fitly chosen, 
although we do not find here such a typical and paroxysmal appearance of the 
pain as in genuine neuralgia, and although, too, a number of other symptoms are 
usually present, which are not seen in genuine neuralgia. Hence the name 
" articular neurosis " is better perhaps than the term " articular neuralgia." 

We see neuralgia of the joints chiefly in nervous, hysterical persons, and there- 
fore more frequently in women and girls than in men. 

We can very often make out a psychical cause for the origin of the disease. 
The most important part in the aetiology of articular neuroses is played by inju- 
ries, which affect the joint, and which would be in themselves without signifi- 
cance, if they were not associated with a decided fright, and did not direct the 
patient's thoughts to the affected limb. 

Either immediately after such an occasion, or often only some weeks later, 
the patient begins to complain of pain. The knee- or hip-joint is almost always 
affected, only rarely the joints of the upper extremity. The pain is continuous, but 
it is more severe at times, especially on motion, or mental excitement. At other 
times, especially if the patient's attention is diverted from the trouble, it seems to 
diminish to a considerable extent. It is mainly localized in the joint, but the whole 
leg is often painful. Patients are usually very sensitive to pressure, or jarring, 
and sometimes we may even discover some painful points on pressure over the 
joints. The patients can not walk at all, or at least walking is very painful and 
they limp badly. In severe cases, especially if the excessive care of those about 
them reduces the patients' power to resist their suffering, they become completely 
bedridden for weeks or months. There is usually a decided weakness in the 
affected leg, which is almost always associated with great muscular rigidity and 
tension. The leg is extended, or flexed and rotated inward, in just the same way 
as in genuine coxitis. 

The diagnosis of articular neuroses is often quite difficult, but it is almost 
always possible, with long observation of the case. At first, of course, the disease 
often seems to be a severe affection of the joint, on account of the great pain, the 
rigid position, and the complete inability to use the leg. The experienced physi- 
cian, however, is usually struck by the absence of any definite physical changes in 
the joint, especially of swelling, and also by the changes in the intensity of the 
complaint, by the influence of mental emotion on the suffering, and finally by the 
general impression he gets from the patients, the way they behave, and the con- 
trast between their great complaint and their usual (though, of course, not invari- 
able) good appearance, appetite, and undisturbed sleep. In doubtful cases an 
examination under chloroform is very advisable. With this contractures appar- 
ently the most severe vanish, and the normal character and mobility of the joint 
become plainly manifest. 



HABITUAL HEADACHE. 



499 



As soon as the diagnosis of an articular neurosis is made the treatment has 
quite definite indications. All embrocations, poultices, bandages, etc., are to be 
laid aside. The patient is to be brought to the conviction that she can walk, if she 
will only first learn to will to walk again. We make the patient practice walk- 
ing methodically ; these attempts at first prove very poor and apparently distress- 
ing to the patient, but they often lead to better results very speedily. These exer- 
cises are very much aided by electrical treatment of the joint, passing a strong 
current through it or using the faradic brush, and also by local cold douches and 
massage. Under some circumstances the use of internal remedies may be indi- 
cated, in many cases with regard only to the mental condition. We give iron 
to anaemic patients, and also the nervines. (See the chapter on hysteria.) 



CHAPTER VI. 

HABITUAL HEADACHE. 

(Cephalcea. Cephalalgia.) 

In addition to the neuralgias, we must speak here of habitual or " nervous " 
headache, an affection which is very often met with in practice, but in regard to 
whose precise causes or whose special nature our knowledge is still in many 
respects very unsatisfactory. 

We do not term the symptomatic headaches, so often observed, " nervous head- 
aches." The former come on in acute febrile infectious diseases, in pronounced 
general anaemia, in the different anatomical diseases of the brain and its mem- 
branes, of the skull, the frontal sinuses, etc. Just as little ought we to confuse 
habitual headache with other painful and well-characterized affections, especially 
typical neuralgia in the frontal branch of the trigeminus, or in the occipital nerves, 
or with genuine migraine or hemicrania (vide infra). Those cases, rather, belong 
to this class in which the headache forms to a certain degree a disease in itself, 
and is the sole, or at least the chief, symptom of which the patient complains, and 
for which he seeks aid. We know no certain anatomical basis for these cases. 
We usually assume disturbances of circulation and of the fine nutrition as the spe- 
cial causes of headache ; but it is only in a very few cases that anything definite as 
to the form of these changes can be stated. We can also state little that is certain 
as to the special place where these pains arise. We do not know whether painful 
irritations may arise in the brain-substance itself. The cerebral meninges, how- 
ever, especially the dura mater, are decidedly sensitive, and hence they may usually 
be regarded as the special seat of headache. 

The manifold character of the circumstances under which headaches arise 
renders it probable that the causes of headache are very different in different 
cases. We have to do either with persons who seem perfectly healthy in other 
respects, or with weak and anaemic people, or again with robust, very well nour- 
ished, " full-blooded " persons with red faces. Hence we look for the cause of the 
pain, according to the general constitution of the patient, either in an abnormal 
hyperaemia or anaemia of the brain and its membranes — a hyperaemic or anaemic 
cephalalgia. We very often find headache, too, as the chief symptom in 
nervous, neurasthenic people — neurasthenic cephalalgia. To this class belong 
especially people who have overworked physically and mentally — scholars, 
officials, students before an examination, etc. If we believe that we can 
make out "rheumatic" influences, like taking cold, or toxic influences, like 
alcohol, nicotine, or chronic lead poisoning, we speak of a rheumatic or a toxic 



500 



DISEASES OF THE SENSORY NERVES. 



cephalalgia. Patients with habitual headache often suffer at the same time from 
chronic gastric disturbances or habitual constipation, so that the latter disorders, 
in many cases, stand perhaps in a causal relation to the headaches. In very many 
cases, however, we can find no definite cause at all for the affection, so that we 
have to do with a genuine idiopathic disease. It is worthy of mention, merely, 
that in not very rare cases a pronounced hereditary predisposition to habitual 
headache seems to exist. 

Habitual headache is a chronic disease. It may last for months or years, or 
even through the whole life, either being present continually, or, what is more 
frequent, coming on in separate attacks and lasting several hours or days. These 
attacks sometimes come without any evident cause, but they may often be referred 
to definite influences, to mental excitement, physical exertion, errors of diet, etc. 
The pain is felt either in the forehead or in the occiput, or sometimes over the 
whole head. It is sometimes limited to a definite and quite sharply denned part 
of the head. The precise form of the pain is described in different ways, either as 
boring, or tearing, or as if the head were pressed together from without, or as if it 
would split open. In many cases the intensity of the pain is not great ; there is 
merely a dizziness and a feeling of "pressure" in the head, but in other cases 
the pain is very severe. In such cases there is also at times a pronounced hyper- 
esthesia of the skin of the head, so that it may cause pain even to touch the hair. 

The general health is almost always disturbed in headache. The patient can 
not work, he is often ill-tempered and irritable, and he loses his appetite. "We 
sometimes see more marked gastric symptoms, especially nausea and vomiting, 
and sometimes copious perspiration. Severe cases of the disease are of great im- 
portance, since by an attack the patient is rendered almost wholly unable to 
attend to his business. 

The treatment of headache is always a difficult task. In the first place, of 
course, we should try to adapt our treatment to the aetiology of the disease if it is 
evident. In such a case the existing primary disease requires special treatment. If 
there is any suspicion of syphilis, which must especially be considered if the pain 
is worse at night, we must first of all try iodide of potassium. For ansemic 
patients we prescribe iron, arsenic, a country residence, strengthening diet, etc. 
We order full-blooded persons, especially if they also suffer from indigestion, to 
drink bitter waters, or we send them to health resorts like Marienbad or Carlsbad. 
Nervous headaches in hysterical and neurasthenic patients require a rational 
general treatment : electricity, general faradization, galvanism to the head, or to 
the sympathetic, cold-water cures, etc. For persons who have overworked, we 
must urgently advise complete physical and mental rest. We send them to the 
country or to try sea-bathing. 

The number of symptomatic remedies recommended to relieve headache is 
very considerable. In most of the tedious cases the patient himself has learned 
to know his disease perfectly well. Many know that there is no remedy for 
"then old headaches," and they merely desire to rest, waiting until the pain 
ceases of itself. Others have become accustomed to employ certain domestic 
remedies ; they put poultices on the head, take a cold or a hot foot-bath, put a 
mustard plaster to the back of the neck, bathe the forehead with cologne-water, 
bind a towel tight about the head, drink strong tea, smell ammonia or " smelling- 
salts," etc. We sometimes see good results, although frequently we do not, from 
the internal remedies. These may be used, either during the attack or for a longer 
period, to prevent the return of the pain. There are no special indications for the 
different remedies, so that we must try to see which one is the most efficacious. 
Among the drugs which should be tried are first of all quinine, three to eight 
grains (grm. 0'2-0"5) a day ; bromide of potassium, fifteen to thirty grains a day 



ANOMALIES OF THE SENSE OF SMELL. 



501 



(grm. 1-2); arsenic, as Fowler's solution, or fagrain. pills (grm. 0*003) three to 
four times a day ; ergotine in hyperaemic headache, one-grain pills (grm. 0*05) 
three to six times a day ; guarana (which contains caffeine), in ten- to thirty- 
grain powders (grm. 0*5-2), etc. In headaches which come on after taking cold, 
as after long exposure to a draught, salicylate of sodium, thirty to sixty grains 
(grm. 2-4) a day, is sometimes very serviceable. If the pain is very severe, nar- 
cotics, like morphine, opium, or chloral, may be necessary. 

Electrical treatment (vide supra) has given decidedly good results in many 
cases, but we must always begin it with great caution, and try first what method 
is best borne. Cold-water cures, too, are sometimes beneficial, or residence in the 
country, at the sea-shore, or in the mountains. 

We can sometimes do the patient good service with the remedies mentioned, 
but in other cases the evil obstinately defies all attempts at cure. Then, however, 
the patient has still the encouragement left that the disease often ceases at last 
spontaneously in advanced age, after lasting years and years. 



CHAPTER VII. 
ANOMALIES OF THE SENSE OF SMELL. 

Anomalies of smell, which depend upon a disease of the olfactory nerve itself, 
or of its terminal apparatus, or of its central termination, are not infrequently 
observed, but they have no great practical interest. It is well known that only 
the upper two turbinated bones and the upper part of the septum of the nares, the 
olfactory region, are supplied by fibers of the olfactory nerve. The branches of the 
olfactory nerve pass into the cranial cavity through the openings of the lamina 
cribrosa and form the trunk of the nerve. Nothing certain is known as to their 
further central course. The hemianosmia, in affections of the posterior portion 
of the internal capsule, is worthy of notice, and also the anosmia of the left nasal 
cavity which has sometimes been claimed to be observed in cases where there was 
also right hemiplegia and aphasia. 

In testing the sense of smell, we use substances which do not at the same time 
irritate the sensory fibers of the trigeminus in the nasal cavity. The best sub- 
stances to use are cologne-water, ethereal oils, like oil of cloves or oil of bergamot, 
oil of turpentine, camphor, musk, valerian, asafcetida, etc. 

Hyperesthesia of the sense of smell makes itself manifest either by a remark- 
ably fine perception of odors, or by an abnormal sensitiveness to them. The latter 
symptom is often noticed, especially in the hysterical. Patients have headaches, 
or attacks of fainting, from slight odors, which healthy persons notice but little. 
Subjective sensations of smell (hallucinations of smell) are quite frequent among 
the insane, and sometimes during the aura of an epileptic attack. 

A diminution of the power of smell (olfactory anaesthesia, anosmia) is also not 
infrequent. We see it in the different diseases of the nose — coryza, etc. — also in 
affections of the base of the skull, like tumors, and acute and chronic meningitis, 
which involve the trunk of the olfactory sympathetically, and also in cerebral dis- 
ease, tumors, etc., and most frequently in severe hysteria. In far-advanced loco- 
motor ataxia we have sometimes found pronounced anosmia, dependent perhaps 
upon an atrophy of the olfactory nerve. It is important to state that in every 
marked enfeeblement of the smell the " taste " for many forms of food suffers, 
since it is well known that their " aroma," as in roast meats, wines, and the differ- 
ent sorts of cheese, is due chiefly to the co-existing sensations of smell. 



502 



DISEASES OF THE SENSOEY NERVES. 



The treatment of anomalies of smell almost always coincides with the treatment 
of the primary disease. In case the disturbance of smell makes special interfer- 
ence desirable, we can try electrization of the nasal mucous membrane, or painting 
it with a one-per-cent. solution of nitrate of strychnine in olive-oil. 



CHAPTER VIII. 
ANOMALIES OF THE SENSE OF TASTE. 

Sensations of taste are obtained from two nerves — the glossopharyngeal, and 
the lingual nerve from the third branch of the trigeminus. The glosso-pharyn- 
geal is the nerve of taste for the posterior third of the tongue and the palate, the 
lingual for the anterior two thirds of the tongue. The gustatory fibers of the lin- 
gual, all, or at least a great part of them, pass over to the chorda tympani, and 
reach with this the trunk of the facial ; they do not remain in the facial, how- 
ever, as many pathological experiences have most plainly shown, but they finally 
come back to the trigeminus ; and, probably chiefly by the great superficial petrosal 
nerve and the Vidian nerve to the spheno-palatine ganglia, in this way they pass 
to the second branch of the trigeminus. There may be some other channels, how- 
ever, by which the gustatory fibers finally unite again with the trigeminus, and 
enter the brain with its trunk. We know nothing definite as to their further 
course and their central termination. 

Hyperesthesia of taste is rare, and has been seen almost exclusively in the 
hysterical. Paresthesia of taste is sometimes found in patients with facial paraly- 
sis, who complain of an abnormal taste in their mouths. In the insane, too, sub- 
jective sensations of taste (hallucinations of taste) may occur. Anaesthesia of the 
gustatory nerves (gustatory anaesthesia, ageusia) is, however, quite frequent. As 
follows from what has gone before, this may be seen : (1) In affections of the 
peripheral terminal organs of the gustatory nerves, as in disease of the mucous 
membrane of the tongue ; (2) in affections of the glossopharyngeal, like com- 
pression ; (3) in affections of the lingual nerve, and of the trigeminus within the 
cranial cavity; (4) in affections of the chorda tympani, from diseases of the middle 
ear ; (5) in affections of the facial nerve between the entrance of the chorda tym- 
pani and the geniculate ganglion; but we know from experience that any obstacle 
to conduction in this nerve above or below the points named causes no disturb- 
ance of the sense of taste. Central disturbances of taste have been observed in 
affections of the posterior portion of the internal capsule. 

The test of the sense of taste must be performed separately for all the different 
varieties of the sensation of taste, since partial paralyses of taste are not infre- 
quent. The test is performed by putting small amounts of the substance to be 
tasted in solution on the tongue with a glass rod or a brush. The anterior and pos- 
terior parts are to be tested separately. A solution of quinine or tincture of nux 
vomica serves as a test for bitter, a solution of sugar for sweet, vinegar or dilute 
muriatic acid for sour, and a solution of common salt for salt. We may also use 
as a test for taste the well-known galvanic taste, which is strongest at the anode, 
but is also detected at the cathode in even very weak currents, and hence is so 
often noticed from by-currents in galvanizing the head, neck, etc. 

An accurate diagnosis as to the seat and cause of disturbances of taste can be 
made only by considering the other symptoms which are also present. Direct 
treatment may best be employed by the aid of electricity. 



KEMARKS UPON THE DISTURBANCES OF MOTILITY. 503 



SECTION II. 
Diseases of the Motor Nerves. 
CHAPTER I. 

GENERAL REMARKS UPON THE DISTURBANCES OF MOTILITY. 

1. Paralysis. 

General Classification of Paralyses— By " paralysis " we mean the loss of vol- 
untary motion in the muscles of the body controlled by the will. We usually dis- 
tinguish between the complete loss of the power of active motion, paralysis, and 
the mere weakening of it, paresis. In complete paralysis of any part of the body, 
or of a single muscle, the slightest voluntary motion can not be produced in it ; 
while in paresis in a diseased part certain movements are still possible, but they 
are more or less below the normal in strength, extent, and duration. 

In every portion of the tract that leads from the motor portions of the cortical 
gray matter of the brain to the muscles — that is, in every part of the so-called great 
" cortico-muscular conduction-path" or "pyramidal tract" — disease may lead to 
paralysis if it takes away from the part affected 
its power to conduct voluntary motor irritations. 
Every destruction or inhibition of function of the 
motor centers in the cerebral cortex, with whose 
integrity the initiation of voluntary innervation 
is associated, must also lead to a paralysis in the 
corresponding muscular region. Finally, it is 
conceivable, at least a priori, that diseases of the 
muscles may also lead to a paralysis, since the mus- 
cles may either have their contractile substance 
injured, or lose their power to respond by a con- 
traction to any nervous irritation that reaches 
them ; but a certain confirmation of such " my- 
opathic paralyses" is associated with great diffi- 
culties, because diseases of the special muscular 
substance can scarcely be separated from diseases 
of the terminal branches and terminal apparatus 
of the motor nerves. 

If we represent to ourselves briefly the precise 
course of the chief tract for exciting voluntary 
movements, as far as it is now known, we must 
put the beginning of this tract, according to all 
recent experiments, in the region of the central 
convolutions of the cerebrum and of the paracen- 
tral lobule. . Here we find the so-called psycho- 
motor centers (see the details in the chapter on 
cerebral localization), from which the motor fibers 
in the corona radiata converge and pass down- 
ward. The latter, after they have united into 
quite a compact bundle, enter the internal capsule, 
which they traverse obliquely. As we see in a 
horizontal section through the cerebral hemi- 
spheres (see Fig. 63), the internal capsule consists of two limbs — an anterior, 
between the lenticular and the caudate nuclei, and a posterior, between the 




Fig. 63.— Horizontal section through 
the right cerebral hemisphere. 
NC. Caudate nucleus. Th. Optic 
thalamus. LK. Lenticular nu- 
cleus (first, second, and third di- 
visions). vS. Anterior limb of the 
internal capsule. hS. Posterior 
limb of the internal capsule. Fa, 
Fibers belonging to the facial 
nerve. Py. Pyramidal tract (mo- 
tor). S. Sensory tract (probably 
cutaneous nerves and those of 
special sense). O. Occipital lobes. 



504 



DISEASES OF THE MOTOR NERVES. 



6 



lenticular nucleus and the optic thalamus. The two limbs form an obtuse angle, 
opening outward, whose top — that is, the junction of the anterior and posterior 
limbs of the internal capsule — is termed the "knee of the capsule." The motor 
tract (Py) lies in the posterior limb of the internal capsule about the posterior end 
of its middle third. In this it runs downward rather obliquely, so that in the 
upper part of the internal capsule it lies somewhat farther forward than in the 
lower. From the internal capsule the pyramidal tract enters the crusta. It lies 
first in the third quarter, counting from the inside, then farther down in the mid- 
dle third of the crusta (see Fig. 64), and from this point it passes into the anterior 
half of the pons. In the pons the fibers of the pyramidal tract are somewhat 

separated, but they come together below it 
into the compact bundle of the pyramids on 
the anterior surface of the medulla. At the 
lower end of the pyramids the decussation of 
the (lower) motor pyramids takes place — that 
is, the motor fibers of each pyramid pass over, 
for the most part, into the lateral column of 
the opposite half of the spinal cord, and here 
form the distinct bundle of the lateral py- 
ramidal tract (Py S, see Figs. 65 and 66). A 
small part of the pyramids, which sometimes 
seems to be entirely wanting, remains un- 
crossed, and passes downward in the anterior 
column of the cord on the same side as the 
so-called anterior pyramidal tract (Py V, 
Fig. 65). From the lateral column, or the 
anterior column of the cord, the motor fibers 
pass into the anterior gray columns of the 
cord, and are here directly connected with 
the large motor ganglion-cells of the an- 
terior cornua. The anterior root-fibers pass out from these ganglion-cells, as is 
well known, and become the anterior spinal roots of the peripheral nerves. 





Fig. 64.— Transverse section through the 
crura cerebri in secondary degeneration 
of the right pyramidal tract. (From 
Charcot.) sn. Substantia nigra, p. The 
degenerated and therefore translucent 
pyramidal tract. III. Oculo- motor 
nerves. AS. Aqueduct of Sylvius. 




Fig. 65.— Transverse section through the cervical 
enlargement of the spinal cord. PyS. Lateral 
pyramidal tract.. PyV. Anterior pyramidal 
tract (in this case present only on one side). 




Fig. 66.— Transverse section through the lumbar 
^enlargement. PyS. Lateral pyramidal tract. 
(The anterior tract is no longer present in the 
lumbar portion of the cord.) 



Through the latter the motor impulses, coming from the cerebrum, finally reach 
the special motor apparatus, the voluntary muscles. 

The long motor tract, just described, the cortico-muscular path or the pyram- 
idal tract, has been quite accurately determined in its details by the results of 
pathological observations (Tiirck, Charcot), and investigations into the history of 
its development (Flechsig). It forms, at all events, the chief path for the conduc- 



EEMAEKS UPON THE DISTURBANCES OF MOTILITY. 505 



tion of voluntary innervation. It is possible that there are other motor paths of 
conduction beside this tract, but we know nothing definite concerning them. 

If we pay attention to the course of the motor tracts described, we shall easily 
understand certain peculiarities in the distribution of motor paralyses, which are 
of great importance in diagnosis. Since the motor centers for separate parts of 
the body, like the face, the arm, or the leg, are separated from one another in the 
cerebral cortex, and are distributed over a comparatively large surface, as we shall 
see more fully later on, it is easily explained why affections of the cortex, if they 
are not very extensive, may lead to paralysis of only a single part of the body. 
We call such an isolated paralysis of one part of the body monoplegia, and thus 
we speak of a cortical facial or brachial monoplegia. Farther downward in the 
brain, in the internal capsule and the crus cerebri, however, as we have seen, all 
the motor fibers are collected into one bundle, whose diameter takes up compara- 
tively little space. Hence we comprehend that any disease of the brain, which is 
situated in this part of the motor tract, may easily make this tract incapable of 
conduction throughout its whole extent, or at least throughout the greatest part 
of it. The result must be, then, a more or less complete paralysis of the facial 
muscles, the arm, and the leg at the same time — that is, of the entire half of the 
body — a form of paralysis which is termed hemiplegia or unilateral paralysis. We 
may note here that, as a result of the passage of the motor fibers to the other half 
of the cord in the decussation of the pyramids, the paralysis must develop on the 
side of the body opposite to the focus of disease in the brain. Farther down in 
the medulla and the cord the fibers coming from both hemispheres, and belonging 
to the two sides of the body, lie quite near each other. Since many diseases of the 
cord have a tendency to affect the two halves of the cord at once, or gradually to 
extend over the whole transverse section of the cord, a simultaneous paralysis of 
the corresponding portion of the two sides of the body will readily arise as a result 
of this. This form of paralysis we call paraplegia. Diseases in the cervical cord 
may have as a result a paralysis of all four extremities or of the two arms, cervi- 
cal, brachial, or superior paraplegia ; diseases in the dorsal and lumbar cord a 
paraplegia of the two legs, inferior paraplegia, often called simply " paraplegia," 
without further prefix. In affections of the peripheral nerves we have, of course, 
again a limitation of the paralysis to the region of the affected nerve. The paraly- 
sis may be quite extensive in diseases of a nervous plexus — paralysis of a periph- 
eral plexus — or it may confine itself wholly to the region of a single nerve, or even 
of a single branch of the nerve — paralysis of a peripheral nerve. 

We will have to add many more details to what has just been said, but as a 
fundamental principle we may now note that hemiplegia is the chief form of 
cerebral paralysis, while paraplegia is the chief form of spinal paralysis. Mono- 
plegias are usually either cortical cerebral paralyses, or peripheral paralyses. 

General -Etiology of Paralysis.— The kind of lesion which leads to paralysis 
may, in the different cases, be very diverse. From easily understood reasons we 
can very rarely decide as to the kind of lesion from the intensity and extent of 
the paralysis, but only from the manifest aetiological factors, from the develop- 
ment and course of the paralysis, from other morbid symptoms that are also 
present, etc. In general, we may divide the paralyses into two groups, according 
to the nature of their cause : into paralyses from causes that can be discovered 
anatomically, and into the so-called functional paralyses, in which no anatomical 
cause for the paralysis can be found ; but since our anatomical, and especially our 
histological, methods of investigation have become better developed and are more 
employed, the domain of functional paralyses has become gradually more and 
more restricted, and a definite anatomical cause has now been found for many 
paralyses which were once regarded as functional. 



506 



DISEASES OF THE MOTOR NERVES. 



All the diseases of the nervous system may be anatomical causes of paralysis, 
if they lie in a spot where they damage or destroy the paths of motor conduction. 
Inflammation, degeneration, new growths, haemorrhages, and severe disturbances 
of circulation, with their results, especially embolic and thrombotic softening, are 
found in the brain, the cord, and the peripheral nerves, and under some circum- 
stances give rise to the appearance of paralysis. Mechanical lesions of the nervous 
system also play a great part in the pathogenesis of paralysis, especially traumatic 
injuries, and compression of the brain, the cord, and the peripheral nerves by 
swellings, new growths, and other diseases in their vicinity. 

We also know certain toxic substances which produce paralysis from their per- 
sistent action on the organism. Of these toxic paralyses, lead paralysis is the most 
important in its clinical relations; but other poisonous substances, like copper, 
arsenic, and certain vegetable alkaloids, may cause paralysis. In regard to lead 
paralysis {vide infra), which was once considered a purely functional paralysis, 
we now know that anatomical changes form its basis. These can be plainly made 
out, especially in the peripheral nerves. 

We may group a large number of paralyses together under the term of " paral- 
ysis after acute diseases." Since in these cases we always have to do with acute 
infectious diseases, we may assume, as their most probable cause, certain changes 
in the nervous system, sometimes in the brain, but more frequently in the cord or 
the peripheral nerves, which stand in direct relation to the specific infectious 
material. We most frequently see paralysis apx3ear after diphtheria, diphtheritic 
paralysis (vide infra), or more rarely after typhoid, small-pox, dysentery, the 
acute exanthemata, etc. It has long been known that the products of certain 
chronic infectious diseases, especially syphilis and tuberculosis, are often localized 
in the nervous system and give rise to paralysis. 

Those paralyses which come on most manifestly because of exposure to cold 
are termed paralyses from exposure to cold, or " refrigeratory," or frequently 
" rheumatic " paralyses. Although many spinal diseases, like myelitis, may per- 
haps be referred to exposure to wet or cold, we usually reckon among rheumatic 
paralyses only certain peripheral paralyses, like that in the region of the facial 
nerve. The functional disturbance of the nerves in these cases probably depends 
upon mild inflammatory changes in them produced by cold, and is accordingly of 
an anatomical and not merely of a functional nature. 

There are, however, quite a comprehensive group of paralyses which we must 
to-day still term functional paralyses. To this class belong the hysterical paralyses, 
the paralyses from psychical causes, like paralysis from fright, the " paralyses from 
imagination," etc. We shall learn to recognize these more fully in the chapter on 
hysteria. 

In conclusion, we must bear in mind the " reflex paralyses," whose aetiology is 
not yet fully explained — that is, paralyses which come on in the course of diseases 
of certain internal organs, especially of the intestine, and of the urinary and 
sexual organs. An attempt has been made to explain their origin, from analogy 
with well-known physiological experiments, by the idea that a " reflex inhibition " 
is excited in certain motor regions by a sensory irritation arising in the diseased 
organs, a theory which has not yet been fully confirmed. Leyden's hypothesis is 
somewhat more probable, but it is by no means proved beyond a doubt. Accord- 
ing to it the paralyses of this class are explained by an ascending neuritis, ai'ising 
from the organs originally affected (see the chapter on neuritis). Lepine has also 
regarded the paralysis of the arm of the affected side, seen in some cases of empy- 
ema, especially as a result of operative interference, as a " reflex paralysis," an 
explanation which may be proper in some cases, but in regard to which we should 
be the more cautious, as metastatic abscesses of the brain are not very infre- 



REMAKES UPON THE DISTURBANCES OF MOTILITY. 507 



quently found in empyema (see the chapters on purulent meningitis and cerebral 
abscess). 

General Symptomatology of Paralyses.— We can recognize the existence of a 
paralysis, except from the patient's statements as to the impossibility of perform 
ing certain motions and functions, only by a careful and thorough physical exam- 
ination of the power of voluntary motion. This examination in patients with 
nervous disease must extend to all parts of the body, and demands an accurate 
knowledge of all the movements that can normally be executed by the different 
joints, and of the muscles and nerves requisite to produce them. In the descrip- 
tion of the different single forms of paralysis we will go more into detail in regard 
to the anomalies of motion to be observed. 

In each individual case of paralysis some other symptoms must be considered 
beside immobility — first the condition of the paralyzed muscles, and then certain 
accompanying symptoms that are often present with the paralysis. 

In regard to the first point, the trophic condition of the paralyzed muscle is of 
the greatest diagnostic and practical importance. In comparing a large number 
of paralyses, a very evident difference in this respect strikes us at once. We see 
on the one hand paralyses where the paralyzed muscles retain their normal vol- 
ume and their normal state of nutrition entirely, or almost entirely, for years, and 
on the other hand we see cases in which there is a considerable atrophy in the 
paralyzed muscles in a few weeks or months. This difference is so effectual that 
all the last-named paralyses have been classed together under the name of " atro- 
phic paralyses." Since muscular atrophy does not occur in every case of paralysis, 
it can not be simply the result of the rest and inactivity of the muscles, but it must 
have its special cause. 

If we once more represent to ourselves the whole course of the motor tracts, 
from the cerebral cortex to the voluntary muscles, we shall remember that the 
nerve-fibers through this long route undergo a single interruption — namely, by 
the interposition of the large ganglion-cells of the anterior cornua of the gray 
matter of the spinal cord. Clinical and anatomical experience teaches us that, in 
all those paralyses where the cause, that is, the break in conduction of the motor 
fibers, lies in their first portion, that is, between the cortex and the cells in the ante- 
rior cornua, there is, as a rule, no atrophy, or only a slight. amount of atrophy, in 
the paralyzed muscles, while in those paralyses where the cause is situated in these 
ganglion-cells themselves, or in the portion of the motor tract peripheral to them, 
a pronounced muscular atrophy rapidly develops. The only possible interpretation 
of this fact is, that the large motor ganglion-cells of the anterior cornua have, as 
we express it, a trophic influence on the muscles. If these cells are intact, and the 
conduction from them to the muscles is not interrupted, the muscles keep approxi- 
mately their normal condition of nutrition, even if they are paralyzed, while an 
affection of the ganglion-cells themselves, or an interruption of conduction in the 
peripheral nerves, rendering the transmission of the trophic influences from the 
cells to the muscle impossible, necessarily results in an atrophy of the muscles. 
This atrophy is not confined merely to the muscles separated from their " trophic 
center," that is, from the ganglion-cells in the anterior cornua of the cord, as we 
must note here, but the nerves proceeding downward from the point of the lesion 
also take part in the atrophy. Since this atrophy, both of nerve and muscle, is 
associated with a destruction of tissue to be more fully described later — a genuine 
" degeneration " of the fibers — we speak of a " degenerative atrophy " of the nerves 
and muscles, in contrast to the simple muscular atrophy which occurs in almost 
all severe diseases, in starvation, etc. The degeneration of the nerves is, of course, 
not evident to our sight and touch during life, but it is proved, as we shall soon 
see, by certain changes in their electrical excitability. 



508 



DISEASES OF THE MOTOE NEEVES. 



From the above statements the following extremely important points in the 
anatomical diagnosis of paralysis are at once evident : that in cerebral paralyses 
there is never a degenerative atrophy in the paralyzed muscles ; that atrophy is 
present in spina] paralyses only when the large ganglion-cells in the anterior 
cornua of the cord, belonging to the muscles, are destroyed or injured in their 
functions by the cause of the paralysis ; but that in all long-continued peripheral 
paralyses a degenerative atrophy of the paralyzed muscles and nerves must inev- 
itably develop. These fundamental principles may suffice for the present ; fur- 
ther deductions from them must be postponed until the special chapters on the 
various forms of paralysis. 

We observe a further distinction in the condition of the paralyzed muscles if 
we perform passive motion in the paralyzed parts. There are paralyses where we 
can perform passive motion in the paralyzed parts at any joint with perfect ease 
and freedom, and without perceiving the slightest resistance. We term such 
paralyses " flaccid paralyses," but there are also paralyses where passive motion 
meets with considerable muscular resistance, so that it can be performed only with 
a certain greater or less amount of exertion, or only within certain limits, or not 
at all. This difficulty in performing passive motion may have different causes. 
It is most frequently caused by the development of persistent shortening in the 
paralyzed muscles themselves, or in their antagonists (the so-called contractures), 
which prevent the free performance of passive motion. In other cases there is no 
special contracture, but the paralyzed muscles exhibit a peculiar rigidity. There 
are all sorts of muscular contractions, which either are to be regarded as symptoms 
of direct motor irritation {vide infra), or have a reflex origin. Paralyses in which 
the performance of passive motion is hindered by such muscular contractions are 
termed " spastic paralyses." The details of all these symptoms will be spoken of 
in the special chapters. 

Finally, in every case of paralysis, we must consider tbe other nervous symp- 
toms which accompany it, since these may also be of great importance in judging 
of the cause of the paralysis. We must first of all investigate the condition of the 
reflexes {vide infra) in the paralyzed parts, from which many conclusions can be 
drawn as to the seat of the lesion which causes the paralysis. We must also test 
the state of the sensibility, both in the skin and in the muscles themselves. Cer- 
tain attendant trophic and vaso-motor symptoms are also to be regarded. The 
skin over the paralyzed parts sometimes appears cyanotic, or marble-like ; it feels 
cool, is cedematous, and sometimes is peculiarly dry, hard, and scaly. 

2. Symptoms of Motor Irritation. 

As we have termed the symptoms of motor deficiency " paralysis," we group 
the symptoms of motor irritation in general together under the name of ''spasm." 
We mean by this all the morbid movements occurring in the muscles involuntarily 
and even against the will. Although we may find spasm in the smooth muscles, 
which generally are not controlled by the will, as in spasm of the bronchial 
muscles, spasm of the vessels, etc., we will concern ourselves here only with the 
spasmodic movements in the voluntary muscles. We must look for the cause of 
these in abnormal irritation exerted in some way on the motor tracts, but we 
know very little of the precise nature and character of this irritation in most 
cases. The abnormal irritation often acts directly on the motor nervous region, 
as in the frequent spasms in affections in the neighborhood of the cortical motor 
centers ; but the motor irritations often seem to be excited secondarily through 
some reflex channel — reflex spasms. 

For a long time two kinds of spasm have been distinguished symptomatically. 



EEMAEKS UPON THE DISTURBANCES OF MOTILITY. 509 



We term those spasms clonic where the abnormal muscular contraction lasts 
only a short time, and then is interrupted by a short period of relaxation, to come 
on again afresh. The affected parts of the body are thus put in a constant con- 
vulsive motion. In distinction from this we term those abnormal muscular con- 
tractions tonic spasms where the muscle remains spasmodically contracted for a 
longer time — minutes, hours, or days. The affected part of the body is thus kept 
motionless in some abnormal position. Both forms of spasm, however, show 
many transitions and combinations, so that we must often speak of " tonic-clonic " 
spasms. 

A more careful examination of the symptoms of motor irritation, however, 
gives a still greater number of different forms. We will here group together the 
most important varieties of morbid involuntary movements without giving a 
completely exhaustive review of the manifold forms of spasm. 

1. Epileptiform convulsions are severe, and usually clonic spasms, at times 
tonic-clonic, spread over the whole body or limited to one half or one portion of 
the body. By them the whole body or the part affected is put into violent 
motion, usually thrashing and shaking movements. The pure epileptic spasm in 
epilepsy is the type of this form of spasm, but precisely analogous spasms, " epi- 
leptiform " spasms, are seen in organic diseases of the brain, in hysteria, etc. 

2. Rhythmical contractions in single groups of muscles are sometimes seen in 
certain cerebral diseases, like apoplexy and sclerosis. In these the part of the 
body affected is put in motion by continuous, separate, weaker or stronger thrusts, 
which follow one another in a regular rhythm. Rhythmical contractions are 
also seen as precursors or at the end of epileptiform spasms. 

3. Trembling motions, or tremor, as we say in ordinary parlance, are moderate 
motions, rapidly following one another, with a not very marked excursion. If 
the tremor is more pronounced, we term it "shaking." Tremor is an important 
symptom, almost pathognomonic in many nervous diseases, like paralysis agitans, 
but we know almost nothing in regard to the more intimate manner of its origin. 
We know that tremor is often present in old people — senile tremor ; and in 
alcoholic subjects — alcoholic tremor. Tremor sometimes appears in muscles at 
rest, that is, not innervated by the will, and sometimes only in those which are 
moved voluntarily. This latter form of tremor, which is seen most frequently 
in multiple sclerosis {vide infra), is termed "intention tremor." 

4. Single contractions, either sudden twifchings, or in the form of a slow con- 
traction of the muscle, are seen with especial frequency in diseases of the cord. 
They are either single, or frequent and persistent. Their mode of origin is not 
always plain. They may depend on direct motor irritation or they may have a 
reflex origin. 

5. Fibrillary muscular contractions are little contractions in the separate 
muscular bundles, which may be seen on a close examination of the muscles, but 
which do not have any special influence on motion. If the fibrillary contrac- 
tions in a muscle are very pronounced, there may develop an actual " wave " in 
the muscular substance. We see this symptom especially in atrophied muscles, 
particularly in progressive muscular atrophy {vide infra). 

6. Choreic movements are either slight contractions or quite complicated and 
extensive movements, which usually appear in the face, in one limb, or some- 
times over the whole body, without regard to rule. In severe cases they are 
almost continuous, but in milder cases they are interrupted by shorter or longer 
pauses. They form the chief symptom of chorea proper, but they are also present 
in other cerebral affections, like symptomatic chorea, post-hemiplegic chorea, etc. 

7. Movements of athetosis is the name we give to peculiar, involuntary, and 
usually quite slow movements, which are seen especially in the arms and hands, 



510 



DISEASES OF THE MOTOR NERVES. 



but also in the head, the trunk, etc. The fingers make slow but often very exten- 
sive movements, are extended, spread apart, flexed, and moved over and around 
one another in the most remarkable way. This form of motor irritation occurs as 
a special disease, '.' athetosis" or as a symptom in certain central nervous diseases, 
especially the cerebral paralysis of children (vide infra). 

8. Constant or co-ordinated spasms are symptoms of motor irritation in which 
the patient performs complicated movements by compulsion — forced movements. 
Among these are classed the compulsory going forward or moving in a circle, the 
turning about the axis of the body (forced attitudes), and also certain peculiar com- 
plicated forms of spasm, like spasms of jumping, laughing, screaming, etc. They 
are seen most frequently in severe cases of hysteria, but epilepsy also may occur 
exceptionally in the form of co-ordinated spasms. The forced movements and 
attitudes mentioned above are seen chiefly in affections of the cerebellum and 
the cerebellar peduncles. 

9. Tonic spasm, as has been said, is the name for all morbid muscular con- 
tractions that continue for a long time. Tonic spasm in the muscles of mastica- 
tion, the masseters, is termed trismus. Tonic spasm in the muscles of the back 
and neck, by which the whole body is drawn backward, and the vertebral column 
is bent into an arch with the convexity in front, is called opisthotonos. Tonic 
rigidity of the whole body is termed tetanus. 

10. Cataleptic rigidity is the name of that tonic condition of the muscles in 
which the limbs are deprived of the influence of the will, but are held in position 
by the muscles in any position given to them passively. It is seen chiefly in cer- 
tain cases of hysteria, but cataleptic states are also present in other cerebral dis- 
eases, like meningitis (see the chapter on catalepsy). 

11. Associated movements are abnormal movements which appear, while mak- 
ing voluntary movements, in muscles which have no connection with the move- 
ment willed. Thus associated movements sometimes take place in the arm when 
the patient wills to move the leg alone. They are most frequent in cerebral dis- 
eases, in hemiplegia ; but we have seen sometimes, even in spinal diseases, that 
on moving one leg the other was always moved with it unintentionally. 

Beside the conditions of motor irritation, other attendant nervous symptoms 
often occur at the same time. Symptoms of motor paralysis and irritation are 
very often combined with each other, since the different forms of spasm may 
appear not only in groups of muscles whose motion is otherwise normal, but also 
in paretic or paralyzed muscles. In general convulsions the state of the con- 
sciousness deserves special attention. Genuine epileptic attacks are usually 
associated with complete loss of consciousness, but in most of the other forms of 
spasm the consciousness is unaffected. Finally, it is worthy of mention that tonic 
spasms especially are attended by a feeling of decided pain, which is probably due 
to an irritation of the intra-muscular sensory nerves. Such painful tonic muscu- 
lar contractions are termed cramps. Among them are the well-known painful 
spasms in the calves after physical exertion. 

3. Ataxia. 

In executing all normal complicated movements we need the simultaneous 
action of several muscles. Consider the numerous muscles which must be put in 
activity in walking, in grasping, and in all the manifold employments of the hands. 
Hence, in order to perform such movements correctly, it is not only necessary 
that all the muscles concerned should be innervated by the will — that is, that they 
be not paralyzed — but that we should also be able so to modify the innervation of 
each individual muscle that its contraction corresponds precisely to the special part 
of the work belonging to it. A prescribed voluntary motion can take place only 



REMARKS UPON THE DISTURBANCES OF MOTILITY. 511 



when, first, all the muscles requisite for it come into no less but also no greater 
action ; second, when each individual muscle contracts only so far and so much as 
its special task requires ; and, third, when the conditions in the time of innerva- 
tion take their normal course — that is, when all the muscles involved contract at 
the same time or in the proper order after one another. A movement which is 
executed in such a prescribed manner we call a co-ordinated movement, and the 
process of properly modifying the innervation of the different muscles necessary 
for a complicated movement we call the co-ordination of motion. We must espe- 
cially bear in mind that the simultaneous action of several muscles is so far neces- 
sary, even for what seem to be the simplest movements, that muscles antagonistic 
to those moved must also come into activity. Only by the aid of the ever-ready 
antagonistic muscles can we grade our movements as finely, or check or hasten 
them as rapidly, as is demanded for the execution of almost all complicated move- 
ments. 

Nervous pathology is rich in facts which can make the idea and the necessity 
of the co-ordination of motion clear to us. We often see disturbances of motility 
which make the patient incapable of any fine motor acts, and yet which do not 
depend at all upon any motor weakness or paralysis, but only upon a disturbance 
in the co-ordination of motion. Such a disturbance we call ataxia, and we speak 
of an ataxia of the arms, of the legs, etc., when the parts named can perform all 
the motions and retain their full strength, but these movements show, usually at 
once, a striking, disordered, uncertain " ataxic " character. 

Many theories have been advanced as to the precise cause of ataxia, upon 
which we must enter in the special chapters. We can remark here only that 
ataxia is seen both in cerebral diseases, especially in affections of the cerebellum 
(cerebellar ataxia), and in diseases of the spinal cord (spinal ataxia). Among the 
latter, degeneration of the posterior columns especially (locomotor ataxia), has 
ataxia as one of its chief symptoms. Therefore we will discuss the character of 
the symptoms and the cause of ataxia more fully in describing this disease. 

4. General Remarks upon testing the Reflexes and upon the Condition 

of THEM. 

In testing the reflexes, which should never be omitted in any case of nervous 
disease on account of its frequent great diagnostic importance, we must distin- 
guish the two chief groups of reflexes from each other : the cutaneous reflexes, and 
the "tendon reflexes." 

Cutaneous Reflexes. — We term the muscular contractions, excited reflexly by 
irritation of the sensory centripetal cutaneous nerves, cutaneous reflexes. These 
are usually present only to a slight degree in the upper extremities ; but we can 
sometimes excite reflexes even here by pricking or pinching the skin, especially 
that of the fingers. The very marked reflex in many people caused by tickling the 
axilla is well known. The test of the cutaneous reflexes in the lower extremities is 
much more important. The soles of the feet are the most sensitive parts for excit- 
ing a reflex. Simply tickling the soles with the finger is a sufficient irritation (the 
tickling reflex), and so is the prick of a pin (the prick reflex), or striking the skin 
hard with a blunt object, usually the handle of a percussion-hammer (the blow 
reflex). Thermal irritants are also very suitable for exciting a reflex, especially 
bits of ice held to the skin (cold reflex). It is often advisable to try all these 
methods, since with diminished reflex irritability a reflex contraction in the leg 
can often be excited only by some one of them. We should also examine the 
reflex irritability of the rest of the skin, as well as the soles of the feet, by a pin- 
prick, by pinching a fold of the skin, etc. We should especially remember that 



512 



DISEASES OF THE MOTOR NERVES. 



in nervous diseases there is often a delay in the reflex, so that the reflex contrac- 
tion appears only when the irritation has lasted for a certain time. Thus in many 
diseases of the cord, as we have repeatedly seen, the reflex follows only after we 
have pinched a fold of skin continuously for several (ten or fifteen) seconds, a 
delay which has a connection with the fact of the "summation of reflex irrita- 
tion" known from physiology. The fact also deserves mention that in many 
patients the reflexes are easily excited in certain parts of the skin, but in other 
parts with difficulty or not at all — the "place of easiest reflex irritability." 

In general, the reflex contractions are confined to the limb irritated. On pricking 
the sole of the foot, a dorsal flexion of the toes or of the foot follows, or a greater 
or less flexion of the leg. The reflex rarely involves the rest of the body, but 
under pathological conditions there is such an increased reflex irritability that, on 
irritating the soles of the feet, both legs, or even the whole body, fall into con- 
traction. Such a condition is sometimes seen in hysteria, in tetanus, in hydro- 
phobia, in strychnine poisoning, etc. 

We must also mention two special forms of cutaneous reflex which are often 
examined : the abdominal reflex, consisting of a contraction of the abdominal 
muscles on the same side, if we stroke the skin of the abdomen with the finger or 
the handle of the percussion-hammer ; and the cremaster reflex — that is, the reflex 
retraction of the testicle, if we stroke the internal surface of the thigh, or exert a 
marked pressure a hand's breadth above the internal condyle. The cremaster 
reflex appears first on the side irritated, but not very infrequently on both sides at 
once. Other cutaneous reflexes, like the gluteal reflex, the mammillary reflex, etc., 
have less significance and are often absent. 

Judgment in regard to any pathological condition of the cutaneous reflexes is 
rendered difficult by the fact that their intensity varies considerably even under 
normal conditions. Many healthy people have much livelier reflexes than others. 
Hence we may judge most accurately of a patient if, in unilateral affections, we can 
compare the reflex symptoms in the two halves of the body with each other. The 
precise condition of the reflexes in the different forms of disease will be spoken of 
in the special chapters. We can state here only that a diminution or a complete 
absence of the cutaneous reflexes must, of course, be seen where the reflex conduction 
— through the centripetal nerve, the gray matter, the special anterior cornu, and the 
motor nerve — is interrupted at any point, as may be the case both in diseases of the 
peripheral nerves and of the spinal cord. On the other hand, however, the cutane- 
ous reflexes may lose their intensity, or even disappear entirely, if the reflex centers 
lose their irritability from an irritation of the reflex-inhibitory centers or fibers. 
We see an abnormal increase of the cutaneous reflexes when either the irritability 
of the parts that aid in producing the reflex is increased, as in many cases of 
cutaneous hyperesthesia, in strychnine poisoning, and in many general neuroses ; 
or when the inhibitory processes which normally act upon the reflex centers are 
abolished, as in certain diseases of the brain and spinal cord. The increase of the 
cutaneous reflexes is shown partly by the fact that the reflex movements are par- 
ticularly lively, and appear with a comparatively slight irritation of the skin, and 
partly by their extension to more distant groups of muscles than usual. 

Tendon Reflexes. — Of almost greater practical importance than the investiga- 
tion of the cutaneous reflexes is the test of the phenomena classed under the name 
of the " tendon reflexes," and first carefully investigated and described by Erb and 
Westphal in the year 1875. We understand by this those muscular contractions 
which arise from the mechanical irritation of the tendons and analogous parts, 
like the periosteum and fasciae. By this the sensory nerves of the tendon are irri- 
tated, and excite a reflex muscular contraction by means of the spinal cord. If 
we give a quick blow to the ligamentum patellae (the tendon of the quadriceps 



EEMAEKS UPON THE DISTUEBANCES OF MOTILITY. 513 



extensor) with the ulnar side of the hand, or, better, with a percussion-hammer, 
while the leg hangs down laxly, or, if the person examined be in bed, while the 
leg is in a passive position of slight flexion, it is followed almost invariably in 
healthy persons by a more or less vigorous contraction of the quadriceps, by which 
the leg is extended. This is termed "patellar reflex," or "knee phenomenon" 
(Westphal). In order to produce it, it is especially necessary for the person exam- 
ined to avoid all active muscular tension in the leg, especially in the extensor. 

The second important tendon reflex to be provoked in the lower extremity is 
the Achilles' tendon reflex. If we give to the foot of the person examined a pas- 
sive position of slight dorsal flexion, so that the tendo Achillis is a little tense, and 
then strike the tendon a quick blow, a marked contraction of the gastrocnemius 
follows. Under normal conditions this reflex is often absent. Where the tendon 
reflexes are abnormally increased, however, it is very vigorous, and then we can 
very often produce it in the following, especially characteristic, manner. If we 
make a sudden short, vigorous, passive dorsal flexion of the foot, the tendo Achillis 
is suddenly made tense, and thus is irritated mechanically. As a result of this, 
there is a reflex plantar flexion of the foot. If now, by persistent passive dorsal 
flexion of the foot, the tendo Achillis is again made tense, there follow by turns 
new plantar and dorsal flexions of the foot, so that the foot is thus put into a vig- 
orous tremor. This symptom, which can only exceptionally be provoked in 
healthy persons, is termed ankle clonus (foot clonus), or "foot phenomenon" 
(Westphal). Where there is a very great increase of the tendon reflexes the 
tremor is sometimes not confined to the foot, but the whole leg falls into a vigor- 
ous clonus, a symptom which was once given the unsuitable name of spinal epi- 
lepsy. We can also obtain the patellar reflex in the form of a clonus if we pull 
the patella firmly down with the finger and force it downward by a sudden blow 
on the finger. 

The two symptoms described— the patellar reflex, and the Achilles' tendon reflex 
or foot phenomenon — are practically the most important, and are the most often 
tested, but they are by no means the only reflexes in the lower extremity. Beside 
the reflexes from the special tendons we also frequently obtain muscular contrac- 
tions by striking the periosteum and the fasciae, which have been termed the peri- 
osteal and fascia reflexes. Thus a contraction in the quadriceps often follows a 
blow on the anterior surface of the tibia. We also see contractions frequently in 
the adductors of the thigh on striking the internal condyle of the femur, contrac- 
tions in the muscles of the posterior aspect of the thigh in striking the calves, etc. 

Under normal conditions the tendon reflexes in the upper extremities are often 
insignificant or entirely absent, but where the irritability is abnormally increased 
we see even here the most various and vigorous reflexes. The most important 
and most constant are the periosteal reflexes in the supinator longus, biceps, and 
deltoid, from a blow on the lower end of the radius and ulnar, and also the tendon 
reflex in the biceps from a blow on the biceps tendon at the elbow-joint, or in 
the triceps from a blow on the triceps tendon above the olecranon. A persistent 
clonus in the hand upon passive volar flexion sometimes occurs, but it is rare. 

In many places in the special chapters we shall go more fully into the exact 
conditions and diagnostic significance of the tendon reflexes. We shall see that 
the absence of tendon reflex is characteristic of certain spinal diseases, like polio- 
myelitis and locomotor ataxia, and also of all peripheral paralyses, traumatic 
paralyses, and neuritis. We see an abnormal increase of tendon reflex in many 
diseases of the cord, especially in that form of spinal paralysis which is termed 
spastic spinal paralysis, and very often, too, in cerebral paralyses. The increase 
of the reflex in these cases is probably always due to a disappearance of certain 
influences which normally inhibit the reflex. 



514 



DISEASES OF THE MOTOR NERVES. 



Although, we have so far tacitly assumed the reflex nature of the symptom 
termed " tendon reflex " as certain — a theory first propounded by Erb, and now 
shared by most nervous pathologists on the ground of many clinical and experi- 
mental facts — we can not conceal the fact that the reflex nature of the phenomena 
in question is not recognized by another party, headed by Westphal. West- 
phal holds the " tendon phenomena " to be the result of a direct mechanical irrita- 
tion of the muscle provoked by the jarring or stretching of the muscle. Since, 
however, careful experimental investigations, repeatedly performed, have of late 
almost without exception decided in favor of the reflex nature of the phenomena 
in question, and since many clinical facts, like the occurrence of contractions in 
distant muscles, crossed contractions, etc., can be explained only in this way, we 
will hold in the sequel to the term "tendon reflex." 

Mechanical Muscular Irritability and Paradoxical Contraction.— In addition to 
the description of tendon reflexes we must make brief mention here of two symp- 
toms which must also be considered in the examination of nervous patients. 
" Direct mechanical irritability of the muscles " is shown by the occurrence of 
contractions from a direct blow on the belly of the muscle, in which, of course, we 
can not definitely separate the direct muscular irritation from some mechanical 
irritation of the muscular nerves. Sometimes the muscular contraction is perhaps 
also a reflex, arising from the mechanical irritation of the fascia drawn over the 
muscle ; but it is worthy of mention that in cases where the tendon reflex has 
wholly disappeared, as in locomotor ataxia, the direct mechanical muscular irrita- 
bility is usually retained. The so-called idio-muscular contractions must be espe- 
cially distinguished. We see these most plainly if we give a vigorous blow with 
the ulnar side of the hand to the belly of a muscle, like the biceps. A circum- 
scribed muscular swelling forms at the point struck, and gradually disappears 
again. The test for mechanical muscular irritability has not yet attained any 
special practical importance. 

" Paradoxical contraction " is the name which Westphal has given to a symp- 
tom seen especially in the tibialis anticus, and rarely also in the flexors of the leg 
and forearm. It is when the foot, after being put in passive dorsal flexion, remains 
in this position even after the expiration of a considerable time (several minutes), 
and a marked prominence of the tendon of the tibialis anticus is usually visible. 
We can not at the present time give an explanation of this phenomenon, which so 
far has been observed in different spinal and cerebral diseases, multiple sclerosis, 
paralysis agitans, etc. 

5. General Remarks upon the Changes of Electrical Excitability in the 
Motor Nerves and Muscles.* 

Electricity, since the investigations of Duchenne, Remak, Benedikt, Moritz 
Meyer, von Ziemssen, Brenner, Erb, and others, has become not only one of the 
most prominent therapeutic aids in the treatment of nervous diseases, but it also 
plays an extremely important part in the examination of nervous patients, since 
the test of the electrical excitability of diseased nerves and muscles gives us a 
large amount of valuable information in regard to diagnosis and prognosis. 

Every complete electrical examination must be made with both currents — the 
faradic or induction current (usually the secondary current), and the galvanic or 
constant current. One " indifferent " pole is usually put on the sternum or the 
back of the neck, and the other "testing 1 ' pole on the nerve or muscle to be 

* In regard to all the details of electrical diagnosis and electro-therapeutics we would refer to Erb's 
" Handbuch der Elektrotherapie." Leipsic, Vogel, 1882. [Translated by Putzel. New York : Wm. 
Wood & Co., 1884.] 



REMARKS UPON THE DISTURBANCES OF MOTILITY. 515 

tested. The excitement of the muscle from the nerve is called indirect ; the excite- 
ment from placing the electrode on the muscle itself (where, of course, the excite- 
ment of the intra-muscular nerves can not be excluded) is called direct. Those 
points on the human body where the different nerves and muscles are most easily 
accessible to the electrical excitement are to be found in Pigs. 67 to 72, taken 
from Erb's hand-book. 

In faradic examination the rule is that we can provoke marked muscular con- 
tractions both from the nerves and from direct excitement of the muscles at the 



Region of the central 
convolutions. 



Region of the third 
frontal convolution 
and the insula 
(speech center). 

Temporalis. 

Facial (upper) in 
front of ear. 

Facial (trunk). 
Posterior auricular. 
Facial (middle br'ch). 
Facial (lower branch). 
Splenius. 

Sterno-cleido-mastoid. 

Spinal accessory. 
Levator anguli 

scapulae. 
Trapezius. 

Dorsalis scapuloz. 
Axillary (circumflex). 

Long thoracic fserra- 
tus magnus). 

Phrenic. Supraclavicular point. Brachial plexus. 
(Erb's point. Deltoid, 
biceps, brachialis anticus, 
and supinator longus.) 

Fig. 67. 

points generally accessible to excitement. We designate the strength of the cur- 
rent required by the position of the cylinder between the two coils of the induc- 
tion apparatus at which the first minimal contraction of the muscle occurs. On 
increasing the current, the minimal contraction gradually passes into a vigorous 
tetanic contraction of the muscles. 

Galvanic examination is performed by the aid of a "current reverser," by 
which the testing pole can be made either the negative pole (the kathode or 
zinc pole), or the positive pole (the anode or copper or carbon pole). By this 
"polar method of investigation" (Brenner) the following law of contraction 
is obtained, which holds equally for the normal motor nerves and for the 
muscles. 

With a weak current no noticeable excitement takes place. If we gradually 
increase the strength of the current, the first weak contraction of the muscle 
occurs at the closure of the kathode — that is, when the current is closed so that 



Frontalis 

Facial 
(upper branch) 
Corrugator supercilii, 

Orbicul. palpebrarum, 
Nasal muscles, -j 

Zygomatici. 
Orbicularis oris, -j 
Facial (middle br'ch). 

Masseter. 

Levator menti. 
Quadratus menti. 
Triangularis menti. 
Hypoglossus. 
Facial (lower branch). 

Platysma myoides. 

Hyoid muscles, -j 



Omo-hyoid. 



Anterior thoracic 
(Pectoralis major). 




516 DISEASES OF THE MOTOR NERVES. 

the kathode is made the testing pole. On opening the kathode, or on closing or 
opening the anode, nothing follows. If we increase the strength of the current 
still more, the kathodic closure contractions become stronger, and the anodic 
closure and anodic opening contractions appear, now the one being earlier and 



Triceps (long head). 



Triceps (internal head) 



Ulnar. 



Flexor carpi ulnaris 
Flexor profundus digitorum, 



Flexor sublimis digitorum 
(II and III). 



Flexor sublimis digitorum 
(I and IV). 



Ulnar. 

Palmaris brevis. 
Abductor minimi digiti. 
Flexor brevis minimi digiti 
Opponens minimi digiti 

Lumbricales. 




_ 


- — * 










' 






i ! 1 



Fig. 68. 



Deltoid (anterior 
half). 



Musculo-cutaneous 
Biceps. 

Brachialis anticus. 



Supinator longus. 
Pronator radii teres. 
Flexor carpi radialis. 

Flexor sublimis digitorum. 

Flexor longus pollicis. 
Median. 

Abductor pollicis. 
Opponens pollicis. 

Flexor brevis pollicis. 
Adductor pollicis. 



stronger, and now the other. Opening of the kathode has still no effect. Only 
with a very strong current, in which the kathodic closure contractions have 
already become tetanic — that is, they still persist after the closure of the currrent— 
can we provoke weak kathodic opening contractions. Expressed in the abbrevia- 



KEMAKKS UPON THE DISTURBANCES OF MOTILITY. 517 

tions now in general use in electrical diagnosis, the law of contraction for normal 
muscles and nerves in man is as follows : * 

1 Lowest degree with weak currents : 

KaSz, KaO—, AnS— , AnO— . 

2. Middle degree with stronger currents : 

KaSZ, KaO—, AnSz, AnOz. 

3. Highest degree with very strong currents : 

KaSTe, KaOz, AnSZ, AnOZ. 



Deltoid (posterior half). 



Radial (muscido-spiral). 
Brachialis anticus. 

Supinator longus. 
Extensor carpi radialis longior. 
Extensor carpi radialis brevior. 



Extensor communis digitorum 

' Extensor indicis 

Extensor ossis metacarpi pollicis 
Extensor primi internodii pollicis 



Dorsal interossei, I and II 




Triceps (longhead). 



Triceps (external head). 



Extensor carpi ulnaris. 
Supinator brevis. 

Extensor minimi digiti. 
Extensor indicis. 



Extensor secundi internodii 
pollicis. 



Abductor minimi digiti. 

) Dorsal interossei, 
f HI and IV. 



The variations from the normal state seen under pathological conditions con- 
sist of quantitative and also of qualitative changes in the law of contraction. We 



* Ka signifies kathode, An = anode, S = closure, O = Opening, z (Zuckung) = weak contraction, 
Z = stronger contraction, Te = tetanus. Sometimes the increasing strength of the contractions is 
abbreviated by the signs Z, Z' and Z". [Many English and American writers on electricity use letters 
derived from the English names. Thus C stands for cathode, closure, and contraction. A and 0 have 
the same meaning. It seems to us clearer and conducive to greater harmony to retain the German 
abbreviations, which are simple and definite. — Trans.] 



518 



DISEASES OF THE MOTOR NERVES. 



term the simple increase or diminution of the electrical excitability in nerves or 
muscles, without simultaneous changes in the quality and order of the occurrence 
of muscular contractions, quantitative changes. The discovery of increased or 
diminished irritability of nerve and muscle can be made most easily in unilateral 
diseases, where we can compare the strengths of current required to obtain the 
minimal contraction on the diseased and healthy side with each other. If we are 
dealing with bilateral or general diseases this is much harder to make out. We 
must then draw our comparisons from the conditions of excitability in normal 
individuals, where the different obstacles to conduction can be carefully estimated 
by the aid of a galvanometer, or by comparing the excitability of the nerve-trunks 
in the different parts of the body with one another. For this purpose we are 
usually content (following Erb's example) with comparing the superficial nerves, 
like the frontal, accessory, ulnar, and peroneal, which are easily excited. An 




Fig. 70. 



increase of electrical excitability is found in many fresh peripheral paralyses, and 
also in tetany. A diminution of electrical excitability is found quite frequently in 
bulbar and spinal paralyses, in progressive muscular atrophy, etc. 

Much more important, however, than the simple quantitative changes of elec- 
trical excitability are those not merely quantitative, but also qualitative deviations 
from the normal law of contraction, which were first discovered in certain forms 
of paralysis by Baierlacher in 1859, and were soon generally confirmed. Erb has 
given these the name of the " reaction of degeneration," because they are closely 
connected with the progress of certain anatomical changes in the paralyzed mus- 
cles and nerves. 



REMARKS UPON THE DISTURBANCES OF MOTILITY. 519 



In order to make the relations of the reaction of degeneration clear, let us 
select as an example any fresh peripheral paralysis and follow the changes in 
excitability to the two currents in the nerves and muscles. In a short time (two 
or three days) after the onset of the paralysis a gradually increasing decline in the 
faradic and galvanic excitability in the nerve begins. After one or two weeks 
the excitability is completely lost, so that from the nerve we can no longer 
provoke any trace of muscular contraction with the strongest faradic or con- 
stant current. During this time the excitability of the paralyzed muscles to 
the faradic current has also rapidly diminished, and finally has wholly disap- 



Gluteus maximus. 



Sciatic. 

Biceps f em oris (long head). 
Biceps femoris (short head). 



Peroneal 

Gastrocnemius (external head), 
Soleus 



Flexor longus hallucis. 




Adductor magnus. 
Semitendinosus. 
Semimembranosus. 



Posterior tibial. 



Gastrocnemius (internal head). 



Soleus. 



Flexor longus digitorum. 



Tibial. 



Fig. 71. 

The case is quite different with direct galvanic excitement of the mus- 
cles. Here we find at first a slight diminution, which in the second week passes 
to a decided increase of the galvanic muscular excitability. We now obtain 
marked muscular contractions with relatively very weak currents. Beside that, 
two other very important peculiarities are to be noted : 1. The muscular contrac- 
tions are not short and lightning-like, as under normal conditions, but they seem 
quite sluggish, protracted, " worm-like," and often persist during the whole dura- 
tion of the closure of the current. 2. The muscular contractions occur not only 
chiefly at kathodic closure (KaS), as under normal conditions, but the anodic 
closure contractions are as strong as the kathodic closure contractions (KaSZ), or 



520 



DISEASES OF THE MOTOR NERVES. 



even plainly exceed them. The kathodic opening contraction (KaOZ) is also fre- 
quently stronger. 3. It may also be mentioned here that the mechanical irrita- 
bility of the muscles in such cases is usually increased. 

This second degree of the reaction of degeneration lasts from four to eight 
weeks. If the paralysis be severe and long continued, or incurable, at the end of 
this period comes a decline of the galvanic muscular excitability. The contractions 
become weaker, the strength of current necessary to produce them greater, and, 
finally, in incurable cases, even with the strongest currents, we can obtain only 
a little slow anodic closure contraction, or none at all. It is different, however, in 
the milder, curable cases. In these the passage to the normal condition gradually 
follows either the increase of the galvanic muscular excitability, or, in more pro- 




Fig. 72. 



tracted cases, its secondary decline. The contractions become more vigorous and 
shorter, the kathodic closure contraction (EaSZ) again predominates, the faradic 
muscular excitability and the faradic and galvanic excitability of the nerves 
finally return, and with them the old normal conditions are restored. A fact to be 
observed in these cases is of great interest, namely, that the voluntary motion in 
such cases often returns decidedly earlier than the electrical excitability of the 
peripheral nerves. We see, then, that a diseased nerve may be capable of con- 
ducting irritations coming from the brain, while the taking up of irritation, its 
direct excitability, is still completely lost.* In such cases we can obtain a mus- 
cular contraction by electrical irritation of the nerve above the point of lesion. 



* This is also connected with the repeated observations by Erb, Bernhardt, and others, that in 
lesions of peripheral nerves, and perhaps also in spinal diseases, reaction of degeneration can some- 



KEMAKKS UPON THE DISTURBANCES OF MOTILITY. 521 



Beside the complete reaction of degeneration just described, there is also a so- 
called partial reaction of degeneration, which is not infrequent in milder cases. 
This is when the diminution of the faradic and galvanic excitability in the nerves, 
and the diminution of faradic excitability in the muscles, is only of a slight degree, 
while the characteristic changes in the direct galvanic excitement of the muscles 
— increased excitability, slow contractions, and predominance of anodic closure 
contractions — are fully developed. In some cases the occurrence of slow contrac- 
tions on faradic excitement of nerves and muscles has lately been observed — 
" faradic reaction of degeneration." 

Anatomical Changes of the Nerves and Muscles in the Reaction of Degenera- 
tion ; its Significance in Diagnosis and Prognosis— As we have seen on page 507, 
all paralyses may be divided into two great groups — into atrophic paralyses, and 
paralyses without marked atrophy of the affected muscles. We have learned to 
recognize the necessary hypothesis of the " trophic " influence of the ganglion-cells 
in the anterior cornua of the spinal cord as the foundation of this distinction. In all 
cases where the disease affects these ganglion-cells, or is situated in the peripheral 
nerves, so that the trophic influence of the ganglion-cells on the muscles can no 
longer be of influence, we have a degenerative atrophy of the peripheral portion of 
the nerve, and of the muscle belonging to it. This degenerative atrophy is the 
anatomical cause of the symptoms of the electrical reaction of degeneration. 

If we have to do with a peripheral paralysis, such as a traumatic lesion of a 
nerve-trunk, the portion of the nerve peripheral to the point of lesion is separated 
from its " trophic center " in the cord, and begins to undergo secondary degenera- 
tion. The first anatomical sign of the degeneration is a breaking down of the 
medullary sheath into large and small flakes and drops. The axis cylinder is also 
soon destroyed, so that the sheath of Schwann finally incloses only homogeneous 
fluid contents, which are in great part rapidly absorbed. At the same time there is 
an increase of the nuclei in the sheath of Schwann, and this increase, when the 
process is long continued, leads to a decided increase of the interstitial connective 
tissue in the nerve. The diminution and final loss of electrical irritability in the 
nerve are perfectly parallel to these anatomical changes, as we can easily under- 
stand. 

The degeneration of the nerve involves its finest terminal branches in the 
muscles ; but the muscle itself does not remain unchanged. The muscular fibers 
undergo a marked atrophy. They become much smaller, their transverse striation 
is less distinct, and they show in part a fatty and " granular " degeneration of their 
contents. Some fibers show that peculiar yellow homogeneous character which 
we call " waxy degeneration." In addition to this, there is a considerable increase 
of the muscular nuclei, and in the later stages a great new growth of interstitial 
connective tissue, often associated with a marked deposit of fat. These muscles, 
thus altered, now react only to the galvanic current, and in the manner above 
described. The particular cause of this remarkable fact is, of course, still com- 
pletely unknown to us. 

In the incurable cases the processes of degeneration just described gradually 
advance, but, in the cases that recover, a number of processes of regeneration begin 
sooner or later. We can not here go into the finer details, which are still, in many 
respects, the subject of controversy ; but it is certain that new nervous and muscu- 
lar fibers are formed, and that, hand in hand with the anatomical processes of 
regeneration, first the voluntary motion, and later the electrical excitability of the 
paralyzed parts, gradually return again. 

times be made out even in those muscles which show no essential limitation of their voluntary mobil- 
ity. In these cases the electrical examination points to finer anatomical disturbances which have not 
led to the loss of voluntary excitability. 



522 



DISEASES OF THE MOTOR NEEVES. 



The same anatomical changes, which we have just described as a secondary- 
degeneration in lesions of the peripheral motor nerves, also develop, if the primary 
disease has its seat in the anterior cornua of the gray matter of the spinal cord — 
that is, in the trophic centers themselves. In these cases, of course, the form of the 
disease has nothing to do with it. Both in the different forms of inflammation 
and of primary atrophy, and also in new growths, which affect the anterior gray 
matter of the cord, a secondary degeneration, with pronounced reaction of degen- 
eration, develops from the anterior roots of that portion of the cord affected to 
the ends of the peripheral nerves, and even to the corresponding muscles. We 
shall also learn to recognize a number of primary degenerations of the peripheral 
nerves, like primary neuritis, diphtheritic and toxic paralyses, etc., which likewise 
show the same anatomical changes, and likewise give, as a result of these, electrical 
reaction of degeneration. In all cerebral paralyses, however, and in those spinal 
paralyses where the cause of the paralysis is situated above the part of the anterior 
gray cornua concerned, the degenerative atrophy, and also the reaction of degen- 
eration, are entirely wanting. 

"We thus see that the reaction of degeneration, in regard to diagnosis, at once 
permits us to decide that the disease is situated in the gray matter of the cord, 
or in the peripheral nerves. It does not permit any further distinction. In regard 
to prognosis, it teaches us that anatomical changes have taken place in the nerves 
and muscles, from which a restoration is still very possible, but at all events it can 
take place only after the lapse of a longer time, at least two or three months. We 
will soon learn to recognize a number of mild peripheral paralyses in which there 
is generally no reaction of degeneration. From the absence of reaction of degen- 
eration we can then draw the conclusion, with certainty, that no coarse anatomi- 
cal changes are present in the nerve, and that we may expect after the trouble a 
much more rapid recovery, perhaps in three or four weeks. The partial reaction 
of degeneration, above mentioned, is also an important symptom in regard to 
prognosis. It shows that severe anatomical changes have taken place in the 
muscles but not in the nerves, and hence it always permits a more favorable 
prognosis as to time than in the cases with complete reaction of degeneration. 



CHAPTER II. 

THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 

1. Paralysis of the Ocular Muscles. 

iEtiology . — The largest part of all the ocular paralyses arise from affections 
which involve either the peripheral nerves or their nuclei in the brain-stem. We 
accordingly make a distinction between peripheral and nuclear paralyses of the 
ocular muscles. As we shall take up the latter more fully in the description of 
chronic bulbar paralysis, we have here to mention only the most important and 
most frequent causes of the peripheral ocular paralyses. These are as follows : 

1. Traumatic injuries, which directly affect the nerve-trunks or their branches : 
blows on the eye, knife-stabs, fractures of the skull involving the orbit or the base 
of the skull, and the like. 

2. Compression of the nerves from morbid processes in their neighborhood. 
Tumors of the base of the skull, especially, very often lead to ocular paralyses. 
Periostitis at the base of the skull or in the orbit may also cause similar symptoms, 
and so do syphilitic diseases of the nerves and their surroundings, the meninges or 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 523 



periosteum, aneurisms of the basilar artery, acute or chronic meningitis in its dif- 
ferent forms, etc. In all these cases we usually have to do with a pure mechanical 
compression of the affected nerves by the morbid new growths in their immediate 
vicinity. More rarely the pathological process directly invades the nerves them- 
selves. 

3. The so-called rheumatic ocular paralyses are quite common. These arise 
after some decided exposure to cold, like a draught from an open window, and 
are in all probability very largely of a peripheral nature. They depend, as is 
supposed, upon an acute neuritis of the affected nerve, and hence are to be regarded 
as completely analogous to the other rheumatic paralyses, like rheumatic facial 
paralysis. Among the " rheumatic paralyses " we usually class the paralyses which 
apparently come on spontaneously and completely recover, for which no other 
special cause can be made out. 

4. The ocular paralyses that sometimes arise after certain acute diseases are 
also of a peripheral nature, and are due to a degenerative neuritis of the affected 
nerves. They are most frequent as a result of diphtheria, and are much more 
rare in typhoid, acute rheumatism, etc. Of chronic diseases, diabetes mellitus 
may sometimes give rise to ocular paralyses, especially to paralysis of accom- 
modation. 

A fuller account of the very important ocular paralyses in locomotor ataxia 
will be found in the description of that disease. 

Symptoms. — Since we must refer to the text-books of ophthalmology in regard 
to the more precise symptomatology, and the more special methods of ophthalmic 
investigation, we will here give only a brief review of the chief symptoms of ocu- 
lar paralyses which are important in nervous pathology. 

The disturbance in the mobility of one eye is noticed by the patient himself 
from the appearance of double images — double vision, or diplopia. These arise 
because, on looking to one side, the eye on the paralyzed side can not be brought 
into the corresponding position, and consequently the retinal images no longer 
fall upon the same spots. In pathological convergence of the visual axes homolo- 
gous double images arise, in pathological divergence crossed images — that is, in 
the first case, on closing one eye, the image disappears on the same side, in the 
second case it disappears on the opposite side. By alternately fixing the gaze on 
one or the other of two fingers held in line with each other, and by regarding the 
disappearance, on closing one eye, of the double image of the finger not fixed, we 
can easily demonstrate this on ourselves. If, then, crossed double images arise, 
for example, on looking to the right, we must have a divergent strabismus — that 
is, an imperfect function of the left internus ; but if there are homonymous 
double images, there must be a convergent strabismus, and consequently a weak- 
ness in the right abducens. It makes it much easier to test the double images 
if we put a colored glass before one of the patient's eyes. False projections of 
the visual field arise, as a result of the double images and of the abnormal 
strength of innervation which the patient exerts, so that the patient's judgment 
of the position of external objects is uncertain. In the more extensive ocular 
paralyses this often leads to a pronounced feeling of dizziness. In order to avoid 
this unpleasantness many patients confine themselves to monocular vision, close 
the affected eye, or put their heads in a position to avoid the double images. 

Physical examination gives the following results, according to the extent of 
the paralysis : 

In complete paralysis of one oeulo-motor nerve (the levator palpebrse superioris, 
the superior, inferior, and internal recti, the inferior oblique, the sphincter of 
the iris, and the ciliary muscle) the first thing that is noticed, beside the disturb- 
ance in the movements of the eye, is the more or less complete drooping of the 



524: 



DISEASES OF THE MOTOR NERVES. 



upper lid — ptosis. If we ask the patient to follow with his eyes the motion of any 
object, like the finger, held before him, keeping his head still, we notice at once 
that the affected eye does not move upward, downward, or inward. The pupil is 
dilated (mydriasis) and no longer contracts to light. Accommodation is lost, and 
distinct vision for near objects is impossible. As a rule, the whole eye seems 
rather prominent (paralytic exophthalmus), because the backward traction of the 
recti is very largely absent. In old oculo-motor paralysis there is often a second- 
ary contracture in the unparalyzed external rectus (and superior oblique), by 
which the eye is persistently drawn outward. Partial oculo-motor paralyses are 
not infrequent, especially isolated ptosis, isolated paralysis of the internal, inferior, 
or superior rectus, or isolated paralysis of accommodation, and they may usually 
be easily recognized from what has been said. 

Paralysis of the abducens is characterized by the inability to move the external 
rectus. The eye can no longer be moved, or it can be moved only imperfectly, 
outward beyond the median line. In old paralysis the eye is drawn inward from 
a secondary contracture of the internal rectus, and convergent strabismus arises. 
Paralysis of the abducens may be isolated, bilateral, or combined with other ocu- 
lar paralyses. 

Paralysis of the trochlear nerve, the superior oblique muscle, is not perfectly 
easy to recognize ; but it is rarely of special practical importance. The action 
of the superior oblique coincides with that of the inferior rectus. The paraly- 
sis of the former, therefore, is soonest recognized by the retardation of the eye 
in movements downward and also inward, and sometimes by the failure of the 
eye to revolve, which rotation normally takes place on looking downward, and is 
due to the superior oblique muscle. This latter movement takes place in each eye 
inward, toward the nose, about a sagittal axis, in such a way that the left eye is 
turned from the left and up to the left and downward, and the right eye from the 
right and up to the right and downward. In regard to diagnosis it is also charac- 
teristic that the double images in trochlear paralysis appear only in the lower 
half of the field of vision, and especially on looking downward. Hence it hap- 
pens that the disturbance of vision is especially manifest in going up or down 
stairs. 

Finally we must mention a symptom to be observed in almost every ocular 
paralysis — the so-called secondary deviation of the healthy eye. If, after the 
sound eye has been covered, we have the paretic eye fix itself upon a point which 
it can not reach at all or which it can reach only after the utmost exertion, we 
see, when the covering hand is taken away from the sound eye, that the latter 
has been moved much too far in the corresponding direction. The abnormal 
exertions of innervation with the affected eye, somewhat after the analogy of 
certain associated movements, pass over to the associated muscle of the healthy 
side and cause in it too extensive a contraction. 

The following must be added in regard to the separate forms of ocular paraly- 
sis : Rheumatic ocular paralysis affects the abducens most frequently, and not 
infrequently the oculo-motor or one of its branches, as in isolated ptosis. A case 
observed by us a short time ago is, at any rate, rare, in which exposure to severe 
cold had been followed by a complete paralysis of all the muscles of the right 
eye, with complete ptosis, and almost absolute immobility of the eye in any direc- 
tion. The rheumatic ocular paralyses are almost always acute in their onset, and 
they are often during the first period associated with sensations of pain about the 
eye and in the head. Vomiting (of reflex origin ?) is also not rare at the beginning 
of the affection. The course of most cases is favorable, since they usually com- 
pletely recover in a few weeks, though sometimes not for months. In some cases 
the paralysis may remain stationary. The diphtheritic ocular paralyses usually 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 525 



appear, like the other diphtheritic paralyses, a week or two after the termination 
of the disease. They most frequently affect the muscles of accommodation, so that 
the patient complains chiefly of indistinct vision for near objects ; but we some- 
times see paralyses of the external ocular muscles also, the abducens or the inter- 
nal rectus. The prognosis of diphtheritic paralyses is almost invariably favor- 
able. Finally, we must mention here the " periodical oculo-motor paralysis," to 
which Mobius and others have lately called attention, and whose nature is still 
almost wholly inexplicable. In the cases of this sort repeated paralyses of one 
oculo-motor nerve, often associated with headache and vomiting, just as in migraine, 
come on at longer or shorter intervals (in women sometimes at the menstrual 
period) in the same individual, who has often had them since childhood. The 
individual attack sometimes lasts only a few days, but often some weeks. The 
attacks usually become gradually more severe later on. 

Nothing generally applicable can be said as to the course and prognosis of the 
other forms of ocular paralyses, since in them everything depends upon the form 
of the underlying disease. 

Treatment. — In regard to the fulfillment of any possible causal indication we 
must remember especially that a syphilitic origin of ocular paralysis is not very 
rare. Iodide of potassium and energetic mercurial inunction may sometimes give 
very good results in such cases. Hence these remedies must also be tried in 
doubtful cases. 

Of other remedies galvanic treatment gives the speediest relief. We pass weak 
currents transversely through the temples, or, what is usually better, put the anode 
to the back of the neck and apply the labile kathode to the closed eye, especially 
to the region corresponding to the paralyzed muscles. Great caution, weak cur- 
rents, and the avoidance of any great variations in the currents are of course 
necessary. We may also try preparations of strychnine internally, or, better, sub- 
cutaneously in the vicinity of the eye. We must refer to special treatises with 
regard to a correction of the double images by prismatic spectacles or in regard to 
operations, like tenotomy, that are sometimes performed. 

2. Paralysis of the Motor Branch of the Trigeminus. 

{Paralysis of the Muscles of Mastication.) 

Paralysis of the muscles of mastication, the masseters and temporals, supplied 
by the third branch of the trigeminus, is a rare affection. It is most frequently 
seen in diseases of the base of the skull which compress the motor branch of the 
fifth. We shall also learn later on to recognize paralysis of the muscles of mastica- 
tion as a rare symptom of chronic bulbar affections. 

The chief symptom of motor paralysis of the trigeminus is the difficulty or 
impossibility of chewing. In unilateral- paralysis the patient can chew only on 
the healthy side ; in bilateral paralysis he can no longer chew at all. The lower 
jaw hangs loosely down and can also no longer be moved sideways, from the 
co-existing paralysis of the pterygoids. There are often sensory disturbances in 
the distribution of the trigeminus at the same time. 

The prognosis and treatment depend upon the primary disease. Local faradi- 
zation or galvanization of the paralyzed muscles is to be tried. 

3. Facial Paralysis. 

{Mimetic Facial Paralysis. Bell's Palsy.) 

iEtiology. — Facial paralysis is one of the commonest peripheral paralyses, as 
we can understand from the exposed position of the nerve and its course through 



526 DISEASES OF THE MOTOR NERVES. 

the narrow Fallopian canal. The most important causes of it are : 1. Exposure 
to cold, draughts, sleeping by an open window, riding in the cars with the win- 
dow open, etc. The paralyses arising in this way are termed " rheumatic," and we 
also include in this class those peripheral paralyses which are apparently spon- 
taneous — that is, those without any marked exposure to cold that can be dis- 
covered. In all these cases we probably have to do with a neuritis of the nerve- 
trunk, which comes on in a way as yet unknown. 2. Diseases of the middle ear 
and caries of the petrous bone. As the facial passes through the Fallopian canal, 
which is in the immediate vicinity of the tympanic cavity, we can easily under- 
stand how, in caries of the petrous bone and in purulent affections of the middle 
ear, inflammation may often invade the trunk of the facial, or how the facial may 
be compressed by inflammatory exudations, etc. 3. In rare cases a pressure 
paralysis of the facial nerve arises in swelling of the parotid gland or tumors in 
its vicinity. 4. Diseases of the base of the skull or brain, tumors, syphilitic new 
growths, and acute or chronic inflammations, often give rise to the development 
of a facial paralysis by invasion of the trunk of the facial or compression of it. 5. 
We shall have to speak repeatedly of the frequent implication of the facial nerve 
in diseases of the brain and medulla in the following sections. 

Symptoms and Course. — The manifold character and different functions of the 
nerves, which unite in the trunk of the facial, are the cause of the quite large array 
of symptoms in facial paralysis. The paralysis of the facial muscles of expression 
is the most striking and characteristic (see Fig. 73). The paralyzed half of the 
face is lax and expressionless, the wrinkles in the forehead are obliterated, the eye 

is abnormally wide open and waters 
(epiphora), the naso-labial fold is 
obliterated, the corner of the mouth 
droops, and saliva frequently flows 
from it. The paralysis becomes still 
more marked on any movement of 
the face, on wrinkling the forehead, 
turning up the nose, laughing, talk- 
ing, whistling, or inflating the cheeks. 
The eye can be only partly closed. 
On attempting it, the upper lid sinks 
down from its weight (a weakening 
of the levator palpebral superioris), 
the eye is turned upward, so that the 
pupil is covered, but quite a wide 
space is left between the eyelids 
(lagophthalmus). This defective 
closure of the lids facilitates the 
entrance of dust, etc., into the eye, 
and sometimes gives rise to con- 
junctivitis, or even to severer in- 
flammation of the eye. Speech is 
rendered difficult and indistinct from 
defective movements of the lips, 
and mastication is rendered difficult 
from the imperfect movement of the 
cheeks. In many cases we also find a paresis of the soft palate on the affected 
side; the fibers from the facial pass through the superficial petrosal nerve to the 
sphenopalatine ganglion, and thence to the soft palate. It droops more, and 
on phonation the soft palate is raised obliquely to the healthy side. No general 




Fig. 73.— Right facial paralysis (after SeeligmEller). 
The folds are smoothed out and in part entirely ab- 
sent on the paralyzed side, while they are strongly 
marked on the left. The mouth and nose are drawn 
to the left. 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 527 



rule can be given as to the position of the uvula, as this varies very much even 
under normal conditions. 

Disturbances of taste in the anterior two thirds of the tongue have been repeat- 
edly found s on the paralyzed side, but they usually attain only a slight degree. 
They are explained by an affection of the fibers of the chorda tympani, which run 
for some distance in the facial, as has been described on page 502. At the begin- 
ning of the paralysis many patients complain of subjective sensations of taste. 
Later on the dullness of taste may often be discovered by careful testing. Tactile 
sensation in the tongue is only exceptionally diminished (sensory fibers in the 
chorda?). There is sometimes a diminished secretion of saliva (fibers in the 
chorda), which produces an abnormal feeling of dryness in the patient's mouth on 
the paralyzed side. Disturbances of hearing are frequent, but they are usually 
due to some complicating aural trouble {vide supra), or to a co-existing affection 
of the acoustic nerve. Paralysis of the stapedius muscle, however, sometimes 
seems to cause symptoms, including a marked sensitiveness to all loud sounds, and 
even an abnormal acuteness of 
hearing, especially for low notes 
(hyperacusis, oxyokoia). This 
symptom is due to the fact that 
in paralysis of the stapedius its 
antagonist, the tensor tympani, 
causes a greater tension of the 
membrana tympani. Reflex 
movements, winking, etc., are, 
of course, lost in complete pe- 
ripheral facial paralysis. For the 
special reflexes, which are often 
seen in the later stages of facial 
paralysis, vide infra. 

By testing all the symptoms 
described, in most cases we can 
decide with accuracy upon the 
place where the break in con- 
duction in the facial must occur. 
If we examine the accompanying 
plan of the facial (Fig. 74), de- 
vised by Erb, we can easily 
understand the following chief 
symptomatic forms of facial 
paralysis : 

1. Paralysis of the facial 
muscles; but taste, secretion of 
saliva, hearing, and soft palate 
normal ; seat of the affection in 
the portion between 1 and 2, 
usually the trunk of the facial 
below the Fallopian canal. 

2. Paralysis of the facial mus- 
cles, disturbance of taste, and 

eventually diminished secretion of saliva ; but hearing and soft palate normal ; 
seat of the affection within the Fallopian canal between 2 and 3. 

3. Paralysis of the facial muscles, disturbance of taste, diminished secretion of 
saliva, abnormal acuteness of hearing ; but soft palate normal ; seat between 3 and 4. 




Fig. 74.— Schematic representation of the trunk of the facial 
from the base of the skull to the pes anserinus. Differ- 
ent localizations of the lesion in paralysis. N.f. Facial 
nerve. N.p.s. Great superficial petrosal. N.c.c.p.t. 
Nerve communicating with the tympanic plexus. N.st. 
Stapedius. Ch.t. Chorda tympani. Gf. Fibers of taste. 
Sps. Nerve governing the secretion of saliva, N.a. 
Acoustic nerve. G.g. Geniculate ganglion. F.st. Stylo- 
mastoid foramen. N.a.p. Posterior auricular nerve. 



528 



DISEASES OF THE MOTOR NERVES. 



4. Paralysis of the facial muscles, disturbance of taste, diminished secretion of 
saliva, abnormal acuteness of hearing, and paresis of the soft palate ; seat in the 
geniculate ganglion between 4 and 5. 

5. Paralysis of the facial muscles, diminished secretion of saliva, abnormal 
acuteness of hearing, paresis of the soft palate, but no disturbance of taste ; seat 
above the geniculate ganglion between 5 and 6. 

The changes in electrical excitability, and some other changes, may be best 
described in connection with the course of facial paralysis. The paralysis usually 
begins quite suddenly ; less frequently it is more gradual. Sometimes there are, 
for a short time, subjective prodromata, like abnormal sensations of taste, slight 
ringing in the ears, and above all painful sensations in the ear and face, which 
symptoms may be referred to the beginning of acute inflammatory processes in 
the nerve. In a few cases the occurrence of herpes vesicles has been observed in 
the distribution of the affected facial, a condition which may be soonest explained, 
in accordance with what was said on page 494, by reference to the numerous 
anastomoses between the branches of the facial and those of the trigeminus. 

In regard to the further course we distinguish the three following forms : 

1. The mild form of facial paralysis, to which especially many rheumatic 
paralyses belong. The affection is usually referred only to the facial muscles, 
disturbances of taste, etc., being wholly absent. Electrical excitability in the 
facial and the paralyzed muscles remains entirely normal. Recovery is rapid, 
usually in two or three weeks. In these cases we may certainly suppose that 
there are generally no severe and deep-seated anatomical changes in the nervous 
or muscular fibers. 

2. The middle form of facial paralysis (Erb). In this there is no complete 
reaction of degeneration, but only a partial one. The excitability of the nerve is 
somewhat diminished, but it is not lost. In the muscles, however, in about two 
or three weeks, there appears a decided increase of galvanic excitability to direct 
excitement. The anodic closure contraction (AnSZ) is also greater than the 
kathodic closure contraction (KaSZ), and the contractions are slow. In regard 
to prognosis we may decide from this that the recovery will still be quite rapid. 
It usually follows in from four to six weeks. 

3. The severe form of facial paralysis is that in which there is a complete 
reaction of degeneration in the nerve and muscles, the details of which we have 
learned in the previous chapter, loss of faradic and galvanic excitability of the 
nerve, loss of faradic excitability of the muscles, and quantitative and qualitative 
changes in the galvanic excitability of the muscles. In this form there are always 
coarse processes of degeneration in the nerve and muscles, so that recovery fol- 
lows, if at all, only after two to six months, or even later, because the processes of 
regeneration require at least as much time for their accomplishment. We often 
see in the later stages of these cases special symptoms of motor irritation (Hitzig). 
These consist, first, of a more or less marked tonic contracture of the paralyzed 
muscles, which is sometimes very striking ; second, of single spasmodic contrac- 
tions of the muscles ; third, of special associated movements — if the patient closes 
his eyes, winks, etc., there always follows a marked distortion of the corner of 
the mouth, which can not be suppressed — fourth, of an increased reflex irrita- 
bility — on pricking the skin, on blowing on it, vigorous muscular contractions 
follow. We have often ourselves seen contractions in the affected facial muscles 
following a blow on the bridge of the nose, on the nasal bone, or on the forehead 
on the healthy side. These reflexes come from the skin, or perhaps in part from 
the periosteum and the fasciae also. All these symptoms may last for a very long 
time — for years in incurable or in imperfectly cured cases. 

Prognosis. — The prognosis of facial paralysis depends, of course, in the first 



THE DIFFEEENT FOEMS OF PEEIPHEEAL PAEALYSIS. 529 



place, upon the primary disease, if any exists. Paralysis in tumors of the base of 
the brain, caries of the petrous bone, etc., is almost always incurable. The course 
of the paralysis in affections of the middle ear depends upon the curability of the 
latter disease. Very important data for the accurate prognosis of rheumatic 
paralysis are given by the electrical examination, as has been carefully described 
above. Of course, we can never form a definite judgment from this at the begin- 
ning of the paralysis, but only at the end of the first week. If, at the end of the 
first week or fortnight, the electrical excitability of the nerve still remains normal, 
we can almost certainly prophesy a rapid and favorable course. If reaction of 
degeneration appears, we can not count upon recovery in the most favorable cases 
before two or three months. As a rule, relapses do not occur, but we saw a man 
of about thirty who had a peripheral facial paralysis four times within a few years, 
which disappeared each time after a few weeks, a condition which possibly is to 
be regarded as analogous to the lt periodical oculo-motor paralysis " (see page 525). 

Diagnosis. — The symptoms of facial paralysis are so pregnant that the paralysis 
itself can always be easily recognized. In regard to the precise form of the 
paralysis and its cause, we can often decide only by considering the setiological 
factors, such as injuries, exposure to cold, or aural affections. In distinguishing 
between peripheral and central (bulbar or cerebral) paralyses, the other co-exist- 
ing bulbar or cerebral symptoms must also be considered. We shall learn to 
recognize more accurately later the different modes in which, in these cases, 
facial paralysis may be combined with paralysis of the other cerebral nerves, or 
the nerves of the extremities. In doubtful cases electrical examination is often of 
decisive value. Eeaction of degeneration can be present only in peripheral paraly- 
sis, or in such bulbar paralyses as affect the fibers of the facial below the facial 
nucleus or affect the nucleus itself. In all the genuine cerebral paralyses the 
electrical excitability is perfectly retained. It may also be mentioned here briefly 
that in all cerebral facial paralyses the frontal portion of the facial is usually un- 
affected, while in peripheral paralysis it also is paralyzed. The ability to close the 
eye is usually not affected in cerebral facial paralysis. 

Treatment. — The treatment of the underlying disease is of the greatest impor- 
tance in all cases where any aural affection, any removable compressing swelling, 
as of the parotid, or syphilis, lies at the bottom of the trouble. The methods of 
treatment indicated in such cases are self-evident. In other cases electricity is 
the only remedy which can exhibit sure results, although we must not overestimate 
its efficiency. In fresh facial paralysis we may recommend the stabile conduction 
of a weak constant current through the auriculo-mastoid fossae, four to six times a 
week for two or three minutes, at first the anode, then the kathode, to the affected 
side. Later on the chief treatment is peripheral galvanization, or eventually 
faradization of the muscles. We place the anode in the auricular fossa and slowly 
stroke the different nerve-branches and the muscles with the kathode. We can 
often confirm the fact, immediately after each sitting, that the eye closes better 
after galvanization of the orbicularis. Faradization perhaps excites a reflex 
irritation of the nerves from irritation of the skin, and hence is of service. 

Of other remedies we may mention subcutaneous injections of strychnine, 
seven to fifteen minims of a one-per-cent. solution of the sulphate three or four 
times a week, although it is only rarely of use. In secondary contractures 
we may obtain favorable results by methodical stretching of the muscles by 
wooden wedges inserted under the cheeks and by massage. 

4. Paralyses in the Eegion of the Muscles of the Shoulder. 

Isolated paralyses of these muscles are rare, with the exception of the practi- 
cally important paralysis of the serratus. Functional disturbances in them are 
34 



530 



DISEASES OF THE MOTOR NERVES. 



more frequent, as one symptom in complicated paralytic states, especially in pro- 
gressive muscular atrophy. The diagnosis of these paralyses in detail is often very 
difficult. 

Paralysis of the Sterno-cleido-mastoid (spinal accessory nerve). — The chin 
is somewhat raised and turned toward the affected side in consequence of the 
antagonistic contracture of the other sterno-mastoid. Motion in the opposite 
direction is difficult. In bilateral paralysis of this muscle it is very difficult to turn 
the head with the chin raised, and it can be done only imperfectly. 

Paralysis of the Trapezius (spinal accessory nerve). — The shoulder sinks 
downward aud forward so that the supra-clavicular fossa becomes deeper. The 
median border of the scapula is not parallel to the vertebral column, as under 
normal conditions, but it runs obliquely from below and inward, upward and out- 
ward. Voluntary raising of the shoulder, " shrugging the shoulder," is impaired, 
and it can be done only by the levator scapulae. The drawing back of the shoul- 
der, approximating it to the vertebral column, is difficult, and can be done only 
by the rhomboidei. Raising the arm above the horizontal is also affected, from 
the impaired fixation of the scapula. 

Paralysis of the Pectoralis Major and Minor (anterior thoracic nerves). 
— Abduction of the upper arm is difficult or impossible. The hand can no longer 
be placed on the shoulder of the healthy side. 

Paralysis of the Rhomboidei and the Levator Anguli Scapula (dorsalis 
scapulae nerve) can be certainly recognized only when the trapezius is also para- 
lyzed. Then the approximation of the scapula to the vertebral column (rhom- 
boidei) and the raising of the scapula (levator anguli scapulae) are completely 
abolished. 

Paralysis of the Latissimus Dorsi (subscapular nerves). — There is no 
deformity when at rest, but the arm can not be strongly adducted, and the hand 
can not be placed on the sacrum. 

Paralysis of the Rotators of the Humerus Inward and Outward.— In 
paralysis of the inward rotators, the teres major and subscapular, innervated by 
the subscapular nerves, the arm, when rotated outward, can not be brought back 
again to its normal position. All manipulations, too, which the paralyzed arm 
tries to make on the opposite side of the body, are considerably impaired. In 
paralysis of the outward rotators — the infra-spinatus, innervated by the supra- 
scapular nerve, and the teres minor, innervated by the axillary— rotation of the 
arm outward is abolished. In writing and sewing (using the needle), the paraly- 
sis causes very marked disturbance. 

Paralysis of the Serratus Anticus Major (paralysis of the long thoracic 
nerve). — This paralysis is quite common, and therefore is of practical importance. 
Its most frequent cause is traumatic action on the nerve. Therefore it is espe- 
cially common hi porters, soldiers, etc. Beside this, serratus paralysis sometimes 
arises from exposure to cold, " rheumatic serratus paralysis," and also as a result 
of infectious diseases, like typhoid, and as one symptom of progressive muscular 
atrophy, especially in the juvenile form. 

As the arm hangs down quietly, the scapula on the paralyzed side stands out a 
little from the chest-wall, from the action of the antagonists (the rhomboidei, the 
levator anguli scapulae, and the trapezius), its lower angle is a little approximated 
to the vertebral column, and therefore its median edge runs obliquely upward and 
outward. If the patient tries to raise his arm, he can raise it only to the hori- 
zontal position, and we fail to see the projection of the tense indentations of the 
serratus on the lateral wall of the chest ; but as soon as we seize the scapula 
firmly and push it forward — that is, supply the missing action of the serratus — the 
patient can at once raise the arm. If the arm is raised upward to the horizontal 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 531 



line, the scapula approaches the vertebral column ; if it is raised forward, there 
appears a very characteristic wing-like projection of the inner border of the scap- 
ula, so that we can touch with the hand the inner surface of the scapula (see 
Fig. 75). Adduction of the arm and laying the hand on the other shoulder are 
also disturbed. The cutaneous sensibility of the chest is, as a rule, normal. 




Fig. 75.— Paralysis of the right serratus. (From a photograph by Dxjchenne.) 



The course of serratus paralysis is usually tedious. Recovery does not take 
place for several months, as a rule. Many cases are incurable. Treatment con- 
sists chiefly in the application of electricity to the paralyzed nerve and muscles. 

5. Paralyses of the Muscles of the Back. 

Of the paralyses of the muscles of the back, which are rarely seen except as 
a complication of more extensive paralyses, paralysis of the extensors of the spine 
in the lumbar region (the erector spinse and its divisions, the sacro-lumbalis and 
longissimus dorsi) is the only one that has a practical interest. This is seen com- 
paratively often in the muscular atrophy or pseudo-hypertrophy of children {vide 
infra), and causes a remarkably characteristic and easily recognizable picture. If 
we make the little patient stand up, the peculiar carriage of the body strikes us at 
once. The lumbar vertebrae are arched forward in lordosis, the belly is very 
prominent, and the upper part of the body is bent backward. The trunk is bal- 
anced on the hips and the gait is waddling. The paralysis of the erectors appears 
most plainly if the child has stooped to get any object and tries to straighten up 



532 



DISEASES OF THE MOTOR NERVES. 



again. He can bring the upper part of his body into the erect posture only by 
supporting himself with his hands on his knees, and slowly climbing up his 
thighs. 

6. Paralyses in the Region of the Upper Extremity. 

Paralysis of the Deltoid Muscle {axillary [circumflex*] nerve). — Deltoid 
paralysis occurs either as one symptom of complicated paralyses arising from the 
brachial plexus, or as an isolated traumatic and rheumatic paralysis ; that is, neu- 
ritic, beginning with pains in the region of the shoulder. It may be recognized by 
the impossibility of raising the upper arm at all. We can easily distinguish it 
from an anchylosis of the shoulder-joint by passive motion. If the paralysis lasts 
a long time there is a very marked atrophy of the muscle, and there is the elec- 
trical reaction of degeneration in it. Paralysis of the teres minor, which is also 
innervated by the axillary, can not be diagnosticated with certainty. 

Paralysis of the Biceps and Brachialis Anticus (musculo-cutaneous nerve) 
is only exceptionally isolated, but is quite often seen combined with other paraly- 
ses. The forearm, when in supination, can not be flexed, but in pronation the 
supinator longus can still display its action of flexion. The action of supination 
by the biceps, which it exerts when the forearm is flexed, is also absent. We 
sometimes see at the same time a disturbance of sensibility on the radial side of 
the forearm from an affection of a cutaneous branch of the musculo-cutaneous 
nerve. 

Radial [Musculo-spiral] Paralysis.— The anatomical course of the radial nerve 
causes pressure paralysis of this nerve to be among the commonest peripheral 
paralyses. It is seen especially when the nerve is pressed against the humerus 
during sleep by the body or head lying on it, in drunkenness, sleeping with the 
arm hanging over the arm of a chair, etc. The paralysis is usually noticed imme- 
diately on waking. Other traumatic influences, direct injuries of the nerve, com- 
pression in dislocation of the shoulder, in fractures of the humerus, in pressure 
from crutches, in bandaging the arm, etc., are also frequent causes of radial 
paralysis. Exposure to coJd, rheumatic radial paralysis, plays a very subordinate 
part. For lead paralysis, which is localized chiefly in the distribution of the 
radial, vide infra. 

The radial innervates the triceps and the muscles on the extensor side of the 
forearm. Paralysis of the triceps is present only in the cases where the point of 
lesion is situated quite high up, as in crutch paralyses, dislocation paralyses, plexus 
paralyses, etc., but it is absent, or at least it is only faintly manifest, in most 
of the ordinary pressure paralyses, in which the place where the radial turns 
about the humerus is the point of compression. Triceps paralysis is readily recog- 
nized by the impossibility of extending the forearm, but we must always make 
the experiment with the upper arm raised, so as to exclude the action of the weight 
of the forearm. 

Paralysis of the muscles on the extensor side of the forearm may at once be 
recognized, since the hand hangs down relaxed in a flexed position (see Fig. 76). 
Any dorsal flexion by the flexor carpi ulnaris and the flexor carpi radialis longus 
and brevis is impossible, and the lateral movements of the hand in abduction and 
adduction are rendered difficult. The fingers are flexed, the first phalanx can not 
be extended by the extensor communis digitorum, extensor indicis, and extensor 
minimi digiti ; but if the first phalanges are extended passively and supported, the 
extension of the terminal phalanges is perfectly normal, from the action of the 
interossei which are supplied by the ulnar nerve. The thumb is flexed and ad- 



* We have followed Henle's nomenclature for the peripheral nerves.— Trans. 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 533 




Fig. 76 



Position of the hand in paralysis of the radial nerve. (From 
Seeligmuller.) 



ducted, and can neither be abducted nor extended actively (extensores ossis meta- 
carpi primi et secundi internodii pollicis). If the forearm be extended and 
pronated it can not be supinated (supinator brevis), but the flexed forearm can 
be supinated by the bi- 
ceps. Flexion of the fore- 
arm in supination, which 
is done by the biceps and 
brachialis anticus, is re- 
tained, but flexion when 
half pronated ("middle 
position ") is weakened, 
from the paralysis of the 
supinator longus. If we 
have the patient make 
short and rapid move- 
ments of flexion of the 
forearm in this position 

we do not see the characteristic normal prominence of the tense supinator longus. 
The very characteristic prominence of this muscle is also wanting if the patient 
tries to hold his pronated and semi-flexed forearm firm against forcible attempts 
at extension. 

The functional disturbance of the hand in radial paralysis is very considerable. 
The action of the flexors is also weakened, since their points of insertion are 
approximated on account of the constant drooping of the hand. We often see, 
too, sensory disturbances as well as motor in the distribution of the radial, but 
these are usually slight. Their chief seat is on the radial half of the back of the 
hand and the dorsal surface of the thumb, and index and middle fingers (compare 
Fig. 60). The electrical excitability of the paralyzed parts corresponds to the laws 
that generally obtain. At the onset, and in mild cases, it is normal ; at a later 
period, in severe cases, there are pronounced atrophy and reaction of degeneration. 
It is worthy of note that in all forms of radial paralysis, especially in lead paraly- 
sis, we very often find a peculiar chronic thickening and swelling of the tendons 
on the back of the hand, the chief cause of which is probably the mechanical ten- 
sion on the tendons. 

Ulnar Paralysis. — Except from the frequent implication of the muscles sup- 
plied by the ulnar nerve in extensive paralyses and atrophies, especially in pro- 
gressive muscular atrophy, ulnar paralysis arises chiefly from traumatic influences, 
pressure, wounds, fractures of the humerus, dislocations of the shoulder-joint, etc. 
Neuritic paralyses are more rare. 

Flexion of the hand, and especially its lateral movement to the ulnar side, is 
disturbed (flexor carpi ulnaris). Flexion of the last three fingers is imperfect 
from partial paresis of the flexor profundus digitorum, and the little finger can 
not be moved at all (hypothenar muscles). Paralysis of the interossei is most 
striking, by which flexion of the primary phalanges and extension of the terminal 
phalanges of the fingers becomes impossible. Spreading the fingers, and still 
more bringing them together again, is also much impaired (interossei, lumbri- 
cales). The thumb can not be firmly adducted against the metacarpal bone of the 
index-finger (adductor pollicis). 

In almost all old cases of ulnar paralysis a very characteristic position of the 
hand is developed, beside the muscular atrophy which is especially noticeable in 
the interosseal furrows of the back of the hand. By the contraction of the mus- 
cles antagonistic to the paralyzed interossei (extensor and flexor communis digi- 
torum), the first phalanges are put in marked dorsal extension, but the terminal 



534: 



DISEASES OF THE MOTOE NERVES. 




Fig. 77.— Claw-shaped hand, main en griffe. (From Duchenne.) 



phalanges are completely flexed, so that the hand assumes an actual clawing- posi- 
tion— " claw-like hand," main en griffe (see Fig. 77). 

The disturbance of sensibility, if it be present at all, affects the volar surface of 
the last two fingers, the dorsal surface of the last three fingers, and a portion of the 
back of the hand (see. Figs. 58 and 59). 

Median Paralysis. — Median paralysis is seen chiefly as a traumatic paralysis. 
It is often, too, one symptom of more extensive paralyses, in progressive muscular 
atrophy, etc. 

The disturbances of motion are very striking. Pronation of the forearm is 
almost wholly abolished (pronator radii teres and quadratus). The hand can be 

flexed only toward the ulnar 
side by the flexor carpi ulnaris 
(paralysis of the flexor carpi 
radialis). The terminal pha- 
langes of the fingers can no 
longer be flexed (flexor sub- 
limis digitorum and a part of 
the profundus), but flexion of 
the primary phalanges is nor- 
mal by means of the interossei. 
The patient can grasp an ob- 
ject only by the last three 
fingers, which can still be 
partly flexed by the flexor profundus digitorum (ulnar nerve). The thumb can 
no longer be flexed or opposed (flexor longus pollicis et brevis, opponens), and 
usually lies on the hand. 

If there is any disturbance of sensibility, it is found on the volar surface of the 
thumb and the two adjacent fingers, and also on the dorsal surface of the terminal 
and middle phalanges of the index and middle fingers, and the radial side of the 
ring-finger (see Figs. 59 and 60). We quite frequently see in severe cases trophic 
disturbances, vesicles on the fingers, a shining atrophic skin, and changes in the 
nails. 

Combined Paralyses of the Arm.— Combined paralyses, in which the affected 
muscles belong to the distribution of several nerves, occur in various forms, espe- 
cially as a result of injuries which affect the brachial plexus in the neck— plexus 
paralyses. To this class belong also a great part of the paralyses following dislo- 
cation of the humerus — dislocation paralyses. 

A combined plexus paralysis, first described by Erb, and since then repeatedly 
observed, deserves special mention. In this the deltoid, biceps, brachialis anticus, 
and supinator longus (muscles whose nerves all rise from the roots of the fifth 
and sixth cervical nerves) are paralyzed at the same time. The arm hangs down 
relaxed, and can not be raised at all, the forearm can not be flexed at all, but the 
hand and fingers have their normal mobility. The cause of the paralysis must 
have its seat at the point where the nerve-fibers for the muscles mentioned lie near 
one another (see Fig. 67). Sometimes the infra-spinatus is also paralyzed, so that 
when the arm is rotated inward it can not be rotated outward. 

This same combination of paralyzed muscles is found in a part of the delivery 
paralyses first described by Duchenne. These are sometimes seen in infants after 
hard labor, and are the result of traumatic injuries of the brachial plexus in turn- 
ing, in the Prague method, in extracting the child by the shoulders, etc. 

In some cases of complicated paralyses of the brachial plexus, which are usually 
traumatic (Seeligmiiller and others), co-existing symptoms on the part of the 
sympathetic have been observed, consisting of contraction of the pupil, narrowing 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 535 



of the opening of the lids, and a retraction of the eyeball on the paralyzed side. 
These symptoms, pointing to a paralysis of sympathetic nerves (vide infra, page 
556), probably depend, as follows from clinical and experimental investigations 
(Klumpke), always upon a lesion of the ramus communicans of the first dorsal 
nerve. Vaso-motor symptoms in the face are usually absent, but we sometimes 
find a peculiar flattening of the cheeks, which has not yet been correctly explained. 

General Prognosis and Treatment of the Peripheral Paralyses of the Upper 
Extremity. — In the prognosis of the peripheral paralyses of the arm the same 
points hold good that have been spoken of in the prognosis of facial paralysis. In 
this, too, there are mild and severe cases, the latter having complete reaction of 
degeneration, and a course that lasts at least several months before recovery. A 
number of traumatic paralyses can be cured only up to a certain point, or are even 
entirely incurable. 

The treatment can fulfill a causal indication only in comparatively rare cases, 
when we can succeed in removing by operation any compressing tumors, cica- 
trices, splinters of bone, formations of callus, etc. 

In other cases the electrical treatment of paralyses promises the best success. 
We use the galvanic current chiefly, although we usually use the faradic current 
at the same time. In regard to the method of application, we may employ the 
stabile action of the constant current on the very point of the lesion, especially in 
fresh cases, but the chief method is the electrical irritation of the paralyzed nerves 
and muscles. We test the nerve above the point of the lesion in order to act in 
some degree against the hindrance to conduction from above and to overcome it. 
The muscles are irritated by galvanism by stroking the kathode over the separate 
paralyzed muscles. If there is reaction of degeneration, with anodic contractions 
predominating or exclusively present, we use the anode for the testing pole. The 
other pole is placed on the back of the neck or on the seat of the lesion. Faradiza- 
tion of the muscles may also be of service, especially if the muscles react to fara- 
dism ; but, even if this is not the case, the sensory faradic irritation has perhaps a 
favorable influence, since it produces a reflex irritation of the motor nerves. The 
single sittings should last five or ten minutes, and should take place daily or three 
or four times a week. The fresher the paralysis, the more favorable, compara- 
tively, is the prognosis, but even in old and severe cases we may sometimes obtain 
noticeable results by patience and perseverance. The treatment must in such cases 
be kept up for months, and even longer, with occasional interruptions. 

Embrocations with spirits and with similar substances must often be prescribed 
in practice, but they act favorably only when associated with methodical massage 
of the paralyzed muscles. We sometimes see a certain advantage, too, from local 
warm bathing, or from the use of the baths in Teplitz, Wiesbaden, Wildbad, etc. 

7. Paralysis of the Diaphragm. 

Isolated paralysis of the diaphragm occurs but rarely, in wounds of the phrenic 
nerve in the neck, as a " rheumatic " paralysis, and finally in hysteria. Muscular 
paresis of the diaphragm seems to develop sometimes as a result of inflammation 
of the serous layer of the diaphragm. The paralysis of the diaphragm which 
comes on as one symptom in more extensive paralyses, is more frequent and prac- 
tically more important. In diseases of the upper cervical cord, in ascending 
myelitis, in progressive muscular atrophy, in multiple neuritis, etc., the develop- 
ment of paralysis of the diaphragm is the cause of the rapidly fatal termination 
which follows the appearance of disturbance of respiration. 

The symptoms of paralysis of the diaphragm are readily recognized, especially 
in the ordinary bilateral affection. We detect the modification of the respiratory 
movements at the first glance. While we are struck by the marked upper thoracic 



536 



DISEASES OF THE MOTOR NERVES. 



respiration, which becomes very labored on the slightest cause, the visible and 
palpable protrusion of the epigastrium on inspiration is entirely absent. Instead 
of this there is usually an inspiratory retraction in the epigastric region. The 
respiration is but little accelerated in uncomplicated cases when the patient is per- 
fectly quiet; but in other cases the development of a severe bronchitis, from the 
defective respiration in the lower lobes of the lungs, causes constant dyspnoea. 
The cause of the bronchitis may be found in the fact that the action of abdominal 
pressure is very much diminished in the constant high position of the diaphragm, 
which may be made out by percussion, and consequently the cough and the 
expectoration of secretion are very imperfect. 

The prognosis is favorable only in hysterical and rheumatic paralyses ; other- 
wise it is usually very unfavorable. In regard to treatment, the only thing that 
can be tried is to excite the diaphragm from the phrenic in the neck by faradism 
or galvanism, while the other pole is placed on the region of the insertion of the 
diaphragm in the thorax. A transverse conduction of the constant current 
through the diaphragm, associated with changes of the current, may also have a 
favorable influence. 

8. Paralyses in the Region of the Lower Extremity. 

Paralysis of the Crural Nerve. — Crural paralysis is but rarely isolated. 
It is seen after injuries, after compression of the nerve by tumors of the pelvis or 
thigh, in disease of the vertebrae, psoas abscess, etc. 

The symptoms are readily recognized. The thigh can not be flexed on the 
trunk, and the trunk can not be raised from the recumbent position (ilio-psoas 
muscle). The leg when flexed can not be extended (quadriceps extensor). Walk- 
ing and standing are very difficult or almost impossible. Paralysis of the sar- 
torius and peotineus causes no special symptoms. If there is any disturbance of 
sensibility it is found in the lower half of the anterior surface of the thigh and on 
the inner side of the leg down to the great toe (saphenous nerve, see Figs. 61 
and 62). 

Paralysis of the Obturator Nerve is very rarely seen as an isolated phe- 
nomenon. The chief symptom is the defective adduction of the thigh (the adductor 
magnus, longus, and brevis, and the gracilis), and the impossibility of crossing one 
leg over the other. Rotation of the thigh outward is also disturbed (obturator 
externus). Some disturbance of sensibility may be found on the inner side of the 
thigh. 

Paralysis of the Gluteal Nerves is also rare. Abduction of the thigh (the 
glutei) and rotation inward (obturator interims) are the movements most impaired. 
Walking, and especially going up and down stairs, are very uncertain. 

Paralyses in the Region of the Sciatic are quite frequently seen. They come 
from traumatic lesions, from compression of the separate nerve-branches in dis- 
eases of the vertebrae, hi pelvic tumors, in hard labors, rarely from rheumatic 
influences, sciatic neuritis, etc. 

Paralysis of the Peroneal Nerve, which is also frequently isolated, may at 
once be recognized by the flaccid drooping of the foot. On walking, this becomes 
very marked, and the tip of the foot often sticks to the floor. The patient, there- 
fore, has to raise the thigh higher, and to put the foot down awkwardly, toe first. 
Dorsal flexion of the foot (tibialis anticus) and of the toes (extensor communis 
digitorum longus and extensor hallucis longus), and also abduction of the foot 
and raising its outer border (the peronei), are almost impossible. In old cases a 
permanent toe-drop (talipes equinus or varo-equinus) develops, usually as a result 
of secondary contracture of the muscles of the calf. 

Paralysis of the Tibial Nerve makes plantar flexion of the foot impos 



THE DIFFERENT FORMS OF PERIPHERAL PARALYSIS. 537 



sible (gastrocnemius and soleus). The patient can no longer rise on his toes. 
Adduction of the foot (tibialis posticus) and plantar flexion of the toes (flexor 
communis digitorum and flexor hallucis longus) are also abolished. As a result 
of secondary contractures, talipes calcaneus sometimes develops, and also a claw- 
like position of the toes with dorsal flexion of the first, and plantar flexion of the 
last phalanges from paralysis of the interossei. 

In Paralyses of the Trunk of the Sciatic there is added to the symp- 
toms mentioned the inability to flex the leg backward on the thigh (to be tested 
when the patient is lying on his side or standing), which is due to a paralysis of 
the biceps, semi-membranosus, and semi-tendinosus. In unilateral paralysis of 
the sciatic, walking is still possible, since the leg is fixed at the knee by the 
quadriceps extensor and is rigid like a wooden leg. 

The distribution of the disturbance of sensibility on the posterior surface of the 
whole leg is given in Fig. 62. Vaso-motor and trophic disturbances, cyanosis and 
coldness of the skin, and atrophy of the muscles, are often present. 

Treatment follows the same rules as are given for the management of periph- 
eral paralyses in the upper extremity. 

9. Toxic Paralyses. 

Lead Paralysis. — Of all the toxic paralyses, that from lead poisoning is prac- 
tically the most important. It is a common symptom of chronic lead poisoning, 
and is seen chiefly in those people whose occupation gives rise to a long-con- 
tinued taking of small amounts of lead into the system, especially, therefore, in 
type-setters, type-cutters and type-founders; in artists and house-painters, from 
lead colors ; in potters, from lead glaze, etc. 

As to the special anatomical causes of ]ead paralysis, we have not yet reached 
a complete harmony in our theories. "While some seek the starting-point of the 
paralysis in the muscles themselves, most authors at present assume, as a cause of 
the paralysis, an affection of the nervous system excited by the toxic action of the 
lead. Since lead paralysis belongs to the genuine atrophic paralyses {vide supra), 
as we shall soon see, we have to do only with a disease of the anterior gray cornua 
in the cord, or with a degeneration of the peripheral motor nerves. The positive 
lesions found at present do not fully agree, but there can be scarcely a doubt, 
after the discoveries of Leyden, Zunker, and others, that, at least in most cases, 
the degenerative atrophy of the peripheral motor nerve-fibers is primary, and that 
the degenerative atrophy of muscles supplied by the nerves follows secondarily in 
the ordinary way. In many cases, however, there is, perhaps, beside the periph- 
eral degeneration, an affection of the cord, especially in the anterior gray cornua, 
caused by the toxic action of the lead ; or perhaps this is sometimes present alone. 
At all events, further anatomical investigations are desirable. 

Lead paralysis shows an extremely typical localization in the great majority of 
cases, and it affects by far the most frequently a part of the radial distribution. A 
paralysis of the extensor communis digitorum comes on rapidly or slowly. Ex- 
tension of the primary phalanx of the middle and ring, and later of the index and 
little fingers, becomes impossible, but the extension of the terminal phalanges by 
the interossei remains normal. There often follows later a paralysis of the 
extensor longus pollicis and the extensor brevis, and of the abductor pollicis and 
the extensors of the wrist, while the supinator longus and the triceps almost 
always remain free in a remarkable way. In much rarer cases lead paralysis 
affects the deltoid, biceps, brachialis anticus, and supinators. Paralysis of the 
lower extremities is also very rare. 

Lead paralysis is usually bilateral. In all severe cases a pronounced atrophy 
and electrical reaction of degeneration develop in the paralyzed muscles. It is an 



538 



DISEASES OF THE MOTOE NERVES. 



interesting point that the latter may sometimes be made out in muscles which can 
be perfectly well moved by the will (see page 520). The sensibility is almost inva- 
riably perfectly normal, so that the sensory nerves are manifestly unaffected by 
the lead. 

Lead paralysis permits a favorable prognosis in the cases where the patient 
can be removed from the injurious influence of the poison. Recovery takes place 
after several weeks, or in severe cases after some months. Relapses and compli- 
cations with other morbid results of chronic lead poisoning, however, are, of 
course, frequent. 

The treatment is the same as in all other peripheral paralyses. Electricity is 
first to be considered. Local sulphur baths and the internal use of iodide of potas- 
sium are also recommended. 

[It is well to mention here that chronic lead poisoning may give rise to symp- 
toms closely resembling those of almost every chronic disease of the nervous sys- 
tem. It is often so difficult to detect the source of the lead that it is well in all 
obscure nervous diseases to test the urine for the metal after iodide of potassium 
has been administered in five- to ten-grain doses thrice daily for a week. For the 
precautions to be observed in carrying out this test the reader is referred to works 
on medical chemistry. If large doses of the iodide are administered there is dan- 
ger lest the lead be liberated too rapidly and cerebral symptoms supervene.] 

Arsenical Paralysis. — Arsenical paralysis is much rarer than that from lead. 
In distinction from that it comes on especially after acute poisoning with arsenic, 
and usually, though riot always, it follows immediately the other symptoms of 
poisoning. The localization of the paralysis is not as typical as in lead paralysis. 
The paralysis is sometimes very extensive over the arms and legs, but it usually 
chiefly affects only the lower extremities. The paralyzed muscles rapidly atrophy. 
It has not yet been certainly decided whether reaction of degeneration occurs. 
, The accompanying disturbances of sensibility are very characteristic, either anaes- 
thesia, or especially parsesthesia and severe pains in the sacrum and legs. Trophic 
disturbances in the nails, hair, etc., have been repeatedly observed. Nothing cer- 
tain is known as to the anatomical cause of arsenical paralysis, but the theory of 
its peripheral origin is most probable on account of the initial pains. 

The course is usually favorable, sometimes rapid and sometimes lasting for 
months. The treatment is the same as in lead paralysis. 



Copper paralysis, zinc paralysis, etc., are very rare, and therefore they will 
not be described fully here. The essentials in regard to alcoholic paralysis may be 
found in the chapter on neuritis (vide infra). We may mention here briefly 
that, after subcutaneous injections of ether on the extensor side of the forearm, 
paralysis of the extensor communis digitorum has been observed in a few cases. 



CHAPTER IH. 
THE DIFFERENT FORMS OF LOCALIZED SPASM. 

1. Spasm in the Motor Distribution of the Trigeminus. 

Tonic spasm of the muscles of mastication is called trismus. As an independ- 
ent disease it is very rare, but it often occurs as one symptom in complicated 
forms of spasm and other nervous affections, as in tetanus, in the epileptic attack, 



THE DIFFERENT FORMS OF LOCALIZED SPASM. 539 



in hysteria, meningitis, etc. Both jaws are pressed firmly together, and we can 
feel through the cheeks the hard and tense masseters. In unilateral spasm of the 
pterygoids the lower jaw is pushed laterally in the opposite direction. 

Clonic spasm of the muscles of mastication — masticatory facial spasm — consists 
of a paroxysmal and constant movement of the lower jaw, almost always in a 
vertical, but rarely in a horizontal direction. The single movements follow 
one another usually in a regular, rapid rhythm, and produce an audible chatter- 
ing of the teeth. The mucous membrane of the mouth and the tongue is often 
injured. 

The cause of these spasms can not always be established. Sometimes they 
seem to be of reflex origin, as in affections of the lower jaw, the teeth, or even of 
distant parts. We once saw a case which lasted for a year which was said to 
have arisen from a severe fright, and also a case of chronic spasm in the masseters 
and inylo-hyoids of hysterical origin in a ten-year-old boy. 

The treatment, apart from the treatment of the primary affection, must aim at 
removing the cause of the disease, if there be one, like decayed teeth. In other 
respects electricity is of value in many cases, applied either by passing the constant 
current through the muscles, or by faradizing them, or by using the wire brush. 
Of internal remedies we may try narcotics, like morphine, cannabis indica, 
bromide of potassium, atropine, arsenic, iodide of potassium, valerianate of 
zinc, etc. 

Artificial feeding is of great importance, if the patient can not take food volun- 
tarily from a persistent trismus. It is best to introduce a small oesophageal tube 
through the nose into the oesophagus. Rectal feeding is insufficient for a perma- 
nent method, but still it is sometimes of service. In some cases a successful 
attempt has been made to overcome the closure of the jaws gradually by push- 
ing wooden wedges between the teeth. 

2. Clonic Facial Spasm. 

(Mimetic Facial Spasm. . Convulsive Tic.) 

We know little that is definite as to the aetiology of facial spasm, the most fre- 
quent, and practically the most important, form of spasm. We can rarely make 
out any cause for its origin. In some cases, perhaps, the disease is to be referred 
to a lesion of the trunk of the facial, from exposure to cold, aural affections, or dis- 
turbances at the base of the skull, or else to a reflex irritation of the nerve in tri- 
geminal neuralgia, and also in diseases of the sexual organs, etc. It may be that 
many cases are not of peripheral, but of central origin, from the facial center in 
the cerebral cortex. The disease may also appear after violent mental excitement. 
Finally, imitation and the habit of grimacing play a part in many cases, espe- 
cially in children, that is not to be underestimated. Repeated observations have 
established the fact that the disposition to the disease is heightened by a general 
hereditary neuropathic taint. 

The symptoms of convulsive tic consist of alternating, short, lightning-like 
contractions in almost all the muscles supplied by the facial. The disease is usu- 
ally unilateral, often extending over the whole distribution of the facial, but some- 
times confined only to individual parts, the partial facial spasm. In many cases 
the contractions are almost constant, though varying in intensity, so that the 
patient involuntarily " makes the strangest faces " ; but they often appear in sepa- 
rate attacks, which last but a short time, and are interrupted by completely free 
intervals. The attacks arise without any special cause, or they are excited by 
talking, voluntary movements, sensory and mental impressions, etc. In some 
very severe cases the contractions also invade the neighboring territory — the mus- 
cles of mastication, the tongue, and the muscles of the neck. Voluntary motion 



540 



DISEASES OF THE MOTOE NERVES. 



in the muscles is perfectly normal, except for the disturbing influence of the spas- 
modic movements. All sensory disturbances are also wanting ; there is neither 
anaesthesia nor pain. 

A common partial form of facial spasm, which is entirely or almost entirely 
isolated, deserves special mention — blepharospasm, or spasm of the eyelids — that 
is, a tonic or clonic spasm in the orbicularis palpebrarum. The tonic form 
may be of reflex origin in affections of the eye, but sometimes it is excited from 
other regions of the trigeminus. It is, as a rule, bilateral, and may last for days 
or weeks, sometimes with occasional interruptions. The pressure points, which 
are found in this form, and which were first carefully described by von Graefe, 
are very remarkable. They are usually found at the points of exit of the branches 
of the trigeminus, but sometimes on the vertebral column or on other parts of the 
body. By pressure on these points the spasm at once ceases, so that the lids " fly 
up as if by a spring. " Clonic spasm of the lids, nictitating spasm, consists of a 
spasmodic winking and contraction of the eyes, which is sometimes almost con- 
stant. Here, too, we can often make out a reflex origin for the spasm, but fre- 
quently we can not find any cause. 

Facial spasm, in its severe forms, is always a troublesome disease for the patient, 
and causes very much disturbance, especially in blepharospasm. The course is 
often very tedious. Sometimes there are long intervals, as we have seen during 
pregnancy, and then the spasm begins anew. In not very rare cases the affection 
becomes habitual and lasts for life. 

Treatment is, therefore, usually a difficult and thankless task. The best results 
may be obtained where we can succeed in removing any reflex cause of the spasm, 
as in extracting decayed teeth, treating affections of the eye, or, in some cases, 
resection of the supra-orbital nerve. In applying electricity, our chief attention 
must be directed to any pressu re-points, to which we make a stabile application of 
the anode of the constant current. If there are no pressure points we put the 
anode on the trunk of the facial and the different branches of the pes anserinus. 
In cases of reflex origin Berger obtained good results by applying the anode to the 
occiput, just under the protuberance, while the kathode was held in the hand — 
galvanization of the medulla. The single sitting should last five or ten minutes. 
The faradic current — a slowly " swelling current " * — has also been recommended. 
Of internal remedies we should first try bromide of potassium, and then arsenic, 
atropine, curare, or oxide of zinc. Tbeir action is always very uncertain. A 
favorable result, however, has been obtained by nerve-stretching, in a part of the 
cases operated on, at least so far that the ensuing paralysis troubles the patient 
less than the constant twitching. When the paralysis ceases the twitchings usu- 
ally begin again, but in some cases the benefit has been permanent. Finally, we 
must mention that the use of the red-hot iron has sometimes been followed by a 
decided improvement of the spasm in old cases. We employ cauterization along 
the cervical vertebrae, on the trunk of the nerve, or on any existing pressure- 
points, by means of Paquelin's thermo-cautery. 

3. Spasm in the Region op the Hypoglossal Nerve. Lingual Spasm. 

Although the tongue is often implicated in complicated forms of spasm, like 
hysterical or epileptic spasms, isolated spasms in it are very rarely seen. They 
occur, however, either in a clonic or a tonic form, and then they cause a marked 
disturbance of speech, or even of respiration, if the spasm draws the tongue back- 
ward. In the latter case it may be necessary to use inhalations of chloroform 
and to draw the tongue forward by force. 



[* A current that begins weak, and is gradually made stronger and then weaker. — Trans.] 



THE DIFFERENT FORMS OF LOCALIZED SPASM. 



541 



4. Spasms in the Muscles of the Neck. 

Tonic and clonic spasms in the region of the muscles of the neck are not very 
frequent, but they appear in very various forms and are at times a very severe and 
persistent affection. We can usually discover nothing- definite as to the aetiology 
of this condition. Only in a few cases can we make out coarse anatomical disease 
of the nervous system or of the cervical vertebras, rheumatic or other evil factors, 
reflex influences, etc. Although the spasms in the different muscular regions are 
often combined with one another, we can still distinguish the chief separate forms. 

Spasms in the Distribution of the Accessory (Circumflex) Nerve. — 
In clonic spasm of the accessory there are paroxysmal twitchings of the head, 
which may attain great severity. Where there is a predominating unilateral 
spasm of the sterno-mastoid, the head is turned to the opposite side at every con- 
traction of this muscle, and the chin is also somewhat raised. In unilateral spasm 
of the trapezius the head is drawn backward toward the affected side against the 
shoulder. In bilateral and combined 
spasm of these muscles we see severe 
shaking and nodding movements of the 
head — the so-called nodding spasms, " sa- 
laam convulsions" — which have been 
observed chiefly in children. They may 
also be excited in like manner by con- 
tractions of other muscles of the neck. 
In tonic spasm of the accessory the head 
is constantly fixed in the abnormal posi- 
tion described above, and it can not be 
brought back passively to its normal 
position at all, or only incompletely. The 
oblique position of the head in unilateral 
tonic spasm of the sterno-mastoid is 
called spastic torticollis {caput ohsti- 
pum spasticum), or rheumatic torticol- 
lis, if exposure to cold is regarded as the 
cause. 

Tonic and clonic spasm of the sple- 
nius (Fig. 78) is also isolated, or com- 
bined with spasm of the accessory. In 
this the head is drawn backward and 
toward the affected side, and thus we can 
feel the muscular swelling protruding 
the trapezius. 

Spasm of the obliquus capitis is probably the cause of the so-called rotatory 
tic, in which there are genuine spasmodic rotatory movements of the head. The 
recti capitis antici and postici are perhaps implicated in many cases of nodding 
spasm. 

The prognosis of the forms of spasm described is usually doubtful. There are 
many mild " rheumatic " cases, which recover in a short time, but, on the other 
hand, many of these forms of spasm develop into a chronic affection ; and many 
cases of combined tonic-clonic spasm of the muscles of the neck form a very 
severe affection, which may last for years or for life, which is extremely distress- 
ing and painful to the patient, and which may also reduce the strength and the 
nutrition to the utmost degree. 

Treatment.— In some cases electricity has brought about recovery, or at least 




Fig. 78.— Spasm of the right splenius capitis. 
(From Duchenne.) 



to the outside of the cervical portion of 



542 DISEASES OF THE MOTOR NERVES. 



improvement. The method of treatment consists in the application of the anode 
to the affected nerves and muscles, or in the use of a swelling faradic current, or 
of the faradic brush to the skin over the affected muscles. Very often we have to 
change the method, and we must try to find out, by testing, the most efficient way 
to employ electricity. Of other remedies, narcotics, such as subcutaneous injec- 
tions of morphine, are indispensable in severe cases. We may also try bromide of 
potassium, atropine, valerianate of zinc, arsenic, and other nervines. In severe 
cases we resort to the use of the red-hot iron to the back of the neck. Other 
observers, and we ourselves, have seen good results from it, but of course benefit 
does not always follow. We may also advise nerve-stretching, but it is of doubt- 
ful advantage. Finally, it must be mentioned that we may give great relief to 
many patients by suitably applied mechanical supports, the more so because in 
some cases the spasms occur only when the head is kept free, but if they lean their 
heads on anything, as in lying or sitting, the spasms cease at once. 

5. Spasms in the Muscles of the Shoulder and Arm. 

Clonic spasms in the upper extremity are probably usually of central origin. 
They are rarely isolated, as in the pectoralis major, but are more frequently com- 
bined with other forms of spasm and other nervous symptoms. They sometimes 
seem to be of reflex origin, as in the clonic spasms associated with brachial neu- 
ralgia, and also the spasms sometimes seen in amputation-stumps. 

Isolated tonic spasms, in single muscles, or groups of muscles, in the upper 
extremity, have been repeatedly observed. Tonic spasm of the rhomboidei causes 
an oblique position of the scapula, so that its inner border runs obliquely upward 
and outward from below and inward. This makes it hard to raise the arm above 
the horizontal line, as in serratus paralysis, but the separation of the scapula from 
the chest-wall, which is so very characteristic of the latter, is wanting. Tonic 
spasm in the levator anguli scapulae is rare, except in connection with spasm of the 
rhomboidei or trapezius. In it the shoulder is raised and the head is bent a little 
to the affected side. Isolated tonic spasms in the pectoralis major, latissimus dorsi, 
deltoid, etc. , are, on the whole, easy to recognize, but are only of very rare occur- 
rence. Tonic flexor spasms of the hand and fingers are more common. We have 
ourselves seen several such cases, which lasted for months. In one case the spasm 
could at once be relieved by placing the anode of a moderately strong galvanic 
current on the median nerve. In another case the flexor spasm of the fingers 
had followed a mild acute inflammation of the wrist- joint. 

The special causes of all these spasms are still wholly unknown to us. Prog- 
nosis and treatment follow the same general rules which are given for other 
forms of spasm. Most is to be expected from electricity: the stabile action of the 
anode, the faradic brush, or faradization of the antagonistic muscles. 

6. Spasms in the Muscles of the Lower Extremity. 

Clonic spasms in the muscles of the lower extremity are always, with rare 
exceptions, a symptom of spinal or cerebral disease. Of the tonic spasms the 
most frequent and the best known are the painful spasms in the calves, or cramps, 
which are apt to come on after great muscular exertion, mountain-climbing, or 
dancing. Many persons have an especially marked predisposition to, such cramps, 
which readily come on, especially after making certain movements or holding the 
foot in a certain position. Similar painful cramps sometimes come m other mus- 
cles beside the calves, as in the abductor hallucis, etc. Other tonic spasms in the 
muscles of the lower extremity are rare, but individual cases of isolated tonic 
spasm in the adductors, in the ilio-psoas, in the muscles of the calves, etc., have 



THE DIFFERENT FORMS OF LOCALIZED SPASM. 543 



been observed. More extensive tonic contractures of the muscles of the leg are 
not very rare in hysteria, especially in the hysteria of children. 

Saltatory Reflex Spasm. — In this place we may mention a peculiar form of 
spasm, to which Bamberger has given the name of "saltatory reflex spasm." 
This shows itself in the muscles of the lower extremities, never when the patient 
is quiet in bed, but only when he tries to stand or to walk. As soon as the soles 
of the feet touch the floor, such vigorous contractions are set up in the muscles of 
the legs as to force the patient to keep up a constant hopping, jumping, or tripping. 
The heels are also usually raised spasmodically, and in many cases the patient 
would certainly fall if he were not supported. In the pure forms of saltatory 
spasm, on physical examination we can usually make out nothing but an extraor- 
dinary increase of the reflexes, especially of the tendon reflexes, but in some cases 
there may also be other nervous symptoms. In general, it seems that saltatory 
reflex spasm is not to be regarded as a special disease, but as a peculiar symptom, 
which may arise in different neuroses in consequence of a very decided exaggera- 
tion of the reflexes. Many cases especially seem to us to belong to hysteria. 
Nothing definite is as yet known as to the precise cause of the unusual increase of 
the reflexes. 

Arthrogryposis. — As an appendix we would here consider briefly a remarkable 
disease, the so-called arthrogryposis, which occurs chiefly in children in the first 
years of life, and consists of persistent tonic spasms and contractures of one, or 
often of all four extremities. The disease usually develops quite acutely, and may 
run its course with fever and rather severe general symptoms. The legs are found 
either in a position of rigid extension, or they are drawn up spasmodically to the 
body, and can not be extended passively even with violence. The arms are flexed, 
and the hands and fingers are also fixed in some position of contracture. The 
milder cases may recover after a few weeks, but we have also seen two cases 
which ended fatally, in which the autopsy gave a perfectly negative result. The 
nature of this quite rare affection is still wholly unknown to us. In regard to 
treatment, prolonged warm baths are especially to be recommended. 

The form of tonic spasm known as tetany will be described in a special chapter. 

7. Spasms in the Respiratory Muscles. 

Tonic spasm of the diaphragm has been seen in a few rare cases. The lower 
part of the thorax is much expanded, the epigastrium is protruded, and the respira- 
tion, which shows intense dyspnoea^ can be performed only by the upper part 
of the thorax. The depression and immobility of the diaphragm can be made 
out on percussion. Many patients have a severe pain in the region of the dia- 
phragm. The condition is not without danger and demands instant interference : 
inhalations of chloroform, subcutaneous injections of morphine, a warm bath 
with a cool shower-bath after it, faradization of the skin in the region of the dia- 
phragm, galvanization of the phrenics, etc. 

Clonic Spasm of the Diaphragm — Singultus. — The well-known "hiccough" 
or " sob," due to a sudden spasmodic contraction of the diaphragm, is in its mild 
forms a very frequent condition, which soon passes off ; but in many cases it 
increases to a persistent, obstinate, and very troublesome affection, which may 
last for weeks or months. It sometimes comes on after mental excitement, and 
is a not very rare symptom of hysteria. Persistent hiccough may also be excited 
reflexly in affections of the stomach, intestines, peritoneum, etc. In some cases 
the hiccough depends upon a direct lesion of the phrenic nerve, as we have seen in 
one case of tubercular mediastino-pericarditis. We have also seen hiccough last- 
ing for hours in cerebral apoplexy, and also in chronic myelitis extending to the 
cervical cord. 



544 



DISEASES OF THE MOTOE NEEVES. 



In the milder cases hiccough soon passes off without special treatment. Hold- 
ing the breath, pressure on the closed glottis, blows on the back, etc., are proced- 
ures generally known by the laity, and often used to suppress hiccough. In 
more severe cases we must try narcotics, opium, cannabis indica, or inhalations of 
chloroform. The faradic brush to the region of the diaphragm, or the direct 
action of electricity on the phrenic nerve, is sometimes of advantage. In hyster- 
ical hiccough we may obtain very rapid results in this way, or sometimes by one 
of the different nervines, valerian, zinc, atropine, or Fowler's solution. 

Complicated respiratory spasms, either in the form of spasmodically accelerated 
and forced breathing, or spasms combined with all sorts of other symptoms, with 
many gurgling noises, eructations, etc., are almost exclusively confined to hysteria. 
We have ourselves counted in one such case over two hundred respirations a min- 
ute ! The best remedy against most of these forms of spasm, and one which often 
acts instantly, is a cool bath with energetic cold shower-baths. The yawning 
spasm (chasmus, oscedo), sneezing spasm {sternutatio convulsiva, ptarmus), 
laughing and weeping spasms, coughing spasm, etc., also belong to the respiratory 
spasms. We once saw a very remarkable example of the latter in a boy ten years 
old. A peculiar, reflex, hollow, barking cough came on, either spontaneously or 
on pinching any part of the skin. The affection lasted for some weeks, and then 
disappeared quite suddenly. 



CHAPTEE IV. 

WRITERS' CRAMP AND ALLIED PROFESSIONAL NEUROSES. 

Writers' cramp (graphospasm, mogigraphia) is the commonest form of a 
whole class of peculiar disturbances of motion, to which Benedikt gave the appro- 
priate name of "professional neuroses of co-ordination." Their characteristic 
feature is that the disturbance in a certain group of muscles appears only when 
these muscles come into harmonious action, in quite a definite, and usually a 
delicate and complicated occupation. Although the persons who suffer from 
writers' cramp can move and use the muscles of their right arm and hand for 
ordinary purposes in a perfectly normal manner, these same muscles at once 
refuse their service when the patient begins to write. In this case the disturbance 
can not lie in the innervation of the individual muscles themselves, but it must be 
referred to the form of their associated action — that is, it must be a disturbance of 
co-ordination; but the details of this disturbance are still entirely unknown to us, 
nor do we know in what part of the nervous system we are to look for the seat of 
the disease. Over-exertion in writing plays the most important part as an serologi- 
cal factor. Writers' cramp is, therefore, seen chiefly, but of course not exclusively, 
in those persons whose occupation is connected with continuous writing, especially 
in secretaries, merchants, bureau officials, etc. A general nervous predisposition 
seems also to increase the tendency to writers' cramp. Attention has also been 
called to the fact that bad pens, like hard steel pens, bad methods of holding the 
pen in writing, etc., may favor the development of writers' cramp. 

Symptoms. — The essential symptom of writers' cramp is the appearance of 
certain disturbances at every attempt to write, which render writing very diffi- 
cult or entirely impossible. The affection usually begins gradually, but increases 
quite rapidly. For the precise characterization of the disturbance Benedikt has 
distinguished three forms of writers' cramp, but they run into one another in vari- 
ous ways. The spastic form is the most frequent. The patient scarcely begins to 



WRITEES' CRAMP AND ALLIED PROFESSIONAL NEUROSES. 545 



write when contractions or tonic spasms come on in the different fingers, so that 
the pen can no longer be held firmly, or it makes abnormal irregular movements, 
or it is firmly pressed into the paper, etc. Writing is wholly impossible, or it is 
done only with the greatest exertion, and the characters are also utterly distorted, 
unequal, and mingled with false strokes and blots. In the paralytic form * the 
disturbance in writing is chiefly a rapidly arising tired feeling, like paralysis, in 
the right arm, which is often associated with painful sensations. Finally, in the 
tremulous form of writers' cramp there is such a marked tremor in the right hand 
at every attempt to write, that the letters are completely illegible. 

As has already been said, motility in every other respect is perfectly normal, 
but sometimes analogous symptoms also appear in the same patient in many other 
fine employments, like sewing, piano-playing, etc. The sensibility is usually per- 
fectly normal, except for the muscular pains already mentioned, and a frequent 
feeling of numbness in the forearm and fingers. A few painful pressure-points 
have sometimes been found on the cervical and dorsal vertebrae. If we are dealing 
with people who are generally neurotic, they often complain at the same time of 
headaches, mental uneasiness, and general weakness. 

The diagnosis of writers' cramp is almost always easy. We must guard against 
confusing it with other nervous diseases, like chorea, paralysis agitans, multiple 
sclerosis, beginning muscular atrophy, or agraphia, which, of course, under some 
circumstances, may lead to disturbances in writing. 

The prognosis is always to be given with reserve. Complete recoveries with- 
out doubt do occur, but many cases are extremely obstinate and others are incur- 
able. Relapses are also very common even after improvement has set in. Many 
patients are obliged to choose another calling in consequence of their trouble. 

The treatment begins first with the command to give up writing entirely for 
several weeks or months. If this command can be obeyed, the mere rest may be of 
service in mild incipient cases. Certain contrivances for writing, which the patient 
can best test himself, are often of advantage, such as sticking the pen-holder 
through a cork, using a large pen-holder, a change in the way of holding the pen 
and in the position of the arm, etc. Nussbaum has lately invented a kind of 
bracelet, to which the pen-holder is fastened, and which is held firmly by the out- 
spread fingers. Learning to write with the left hand, which is often tried by 
patients, usually leads to no good result, since the cramp very soon appears in the 
left hand also with remarkable rapidity. 

Of the special methods of treating writers' cramp the application of galvanism 
deserves the first mention. Avoiding all strong currents and variations of the 
current, we apply the stabile anode to the brachial plexus, and also the different 
nerves and the affected muscles, for five or ten minutes. The kathode is placed in 
the vicinity of the cervical vertebrae. If painful points are found, they receive 
special treatment. We may also use galvanism, as an experiment, through the 
head. Of late, massage and methodical gymnastics have shown still more favora- 
ble results than electrical treatment, but the use of them demands special tech- 
nical skill, and therefore they have so far obtained excellent results chiefly in the 
hands of certain specialists. We can very rarely promise success from internal 
remedies, such as subcutaneous injections of strychnine, atropine, etc., but those 
methods of treatment often act favorably which aid the general strength of the 
nervous system, like cold-water cures, sea-bathing, and mountain residences. 

As an appendix we will mention here some other professional neuroses that 
are occasionally seen. They are the piano-players' cramp, which is seen espe- 



* It is particularly illogical to class this disturbance with writers' cramp, since we can not speak 
of the " paralytic " form of a " cramp." 
35 



546 



DISEASES OF THE MOTOR NERVES. 



cially in young conservatory pupils, violin- and 'cello-players' cramp, telegraphers 7 
cramp, tailors' cramp, milkers' cramp, the peculiar disturbances of innervation in 
the hands which often occur in cigar-rollers, etc. In the lower extremities there 
seems to be an analogous affection in ballet-dancers, and also in sewing-machine 
girls, turners, etc. We have seen a professional cramp in the tongue in a clario- 
net-player. The special points in the symptomatology and treatment of all these 
forms of cramp are in large part analogous to the conditions described in writers' 
cramp. In piano-players the neurosis appears chiefly in the paretic form — mild 
fatigue — and is usually associated with quite severe pains, that come on during 
playing, in certain parts of the arm. In regard to treatment, the best results are 
obtained by energetic massage. Finally, it may here be noted that, in certain 
laborious occupations that are persistently practiced, a severe group of nerv- 
ous symptoms may also arise. For example : B. Hirt has lately described an 
affection, which occurs in sewing-machine girls, and is characterized by disturb- 
ances of sensibility, pain, paraesthesia, and in some cases anaesthesia, ataxia, absence 
of the tendon reflexes, and swaying with the eyes shut. The disease thus recalls 
very closely the picture of locomotor ataxia, but it is curable with proper treat- 
ment. Therefore, Hirt suspected an affection of the peripheral nerves. Like 
symptoms are also seen in other classes of laborers, as in farm-hands after labori- 
ous toil in the fields. 



CHAPTER V. 

SIMPLE AND MULTIPLE DEGENERATIVE NEURITIS. 

JEtiology and Pathology. — We term those changes in the nerves acute neuritis 
(inflammation of the nerves) where their vessels become very hyperaemic, and 
where the transudation of fluid and cellular elements takes place from the walls 
of the vessels into the surrounding tissue. The inflamed nerve is therefore swollen 
and thickened, its color is manifestly reddened from the marked vascular hyper- 
aemia, and we can often recognize with the naked eye a few or many small haem- 
orrhages. Microscopic examination shows an abundant infiltration of round cells 
into the nerve-sheaths and the interstitial tissue, and these may be so numerous 
that the inflammation in some cases may be recognized, even on macroscopic 
examination, as a purulent neuritis. The nerve-fibers themselves sometimes show 
no visible changes, but in more severe neuritis we usually find an evident disin- 
tegration of the medullary sheaths and the axis-cylinders, and finally a complete 
destruction of the nerve-fibers. The "fatty granular cells," which are seen in 
these cases, are probably white blood-corpuscles (perhaps, also, endothelial cells ?), 
which have taken up the fat from the disintegrated medullary substance. The 
destruction of the nerve-fibers, " parenchymatous inflammation," is partly a 
mechanical result of their compression by the surrounding exudation, but very 
largely probably the result of the direct injury which the nerve-fibers undergo 
from the causes that provoke the inflammation. 

In its further course the neuritis advances to the stage of the new formation of 
connective tissue and the regenerative processes. The nerve appears firmer and 
denser than normal; a large amount of interstitial connective tissue is formed 
between the single nerve-fibers that' are still preserved, which, if produced in 
excess, like a sort of callus formation, may lead to quite considerable partial thick- 
enings of the nerve, the so-called neuritis nodosa. The capacity for regeneration 
of the peripheral nerves is relatively very considerable, so that in moderate, and 



SIMPLE AND MULTIPLE DEGENERATIVE NEURITIS. 547 



even in severe degrees of neuritis we may have a complete restitutio ad integrum. 
There may be a partial regeneration of the nerve-fibers even in the worst cases. 
Chronic neuritis either proceeds from acute neuritis, or it develops de novo in an 
insidious fashion. In the latter case the first acute stage of hyperemia and cellular 
infiltration is entirely absent, and the destruction of the nerve-fibers and the new 
growth of connective tissue proceed in a chronic manner from the beginning. In 
such cases the interstitial inflammatory changes in the connective tissue and the 
vessels are often so subordinate to the degenerative processes in the nerve-fibers 
themselves that we have almost a genuine parenchymatous degeneration. Such 
conditions, perhaps, can not be properly termed "neuritis" at all, but rather 
"primary chronic degenerative atrophy of the nerves." They arise especially 
as a result of certain infectious and toxic influences {vide infra), which have a 
directly deleterious action upon the nerve-fibers. They often appear in many 
nerves at the same time, and consist of a slowly progressive disintegration of the 
medullary sheath, and later of the axis-cylinders also. It is possible that these 
last-named changes begin in the terminal branches of the peripheral nerves, and 
gradually advance from them toward the centers, but this has not yet been certainly 
confirmed ; at any rate, the affection often remains confined to the peripheral nerves. 
The anterior spinal roots and the cord itself in such cases are found perfectly intact, 
or altered only in a subordinate way. 

In inquiring into the causes of neuritis we encounter first the same injurious 
influences which play the chief part in the inflammations of other organs. We 
very often speak of a traumatic neuritis, which is supposed to mean a neuritis 
produced by various mechanical injuries of the nerve. As far as this implies 
open wounds — like stabs, cuts, gun-shot wounds, etc. —that involve the nerve, the 
development of a genuine traumatic neuritis can not be doubted ; but in such cases 
we not only have to do with mechanical lesions, but with an accidental complica- 
tion of the wound, with the entrance of organized agents of inflammation through 
the wound into the nerves. Only in this case can there be an inflammation 
(ascending neuritis, neuritis migrans) advancing continuously or by leaps in 
the nerve-trunk from the point of lesion in the nerve, whereas, if the wound 
remains aseptic, as the experiments of Rosenbach and Kast have shown, such a 
propagation of the inflammation above the point of lesion never occurs. In the 
subcutaneous injuries of the nerve-trunk from a blow, from pressure, from dislo- 
cations of the bones, etc., we are, of course, not justified in speaking of a traumatic 
neuritis; but in such cases we have a purely mechanical destruction of the nerv- 
ous elements, which is followed by the regular processes of secondary degeneration 
{vide supra), increase of connective tissue, and final restoration. 

Another cause for the origin of a genuine neuritis lies in the extension of an 
inflammation from the neighboring organs to the nerves. In inflammations of 
the bones, as in caries of the bones of the skull and of the vertebrae, of the joints 
and of the different internal organs, the inflammatory process may directly involve 
a nerve-trunk by contiguity. In this way, perhaps, are developed the atrophy 
and paralysis of the neighboring muscles which are often seen after affections of 
the joints. Leyden has also tried to explain a number of the so-called " reflex 
paralyses "—that is, paralyses which sometimes develop as a result 'of inflamma- 
tory affections of certain internal organs, especially the intestines and the urinary 
and sexual organs — by a neuritis arising from the organ originally affected, and 
even extending to the spinal cord. 

Primary neuritis, however, is of special interest. This may either be caused 
by some evident agency, or it may develop, apparently spontaneously, without 
any cause as far as known. We have already learned to recognize one group of 
these primary neuritides in the preceding chapters : those which, in all probabil- 



548 



DISEASES OF THE MOTOK NERVES. 



ity, underlie most of the " rheumatic " paralyses on the one hand, and certain 
forms of neuralgia, like sciatica, intercostal neuralgia with zoster, etc., on the 
other. As we have said, little that is definite is known as to the precise cause of 
these neuritides. Some of them seem to arise from external agencies, like 
exposure to cold ; others, perhaps, from infectious influences. Certain toxic 
paralyses belong to a second group of primary neuritides, among them, for 
instance, the lead and arsenic paralyses already described, and the disease of the 
nerves produced by chronic alcoholism, which will be more fully described below. 
Finally, the so-called multiple neuritis forms the third recognized group, a special 
form of disease in which several nerves are usually affected at the same time or 
sqoii after one another. As will be stated in the description of the course of the 
disease, we probably have in these cases a definite form of infectious disease, 
which is localized exclusively, or at least mainly, in the peripheral nerves. In 
the acute cases the anatomical changes in the nerves seem to be really of an 
inflammatory nature, but in the chronic cases a simple degenerative atrophy of 
the nerves underlies the morbid symptoms. The serological position of these 
chronic cases of multiple neuritis, however, is, in our opinion, to be judged with 
caution, since at least a part of the cases so far published are certainly to be classed 
with alcoholic neuritis {vide infra). 

Clinical History of the Different Forms of Neuritis. 

1. Secondary Neuritis. — The chief symptom of secondary neuritis, following 
wounds, inflammations of neighboring organs, etc., is pain, which comes on with 
great intensity, not only in the region of distribution of the affected nerve, but 
also along the whole trunk of the nerve. In these cases there is also a marked 
sensitiveness of the nerve to pressure. In many cases we can succeed in feeling 
the thickened nerve plainly through the skin. 

Beside these direct symptoms, the inflammation soon renders the necessary 
results of disturbed nervous conduction apparent. There is a dullness of sensibility 
in the distribution of the affected nerve, at first in the form of a subjective feeling 
of numbness, but later as a manifest objective anaesthesia, which, however, rarely 
reaches a very high degree. The motor symptoms at first show themselves as 
motor weakness, which in severe cases becomes a pronounced paralysis. It goes 
without saying (see page 507) that the paralysis, in all severe cases, is followed by a 
degenerative atrophy of the paralyzed muscles, and the appearance of electrical 
reaction of degeneration. In the skin, trophic and vaso-motor disturbances have 
been repeatedly observed, especially slight oedema of the subcutaneous cellular 
tissue, eruptions of herpes, etc. 

The course of simple secondary neuritis may vary. Its onset is usually quite 
acute, or more rarely it begins gradually. Many cases seem to recover before the 
severer consequences are reached, while others take a chronic, tedious course, and 
lead to permanent disturbances of function. 

2. Primary Multiple Degenerative Neuritis. — Primary multiple neuritis is 
probably not a very rare disease, but yet it has been carefully investigated only in 
the last few years. The first definite observations upon it were made in the years 
1864 and 1866 in France by Dumenil. Since then a whole series of well-established 
cases have been published by Eichhorst, Eisenlohr, Joffroy, Leyden, Vierordt, the 
writer, and others, so that the type of the disease is at present quite accurately 
known. Probably in former days multiple neuritis was often confused with 
poliomyelitis and certain cases of "acute ascending paralysis" (vide infra). An 
interesting discovery was first made by Scheube, that the peculiar disease, of 
endemic occurrence, long known in Japan and the East Indies as " kaJc-Jce " or 



SIMPLE AND MULTIPLE DEGENERATIVE NEURITIS. U9 



11 beri-beri," is, in its clinical and anatomical relations, a well-characterized multi- 
ple peripheral neuritis. 

Multiple neuritis usually begins acutely, sometimes almost in an apoplectiform 
manner, and without any definite occasion, precisely like an acute infectious disease. 
Febrile symptoms, with temperatures from 102° to 104° (39 o -40° C), come on in 
persons previously in good health, usually in adults in youth or middle life, with 
severe general disturbance, loss of appetite, dullness, headache, and sometimes 
even mild delirium. In these acute cases albuminuria and a slight enlargement 
of the spleen have sometimes been observed, which symptoms also point toward 
the infectious nature of the disease. The pains, which are hardly ever absent, are 
very characteristic. They are described as pulling and tearing, are felt chiefly in 
the loins and the extremities, and sometimes follow approximately the course of 
the large nerve-trunks. Since in some cases a number of the joints are swollen, the 
disease at first may be mistaken for acute articular rheumatism. The first symp- 
toms of paralysis, usually in the lower extremities, appear very soon after these 
initial symptoms, or at the same time with them. The patient notices that he can 
not readily move one leg, and soon after he notices the same of the other. The 
paralysis often extends rapidly to one or both arms. If we examine the paralyzed 
parts more carefully we find a perfectly atonic and more or less extensive paralysis. 
The reflexes are constantly diminished, the tendon reflexes are usually entirely 
absent, and the cutaneous reflexes are weak, or have also almost wholly disappeared. 
We can usually make out, after a few days, a decided diminution of electrical 
excitability in the affected nerves and muscles, which finally becomes a pronounced 
reaction of degeneration. If the paralysis is of longer duration, there is a decided 
atrophy of the muscles. In these cases the severe initial symptoms of sensory 
irritation, as a rule, rapidly disappear, although slight pains, paresthesia, and 
especially a considerable sensitiveness of the paralyzed parts to pressure and 
to passive motion, often last for a long time. In many acute cases the hyperses- 
thesia of the skin and of the deeper parts reaches a very high degree, but it is very 
remarkable that the objective disturbances of sensibility are very slight in the 
great majority of cases. Marked anaesthesia is a rare exception, so that we may 
rightly suppose that primary multiple neuritis affects chiefly the motor nerve- 
fibers. We usually find no disturbances in the distribution of the cerebral and 
bulbar nerves. An affection of the optic nerve has been mentioned in only a few 
cases. The marked increase in the frequency of the pulse, which is usually pres- 
ent, is important, and probably depends upon a disturbance of the vagus. Trophic 
disturbances in the skin, hair, and nails, are not very rare. CEdematous swelling 
of the affected extremities has also been repeatedly observed. The functions of 
the bladder and rectum, however, almost always remain undisturbed. 

In regard to the course of the disease, in the severest cases it may soon termi- 
nate fatally, almost always because the paralysis extends to the muscles of respira- 
tion. The inspirations are labored,- and are performed with the upper part of the 
thorax only, while the epigastrium is motionless, or sinks in on inspiration from 
the paralysis of the diaphragm. There is also paralysis of the other muscles of 
respiration, the abdominal muscles, etc., so that, after the disease has lasted a week 
or ten days, death ensues with all the signs of respiratory insufficiency. A second 
class of cases also begins quite acutely, but then takes a chronic course. The ini- 
tial acute febrile symptoms cease after a few days, and the paralysis develops 
to some extent. Then the affection seems to come to a stand-still, and the first 
signs of improvement gradually begin to appear. Since there is always a more or 
less pronounced atrophy of the muscles in these cases, it always takes quite a long 
time — usually several months — for recovery. A third class of cases follow a chronic 
course from the outset, although even in these cases there may be more acute exacer- 



550 



DISEASES OF THE MOTOR NEEYES. 



bations of the disease. In these cases quite extensive atrophic paralysis gradually 
develops in the lower extremities, and usually in the upper extremities also. The 
reflexes disappear, the sensibility is as a rule somewhat, but very rarely much 
diminished. Pains are always present at first, but later on in the disease they 
often become subordinate. The bladder and rectum usually remain intact in their 
functions. If the disease advances gradually it may terminate fatally even at a 
late period, after a course of months, usually from a final paralysis of respiration ; 
but, on the other hand, even after a protracted course, the disease may come to a 
stand-still and even to a complete, or at least to a partial, recovery. It is worthy of 
note that a combination of multiple neuritis and pulmonary tuberculosis has quite 
frequently been observed ; but nothing definite is yet known as to the form of 
connection between the two diseases. 

The diagnosis of multiple neuritis is, as a rule, easy, for one who is acquainted 
with the disease, and notes the different symptoms carefully. In regard to diagu osis, 
the chief importance should be placed on the generally acute beginning, with pro- 
nounced symptoms of sensory irritation, with frequently a very considerable sen- 
sitiveness of the nerves to pressure and general cutaneous hyperesthesia ; and also 
on the appearance of a rapidly extending paralysis, whose peripheral nature may 
be attested by the presence of reaction of degeneration, muscular atrophy, and the 
absence of the cutaneous and tendon reflexes. Such a paralysis can be produced 
by nothing but an affection of the peripheral nerves or poliomyelitis (vide infra). 
As we have shown above, this latter disease may, in fact, often be confused with 
multiple neuritis, but a careful attention to the initial symptoms, especially to the 
disturbances of sensation, will usually make the differential diagnosis possible. 

The prognosis of multiple neuritis is doubtful, as is shown by the description 
of the course of the disease, but it is by no means very unfavorable. If the first 
acute stage of the disease has been gone through with, without accident, we may 
hope for recovery, or at least actual improvement, even with extensive paralysis. 
Such striking results in the way of recovery, after paralysis that has lasted for 
months, are also important in regard to diagnosis, since such extensive processes 
of regeneration are possible in affections of the peripheral nerves, but scarcely in 
spinal diseases ; and hence they are sometimes an additional confirmation of the 
diagnosis of a neuritis. 

Treatment. — In the first stage of the disease, especially if severe pains, swelling 
of the joints, or high fever be present, it is advisable to try the exhibition of sali- 
cylic acid, from which several observers have seen a favorable effect. We give ten 
grains (grm. 0*5) of the acid every hour, or a few larger doses, a drachm to a 
drachm and a half (grm. 4-6) of salicylate of sodium. When the pain is very 
severe we must use narcotics, such as injections of morphine. Embrocations of 
chloroform, and sometimes protracted warm baths, have also a palliative effect. 
In the further course of the disease proper care, a suitable position for the limbs, 
and diet — nourishing food — are the main things for the patient. The regenerative 
processes of recovery begin spontaneously, if at all, but we may hasten recovery 
and make it complete by a subsequent electrical treatment, especially galvanism. 
For the completion of the recovery, bathing (simple warm baths, salt baths, etc.) 
is serviceable, and also the baths at Teplitz, Wiesbaden, and Eehme. 

3. The Chronic Neuritis of Alcoholic Subjects. 

(Pseudotabes of Alcoholic Subjects, Ataxia of Drinkers.) 
It has long been known that peculiar nervous affections often occur in alco- 
holic subjects (M. Huss, Lendet, and others) ; but up to the present time a disease 
of the spinal cord has been assumed to be the cause of the symptoms, and only of 
late have we obtained the knowledge that at least a great part of the cases of this 



NEW GEOWTHS IN THE PERIPHERAL NERVES. 551 



class are to be regarded as a special form of chronic multiple neuritis (Lancereaux, 
Moeli, and others). The practical importance of this alcoholic neuritis is not 
slight ; first, because it may easily be confused with other nervous diseases, espe- 
cially with locomotor ataxia, and, second, because its proper and timely diagnosis 
is of great significance in regard to treatment. 

Alcoholic neuritis occurs chiefly in two forms : in one form actual atrophic 
paralysis develops, chiefly in the lower extremities, but in the other form the 
paresis is subordinate to the other disturbances of innervation. The first symptom 
of the disease is usually tearing and drawing pains in different parts of the 
lower, or, more rarely, of the upper, extremities. The pains are usually quite 
severe, but sometimes only of moderate strength. Sooner or later, but some- 
times not for years, a pronounced disturbance of the gait is added to the pains. 
More careful examination shows that, in such cases, there is partly an actual 
paresis of the muscles of the legs, and partly a form of ataxia — a defective inner- 
vation which is manifest by an uncertainty, a staggering and reeling in the 
gait. If there is marked paresis, the affected muscles are quite atrophic, and elec- 
trical examination usually gives a decided diminution of excitability, or even pro- 
nounced reaction of degeneration. The patellar reflex is usually lost quite early. 
The sensibility, too, is very rarely perfectly normal ; we find sometimes quite 
marked ansesthesia, especially in the lower legs, and also in other parts of the skin. 
The cutaneous reflexes are also often feeble and slow. There is sometimes con- 
siderable tenderness on pressure on the deeper parts and over the nerves. The 
course of the disease is usually chronic. If the cause of the evil, the abuse of 
alcohol, be removed in time, perfect recovery is possible ; but, in far-advanced 
cases, the disease may go on to complete paralysis, even of the upper extremities, 
and to a fatal termination. 

As may be seen, the disease is decidedly like locomotor ataxia, and, in the early 
stages, with pain, ataxia, and absence of patellar reflex, the differential diagnosis 
has no slight difficulty. In regard to this it must be borne in mind that the 
reflex immobility of the pupils, the girdle sensation and disturbances of the bladder, 
seem to be absent in alcoholic neuritis, at least as a rule, while, on the other hand, 
the development of atrophic paralyses may almost certainly exclude locomotor 
ataxia. 

The treatment demands, in the first place, the entire abandonment of the 
further use of alcohol, if possible. In mild cases we can obtain a decided improve- 
ment by this alone. In more advanced cases electrical treatment and tepid baths 
do the best service. We would also recommend the internal or subcutaneous use 
of preparations of strychnine. 



CHAPTER VI. 

NEW GROWTHS IN THE PERIPHERAL NERVES. 

The new growths in the peripheral nerves are usually divided into false and 
true neuromata. The former are not newly-formed nervous tissue proper, but are 
fibromata, myxomata, sarcomata, etc., which develop on the nerves. Infectious 
tumors, also, especially syphilitic gummata, and still more frequently the new 
growths arising in leprosy, may have their seat on the peripheral nerves. The 
true neuromata consist of newly formed, usually medullated, nerve-fibers (neu- 
roma myelinicum of Virchow), which are imbedded in a frequently very abun- 
dant connective-tissue stroma. These neuromata develop most frequently in the 



552 



DISEASES OF THE MOTOR NERVES. 



cut ends of nerves in amputation-stumps (amputation neuromata), but they may 
form after other injuries of the nerves. The multiple occurrence of neuromata, 
which has also been repeatedly observed, is very remarkable. These develop by 
hundreds in the same individual, chiefly on the spinal nerves, only occasionally 
and exceptionally on the sympathetic or cranial nerves. In such cases the differ- 
ent tumors are by no means metastases from one original tumor, but are the 
expression of a general and often hereditary predisposition of the peripheral 
nervous system to the formation of tumors. Sometimes multiple neuromata are 
combined with other anomalies of the nervous system, like cretinism. Beside 
the medullated neuromata, there are also new growths of non-medullated nerve- 
fibers (neuroma amyelinicum), but their histological diagnosis is always very 
difficult. 

The symptoms of neuromata vary very much in different cases. Many of 
them cause no symptoms at all, but in other cases they are the cause of extremely 
severe and persistent neuralgias and neuralgiform pains, which come on with 
varying intensity, are usually remittent or intermittent, and are often- increased 
by external causes, the influence of the weather, etc. Marked symptoms of 
pressure, especially anaesthesia and motor paralysis, are only exceptionally devel- 
oped, but they sometimes do occur, especially in neuromata of the cauda equina. 
Direct or reflex symptoms of motor irritation, like tremor or tonic spasms, are 
somewhat more frequent. 

The so-called tubercula dolorosa deserve special mention. By this term we 
mean little nodules, which may be felt beneath the skin, and are usually readily 
movable and very sensitive to pressure. They are not very rare, and are usually 
associated with drawing pains, which are rarely decidedly neuralgic and are not 
very strictly localized. They are situated in the extremities, especially in the 
arms, and in the back, the neck, etc. It is worthy of note that the symptoms are 
only at times very prominent, and then they disappear again, and that with this 
disappearance is certainly sometimes associated a spontaneous disappearance of 
the nodule. The anatomical nature of the tubercula dolorosa is not always to be 
established with certainty. Many of them are true neuromata, but others belong 
to other kinds of new growths. 

The course of neuromata is, of course, very chronic. In some cases the per- 
sistent severe pain may give rise to considerable general disturbance, but a final 
spontaneous cessation of the symptoms, and even a disappearance of the new 
growths, have also been observed. 

The diagnosis of neuromata is possible only when the tumors can be felt 
through the skin, and when their seat, as well as their clinical symptoms, corre- 
sponds to the course and distribution of a nerve. In multiple neuromata the 
diagnosis has been repeatedly confirmed by the excision and examination of 
one of the tumors. 

The only successful treatment of neuromata is extirpation, which is to be 
undertaken only when the symptoms are very severe. If extirpation be not 
practicable, or if we have to do with multiple neuromata, the patient's trouble 
can be alleviated only by symptomatic means, narcotics, and electricity. If we 
can compress the nerve above the neuroma, we can often cause by this means a 
temporary cessation of the pain. 



VASO-MOTOR, TROPHIC, AND SECRETORY DISTURBANCES. 553 



II.— Vaso-motor and Trophic Neuroses. 



CHAPTER I. 

PRELIMINARY REMARKS UPON VASO MOTOR, TROPHIC, AND 
SECRETORY DISTURBANCES. 

Beside the disturbances of sensibility and motility described in the preceding 
sections, we also see in nervous patients frequent anomalies of the vaso-motor and 
trophic functions, but up to the present time we know comparatively little that is 
certain as to the precise nature of their occurrence. 

Physiology, as is well known, distinguishes two varieties of vaso-motor nerves 
— the vaso-constrictors and the vaso-dilators ; but since experiments have detected 
the latter variety in only a few places — for example, in the chorda tympani, the 
nervi erigentes, and the sciatic — they have not acquired a very great significance in 
human pathology. We are at present much more disposed to refer every abnor- 
mal constriction of the vessels to an irritation, and every abnormal dilatation of 
the vessels to a paralysis of the vaso-constrictor nerves, although perhaps patho- 
logical conditions of irritation of the vaso-dilators may not be at all rare. In 
regard to the precise anatomical course of the vaso-motor nerves, we must first 
state that vaso-motor irritations may certainly proceed from the cerebrum, as is 
shown by the well-known symptoms of blushing and pallor from mental emo- 
tions. In experiments on dogs, Eulenburg and Landois have succeeded in pro- 
ducing a fall of temperature on the opposite side by irritating certain portions of 
the cortex in the immediate vicinity of the motor centers, and by extirpation of 
the same parts they have produced a rise in temperature. Furthermore, we know 
with certainty that there is an important vaso-motor center in the medulla oblon- 
gata (in the region of the upper olivary body in puppies), the irritation of which, 
directly or reflexly, is followed by an almost universal vascular constriction, and 
its destruction by an almost universal vascular dilatation. We must probably 
seek the further course of the vaso-motor ■ nerves very largely (or exclusively ?) in 
the lateral columns, from which they pass out chiefly by the anterior roots ; but 
there are also experimental data (Strieker) suggesting the presence of vaso-motor 
nerves in the posterior roots. It is not known with certainty whether there is 
any decussation of the vaso-motor fibers, or, if there is, where it occurs. The 
larger part of the vaso-motor nerves collect, at any rate, in the principal trunks 
of the sympathetic, from which, as is well known, the separate plexuses that sur- 
round the vessels arise. It is not improbable, however, that there is also in part a 
direct passage of vaso-motor fibers from the cord into the peripheral nerves. In 
conclusion, we must mention that, according to Ooltz's experiments, there are 
reflex vaso-motor centers in the cord for the different parts of the body. 

The clinical vaso-motor symptoms are chiefly to be observed in the external 
skin. We distinguish them as follows : 

1. Symptoms of Vaso-motor Paralysis. — We conclude that there is a paral- 
ysis of the vaso-motors if there is an abnormal redness of the skin. Such a 
redness is almost always associated with an objective and often a subjective feel- 
ing of an increase of temperature. Such conditions are observed either in con- 
nection with other nervous symptoms — as in fresh spinal or cerebral paralyses, 



554 



VASOMOTOR AND TROPHIC NEUROSES. 



and also very often in certain functional neuroses, like hysteria and neurasthenia 
— or in the form of independent affections — the pure vaso-motor neuroses, injuries 
of the cervical sympathetic, etc. There are cases in which the only symptoms 
are a persistent or paroxysmal redness of the skin, especially of the head, asso- 
ciated with a great feeling of heat, with palpitation of the heart, strong pulsa- 
tion of the arteries, anxiety, ringing in the ears, and sweating. If the affection 
is confined to a single extremity, in which there are paroxysmal redness, diffuse 
swelling, and pain, we have the condition described by Weir Mitchell as erythro- 
melalgia. As was stated above, it is at present impossible to decide whether 
many of the symptoms just mentioned do not perhaps depend upon an irritation 
of the vaso-dilator nerves. 

2. Symptoms of Vaso-motor Spasm. — Spasm of the small vessels becomes 
apparent by a striking pallor and coolness of the skin. There is often, with this, 
a decided feeling of formication and stiffness in the affected parts, which may 
even increase to an actual feeling of pain. Such vaso-motor spasms affect the 
hands especially, and form a chronic trouble that is not very rare. They are 
usually seen in people who are generally nervous and irritable, and sometimes 
also in washerwomen. A vascular spasm is sometimes seen in the extremities as 
one symptom of complicated paroxysms, like nervous angina pectoris (q. v.), 
especially at the beginning of the paroxysm. A persistent spasm of the small 
arteries may give rise to considerable subsequent trophic disturbance. At least, 
the rare cases of so-called " spontaneous symmetrical gangrene " of the extremities, 
and also certain forms of scleroderma and some similar affections, are referred by 
many observers to a primary spasm of the vessels. There is a condition, seen 
especially in the hands, in which, without known cause, the skin becomes dark 
blue and icy cold, and the epidermis is raised in different parts into bullae. This 
condition may even attain to a circumscribed gangrene — spastic gangrene. 

We have much less information concerning the trophic nerves than we have 
concerning the vaso-motor. As is well known, the controversy is still going on 
as to whether we have any right to assume the existence of special trophic nerves. 
Clinical facts speak decidedly in favor of this assumption, although we have 
already stated that many trophic disturbances are probably due to vaso-motor 
changes, and also that the anaesthesia of many parts is a very favorable circum- 
stance for the occurrence of disturbances of nutrition (compare what was said in 
regard to anaesthesia of the trigeminus on page 483). 

Those changes in the skin which depend essentially upon an abnormally great 
exudation from the vessels, form a transition between vaso-motor and trophic dis- 
turbances. Among them are, first, peculiar cases of disease which have been termed 
"acute angioneurotic oedema" (Quincke, Strubing, and others). In these cases 
cedematous swellings appear suddenly in various parts of the body, and sometimes 
disappear after a few hours, but they may be very often repeated. Dangerous symp- 
toms may arise if the oedema affects the pharynx or the entrance to the larynx. 
The patient's health otherwise is sometimes perfectly good, but in other cases it is 
more or less affected. Gastric disturbances especially (attacks of vomiting and 
gastralgia) have been observed at the same time in such patients. " Acute angio- 
neurotic oedema " is manifestly closely allied to urticaria and erythema exuda- 
tivum. In regard to the occurrence of herpes zoster in nervous diseases, compare 
what was said on page 487. Vesicle formations analogous to herpes zoster inter- 
costalis may also occur along the track of other nerve-trunks in peripheral, or 
even in purely spinal (?) nervous affections. 

Among those symptoms which chiefly support the theory of the existence of 
specific trophic nervous influences, we have already learned to recognize the 
degenerative atrophy of the muscles and nerves (see page 507). Various other 



VASO-MOTOR, TROPHIC, AND SECRETORY DISTURBANCES. 555 



sorts of trophic disturbances in the skin and the deeper parts are seen in nervous 
diseases. Especially after wounds of the peripheral nerves we often notice a 
peculiar shining, smooth, atrophic condition of the skin — the " glossy skin " or 
"glossy fingers" of the English authors. In other cases anomalies in the pig- 
mentation of the skin seem to be connected with the nervous disturbances ; thus 
spots deprived of pigment {vitiligo) often develop as a result of severe neural- 
gias. We must also bring to mind here the appearance of changes in pigmenta- 
tion from nervous causes, especially the aetiology of Addison's disease (vide infra) 
and the occurrence of the so-called nervous nsevi. Among the severe neuro- 
trophic disturbances of the skin many observers, especially Charcot, class the 
appearance of acute bed-sores in many spinal and cerebral paralyses, but we 
have never been able to convince ourselves of the occurrence of a " neurotrophic 
decubitus," and we believe that every bed-sore is due in the first instance to exter- 
nal influences, uncleanliness, and pressure on the skin. Finally, a disease lately 
described, especially in England, by William Gull and Ord, is very remarkable, and 
may be briefly mentioned here. In this there is a marked cedema-like swelling of 
different parts of the skin, especially in the face, but also in the extremities, and also 
of the trunk, the tongue, and the internal organs, which is due to the development 
of a form of myxomatous new growth in the connective tissue ; from this growth 
it is called myxcedema. Other trophic disturbances are usually found at the same 
time : atrophy of the teeth and nails, loss of hair, failure of the secretion of sweat, 
and consequent dryness of the skin. A general physical and mental weakness 
almost always gradually develops, and the latter may increase to complete demen- 
tia. Disturbances in the functions of the special senses are also present. A dimi- 
nution in the size of the thyroid gland seems to be constant. Charcot regards the 
disease as of trophoneurotic origin, and calls it " cachexie pachydermique." 

Beside the trophic disturbances in the skin, we often see analogous changes in 
the nails and hair in nervous patients. The nails become brittle and cracked, 
assume a darker color, and often show a considerable thickening (onychogryphosis). 
We also see at times a loss of the nails. A loss of hair is seen in frontal neuralgia, 
in certain forms of headache, and not infrequently as an apparently independent 
nervous disease (alopecia). A very rapid whitening of the hair after mental 
excitement is well known to have occurred in some cases. 

Among the trophic disturbances of the deeper parts the symptoms sometimes 
seen in the bones and joints deserve a brief mention. The implication of the bones 
in atrophic processes is seen chiefly in progressive unilateral facial atrophy (vide 
infra). A retarded growth of bone in the affected extremities is also a symptom 
frequently seen in the spinal, and even in the cerebral paralyses, that develop in 
childhood, which proves most plainly that the processes of growth depend upon the 
nervous system. Trophic affections of the joints have been repeatedly confirmed in 
cerebral and spiual diseases, especially in locomotor ataxia (vide infra). As a 
special vaso-motor-trophic articular neurosis we may mention here the so-called 
hydrops articulorum intermittens. We mean by this a very rare but perfectly typ- 
ical disease, in which large swellings, usually of the knee-joint, but sometimes of 
the other large joints, develop at perfectly regular intervals of one to four weeks. 
They continue without fever, and usually without any great pain, and disappear 
again in a few days. Such attacks may be repeated at intervals of different 
lengths, during years and years. Their nervous character is attested especially by 
the rapid onset and disappearance of the affection, and also by the combination of 
it with other nervous disturbances, like angina pectoris, exophthalmic goitre, vaso- 
motor symptoms, etc., which combination has often been observed. In regard to 
treatment we may try salicylic acid, quinine, Fowler's solution, and subcutaneous 
injections of ergotine. 



556 



VASO-MOTOR AND TEOPHIC NEUROSES. 



In addition to the trophic disturbances we must consider the disturbances of 
secretion. These are not infrequent. We have already learned to recognize 
anomalies in the secretion of saliva in facial paralysis, and of the lachrymal secre- 
tion in trigeminal neuralgia. Analogous symptoms are occasionally noticed in 
other nervous diseases. Disturbances of the sweat secretion are the easiest to con- 
firm. Our understanding of them comes substantially from the discovery of the 
" sweat nerves," arising mainly from the sympathetic, which was first made by 
Luchsinger. In nervous patients we have seen quite frequently, on the one hand, 
an abnormal increase of the sweat secretion {hyperidrosis, ephidrosis), and, on the 
other, a diminution or a complete disappearance of it. The former is seen on 
the paralyzed side in many hemiplegias and in spinal paralyses, the latter in loco- 
motor ataxia. Anomalies of the sweat secretion are quite frequent, and are 
usually combined with vaso-motor disturbances, in certain general neuroses, like 
hysteria and neurasthenia. In a few rare cases a genuine haeinatidrosis (bloody 
sweat) has been confirmed. The condition known as unilateral hyperidrosis (uni- 
lateral sweating) is also especially interesting. In this there is an abnormal secre- 
tion of sweat, chiefly in one half of the face, more rarely in one arm or over the 
whole of one side. The affection has usually been observed in connection with 
hemicrania, exophthalmic goitre, hysteria, etc., and, in at least a number of cases, 
it is due to direct lesions of the sympathetic. On the other hand, we have repeat- 
edly seen persons, who were otherwise perfectly healthy, in whom the secretion of 
sweat, coming on under normal conditions from heat or physical exertion, remained 
limited to one half of the body, especially the face. 

In conclusion, we would briefly mention here the symptoms which have been 
observed in direct injuries of the cervical sympathetic, wounds, pressure of neigh- 
boring tumors, etc. If we have to do with a paralysis of the sympathetic, we see 
almost constantly on the affected side a contraction of the pupil from paralysis of 
the dilatator pupillse supplied from the sympathetic, in many cases associated with 
a slow reaction to light. We also frequently see a narrowing of the opening of the 
lids from paralysis of Muller's muscle, and in old cases a retraction of the bulbus 
oculi, and occasionally increased redness and warmth in the ear and cheeks from 
vaso-motor disturbance. In a few cases we see an increased sweat secretion. We 
may add that, according to Mobius, the normal reflex dilatation of the pupil, from 
a painful irritation of the skin of the face, is absent in paralysis of the sympa- 
thetic. The opposite symptoms are found in conditions of irritation of the sym- 
pathetic. In both cases there are sometimes slight trophic disturbances in the 
cheeks. It is also worthy of note that in tumors of the neck, and after injuries of 
the brachial plexus, there are sometimes disturbances in the sympathetic, especially 
changes in the pupils, which are due, as is supposed, to a lesion of the communi- 
cating branches between the principal trunk of the sympathetic and the brachial 
plexus. The occurrence of sympathetic symptoms in certain injuries of the bra- 
chial plexus has already been mentioned above (page 535). 



CHAPTER II. 

HEMICRANIA. 

{Migraine) 

iEtiology. — By hemicrania we mean a peculiar form of unilateral headache, 
due probably to vaso-motor disturbances, or at least almost always associated with 
vaso-motor symptoms. The affection occurs especially in women, more rarely in 



HEMICEANIA. 



557 



men, and almost always begins in youth, generally at the period of puberty, but 
typical cases of migraine have been repeatedly observed in school-children. Quite 
frequently, but not always by any means, the disease affects women who must be 
regarded as " generally nervous," who are anaemic, or who suffer from disturbances 
of menstruation. Heredity often plays a part, since hemicrania is both hereditary 
as such, and often appears in families which have suffered from other nervous 
diseases, like epilepsy, hysteria, or the psychoses. We may mention as exciting 
causes, which may be made answerable both for the onset of the disease, and quite 
often for the individual attacks, physical and mental over-exertion, great mental 
excitement, and disturbances of digestion. 

We do not know the special cause of hemicrania. Considering the accompa- 
nying vaso-motor symptoms, which are present in migraine as a rule (vide infra), 
it is almost universally assumed that we must regard the disease, from its chief 
cause, as an affection of the sympathetic ; but we must agree with Mobius that this 
assumption is by no means confirmed, and that it is possible that the accompany- 
ing sympathetic symptoms may be only secondary and of reflex origin, in conse- 
quence of the pain. We also have no definite information as to the special seat 
of the pain in migraine, but it is most probably to be placed in the meninges — the 
pia and dura mater. 

Symptomatology. — Migraine always comes on in separate attacks, which are 
repeated at intervals of varying lengths, although some cases often show a 
remarkably great regularity. The onset of the attack in women often has some 
relation to the menses. The left half of the head is much more frequently affected 
than the right. In some cases it happens that the pain affects the right and 
the left sides alternately ; in others it is not generally very strictly limited to one 
side. 

The attack of migraine usually begins with certain prodromal symptoms, which 
the patient soon recognizes as sure signs of his approaching suffering. These 
prodromal symptoms consist of general uneasiness, discomfort, pressure in the 
head, vertigo, at times tinnitus, spots before the eyes, chills, malaise, abnormal 
yawning, etc. In a short time the pain begins. It is felt most either in the anterior 
frontal region or in the temporal or parietal region, it generally shows a con- 
tinuous character, not intermittent as in neuralgia, and may increase to a very 
great intensity. Special painful points are usually absent, but the whole skin 
over the head on the affected side is usually hyperaesthetic. The general malaise 
continues with it ; the patient has absolutely no appetite, there is often great 
nausea, and almost always a great sensitiveness to external impressions, to any 
bright light, or to any noise. In many cases of ophthalmic hemicrania, ocular 
disturbances are especially prominent ; bright scintillations before the eyes, scin- 
tillating scotoma, and quite often a pronounced hemianopsia, may be made out 
during the attack. 

The vaso-motor symptoms are of special interest because they are of value in 
the theory of the disease. From them migraine is usually divided into two sub- 
divisions — hemicrania sympathico-tonica or spastica, and hemicrania sympathi- 
co-paralytica or angio-paralytica. 

In hemicrania spastica, first described by Du Bois-Eeymond from observations 
on himself, the forehead and ear on the affected side are pale, the skin is cool, the 
temporal arteries contracted, the pupil is often decidedly dilated, the secretion of 
saliva increased — in short, there are a whole row of symptoms present which all 
agree in pointing to a condition of irritation in the sympathetic (vide supra). 

In hemicrania paralytica, however, which was first described by Mollendorff, 
also from observations on himself, the face is reddened on the affected side, it feels 
hot, the temporal arteries are dilated and pulsate strongly, there is sometimes 



558 



VASO-MOTOE AND TROPHIC NEUROSES. 



unilateral sweating of the face, the pupil is contracted — all symptoms which can 
depend only on a paralysis of the sympathetic. 

As has already been hinted, the significance of all these symptoms is not abso- 
lutely certain, and we must also add that the cases which occur in practice can 
not by any means always be inserted into one or the other typical scheme without 
further ceremony. The vascular symptoms are sometimes but slight, conditions 
of paralysis and of irritation of the sympathetic sometimes seem to alternate with 
each other in the same attack, and we may even frequently meet with apparently 
contradictory symptoms at the same time, like pallor joined with contraction of 
the pupil. The peculiar method of the origin of the pain is at present, also, almost 
wholly unexplained. If we assume primary vascular changes in hemicrania, we 
must look for the cause of the pain in the disturbance of the circulation, or per- 
haps, in spastic hemicrania, in the spasmodic contraction of the vessels itself. 

The duration of the attacks of migraine differs very much in different cases. 
It usually lasts several hours, or a whole day ; then the pain gradually disappears, 
and there is often considerable vomiting toward the end of the attack. In the 
intervals between the different attacks most patients are perfectly well and free 
from pain. 

The whole course of migraine is very chronic, and may last for years and 
years. It is usually a trouble to which the patient finally becomes accustomed. 
We must generally be quite guarded in our prognosis, for many cases resist very 
obstinately all attempts at cure. We can give the patient only the consolation 
that the trouble generally disappears of itself in advanced life. It is not usually 
attended with any special danger. In only a few cases has it been noticed that 
attacks of hemicrania of years' duration have preceded a severe cerebral disease 
that developed later, or locomotor ataxia. 

Treatment. — Very many patients who suffer from migraine finally renounce 
any special treatment, after they have exhausted all possible remedies. They 
withdraw to then rooms when the attack comes on, darken the windows, take 
nothing but some tea, Seltzer-water, or cracked ice, put a cold compress about 
the head, perhaps try a foot-bath, and for the rest wait quietly until the attack is 
over. In fact, our remedies for cutting the attack short are quite uncertain. They 
sometimes aid, but they often leave us in the lurch, especially if used repeatedly. 
We must note especially that narcotics, like morphine, are almost always ill borne 
in migraine, and do no good. In spastic hemicrania, inhalations of nitrite of 
amyl, three to five drops on a napkin, have been recommended on theoretical 
grounds, and sometimes really act well. In paralytic hemicrania, subcutaneous 
injections of ergo tine are at times of advantage; aqueous extract of ergot, 2*5; 
dilute alcohol and glycerine, each, 5 ; or dialyzed ergotine in distilled water, one 
to four, injecting of either seven to fifteen minims. Of the other remedies used, 
we may mention guarana, half a drachm to a drachm (grm. 2-4) of the pow- 
der, caffeine in one-grain (grm. 0*05) doses, and, what is perhaps most efficient, 
salicylate of sodium, half a drachm to a drachm (grm. 2-4), best taken in 
strong cafe noir. These remedies, and many other nervines, like bromide of 
potassium and Fowler's solution, have been recommended for continued use, 
and also extract of cannabis indica; and, lately, nitrite of sodium, two parts in 
120 of water, a teaspoonful one to three times a day. Its action is analogous to 
that of nitrite of amyl. Nitro-glycerine, in troches containing to grain 
(grm. 0*0005-0 '001), also has the same dilating action on the vessels. 

In many cases the general treatment is very important. Preparations of iron, 
sea-bathing, a mountain residence, and cold-water cures, are often of distinct serv- 
ice. The persistent application of electricity has also shown some good results, 
but we must not build very great hopes upon it. In the spastic form the action of 



PROGRESSIVE FACIAL HEMIATROPHY. 



559 



the anode on the sympathetic is to be especially tried, and in the paralytic form 
the action of the kathode, while the other electrode is to be placed on the cervical 
cord, or as high as possible on the occiput in the region of the medulla. Cautious 
galvanization of the head, and weak primary f aradic currents, may also be used. 



CHAPTER III. 

PROGRESSIVE FACIAL HEMIATROPHY. 

{Unilateral Progressive Facial Atrophy.) 

Unilateral facial atrophy is an extremely rare disease, of which only about 
thirty cases have been recorded in literature up to the present time. The disease 
consists in a very slow and gradual but usually constantly progressive atrophy of 
one half of the face, and affects the skin, and also the fatty tissue, the muscles, 
and the bones, either in a uniform or a very diverse manner. The affection 
usually begins in youth. The female sex seems to be more disposed to the disease 
than the male. 

The atrophy, which has its seat much more frequently on the left side than on 
the right, begins usually in a circumscribed spot, either on the cheeks or on the 
chin. The skin, as a rule, gradually assumes a whitish or brownish color. The 
affected part, and finally the whole 
half of the face, gradually sink in 
more and more, so that the disease 
can be recognized at the first glance. 
The atrophy shows a sharp limita- 
tion at the median line. In many 
cases the muscles apparently re- 
main almost wholly intact, but in 
some cases they show a marked 
atrophy, especially the muscles of 
mastication. The corresponding 
half of the tongue and the soft pal- 
ate has sometimes been found im- 
plicated. Exceptionally, the atro- 
phy involves the neighboring re- 
gion of the shoulder and the upper 
extremity. The bones also atrophy, 
especially in the cases which arise 
in early youth. The hair on the 
affected half of the head often falls 
out in great amount, and it becomes 
thin and atrophic. The sensibility 
remains perfectly intact. Marked 
vaso-motor and secretory disturb- 
ances have only rarely been ob- 
served. The accompanying illustration (Fig. 79) shows a patient who was described 
by Romberg about thirty years ago, and who at present still frequents the Ger- 
man cliniques in order to show himself. 

Nothing definite is known in regard to the nature of the affection. Most 
observers at present agree that it is a trophic neurosis, an affection of trophic 
nerves or nerve-centers, but where we are to look for the special seat of the dis- 




Fig. 79.— Left facial hemiatrophy. 



560 



VASOMOTOR AND TROPHIC NEUROSES. 



ease, whether in the trigeminus (especially in the spheno-palatine or the Gasserian 
ganglion ?) or in the sympathetic, we do not know, as post-mortem examinations 
are still entirely wanting. 

The disease is not dangerous in itself, and usually causes no special subjective 
disturbance, but it seems to be incurable. In cases at their beginning we can at 
most make an attempt to bring the disease to a stand- still by a long-continued 
application of electricity. 

As an appendix it may be briefly mentioned here that there is a unilateral 
hypertrophy, which is also possibly connected with neurotrophic disturbances. 
We have at present under observation a ten-year-old boy, otherwise perfectly 
healthy, in whom a striking hypertrophy of the left side of his face and of the 
left arm has gradually developed. 



CHAPTER IV. 

EXOPHTHALMIC GOITRE. 

(Graves's Disease. Morbus Gravesii. Basedow's Disease. Morbus Basedoivii. GlotzaugenTcrankheit.) 

iEtiology. — The special group of symptoms to which the name of exoph- 
thalmic goitre has been given, and whose three cardinal symptoms are accelera- 
tion of the pulse, goitre, and exophthalmus, was first carefully described in Ger- 
many, in the year 1840, by the Merseburg physician Basedow, although similar but 
less precise observations had been published in England by Graves five years ear- 
lier. The anatomical cause of this disease is still entirely unknown to us, but the 
whole type, and almost all the single symptoms of the affection, point definitely 
to an affection of the nervous system, which, with regard to the most prominent 
symptoms, is usually considered a " vaso-motor neurosis " or an " affection of the 
sympathetic " ; although, as may be seen from what follows, exophthalmic goitre 
might be more properly regarded as belonging to the general neuroses. 

With reference to the special aetiology of the disease all those factors are 
prominent which generally play the first part in the aetiology of neuroses. In 
many cases a hereditary predisposition can certainly be discovered. The disease 
has been repeatedly seen in several members of the same family. Further- 
more, exophthalmic goitre is also quite frequent in those families in which there 
is a hereditary predisposition to neuroses in general — epilepsy, the psychoses, or 
hysteria. Among the exciting causes we must first mention great mental excite- 
ment — grief, terror, anger. Sometimes real injuries, as well as these " psychical 
injuries," seem to have an influence on the development of the disease — that is, 
great general bodily concussion, like a fall. Many authors have laid considerable 
weight on diseases of the female sexual organs, but the importance of this factor 
seems to us to be exaggerated. It is certain, however, that the first symptoms of 
exophthalmic goitre often develop at the period of pregnancy. 

The influence of sex upon the origin of the disease is plain, since women, espe- 
cially somewhat anaemic, " nervous " women, are much more frequently affected 
than men. Exophthalmic goitre usually appears in middle life, while it is seen 
only exceptionally in children and old people. 

Symptomatology. — Of the three cardinal symptoms of exophthalmic goitre 
named above, of which, of course, one or another is often absent or only slightly 
developed, the acceleration of the pulse is the most constant and usually the ear- 
liest. The frequency of the pulse averages 100 to 120, sometimes only 80 or 90, 



EXOPHTHALMIC GOITEE. 



561 



but in other cases even 140 or 160. It is not alike at all times, but has many vari- 
ations ; the symptoms lasting" for long periods and coming on in single parox- 
ysms. A very vigorous action of the heart, and as a rule the subjective feeling 
of palpitation, are usually associated with the acceleration of the pulse. There is 
a vigorous pulsation of the carotids, and sometimes of the smaller arteries. We 
do not discover any qualitative changes of the pulse. The pulse is usually quite 
regular, but arhythmia has been repeatedly observed. In some cases the patients 
suffer from pronounced angina pectoris. 

Physical examination of the heart in many cases shows nothing particular, 
except an accelerated and violent action of the heart, but we sometimes find, as 
we can affirm from several cases in our own experience, a manifest hypertrophy 
of the left ventricle, and also dilatation of the heart, and even actual valvular 
disease. In the diagnosis of the latter some caution is necessary, because functional 
heart murmurs are often present in exophthalmic goitre. 

The goitre usually develops somewhat later than the first symptoms in the 
heart. In many cases it is entirely absent, or present only in a slight degree. 
The swelling of the thyroid gland is generally only exceptionally very marked. 
There are sometimes marked variations in it in the course of the same case. The 
comparative softness of the tumor, the frequent and strong pulsations in it, and the 
loud vascular murmurs, which are often, but not always, heard, and which arise 
in the dilated vessels of the thyroid gland, are characteristic of the goitre in 
Graves's disease. By laying the hand on it we can often feel the thrill and pul- 
sation. 

The exophthalmus, the protrusion of the eyeballs from their orbits, is always 
bilateral, although it is sometimes more marked on one side than on the other. It 
differs very much in intensity. In many cases it is entirely absent ; in others it 
may attain so high a degree that an actual 14 dislocation of the eyeball " has been 
described. In the marked degrees of exophthalmus there is often a peculiar star- 
ing expression to the countenance. A peculiar symptom, first described by Von 
Graefe, is also worthy of mention. On raising and lowering the eyes, the cor- 
responding associated movements of the upper eyelid, which are always present 
under normal conditions, are absent. This " Graefe symptom " may sometimes 
be one of the earliest signs of the disease, and may therefore be of diagnostic 
value ; but we must lay stress upon the fact that, in our own experience, this 
symptom is at any rate very rare. Sometimes severe inflammatory processes 
have been seen in the eye, which are probably to be referred to the impaired 
protection of the eye by the upper lid as a result of the exophthalmus. Dis- 
turbances of the pupils and of accommodation are unknown in exophthalmic 
goitre, but we have ourselves repeatedly observed anomalies in the movements of 
the eyeball, especially temporary strabismus. We might mention one symp- 
tom, which Mobius has first noticed, and which we also have repeatedly but 
not constantly seen, especially in patients with more marked exophthalmus. It 
consists in the fact that one eye very soon deviates outward (insufficiency of one 
internal rectus) if we have the patient converge the eyes strongly, as in fixation of 
a near object. 

Beside the chief symptoms of exophthalmic goitre thus far described, we must 
also mention a list of other symptoms which come to our observation, both in 
the typical cases, and still more often in anomalous cases — the so-called u formes 
frustes " of the French. Among them are some other nervous symptoms, especially 
a peculiar tremor to which Marie in particular has lately called attention. This 
tremor affects the whole body, or the extremities alone ; it shows at times temporary 
remissions and exacerbations, and it may be so severe as to form the patient's chief 
complaint. In a case under our observation marked tremor was one of the first 



562 



VASO-MOTOK AND TROPHIC NEUROSES. 



symptoms of tlie disease. It may become so violent at times that there are even 
spasmodic twitchings in the extremities and in the muscles of the face. We have 
repeatedly seen lesser degrees of tremor, especially in the hands, and we regard it, 
indeed, as quite characteristic. We may also mention among the nervous symp- 
toms which are sometimes present, headache, vertigo, weakness of memory, and 
sleeplessness. The peculiar nervous anxiety and the irritable disposition of the 
patient are, however, very frequent, and in fact very characteristic, in many cases 
of the disease. The anxiety and the haste in all movements, in speaking, etc. , often 
show themselves, even during the physician's examination, in so striking a way 
that they must be regarded as not unimportant factors in diagnosis. Exoph- 
thalmic goitre is sometimes complicated with other neuroses — with actual hysteria, 
epilepsy, chorea, the psychoses, etc. The marked subjective feeling of heat, from 
which many patients suffer, is probably due to vaso-motor disturbances. Object- 
ive elevations of temperature up to 100° or 101'5° (38°-38'8° C.) have also been 
repeatedly confirmed by others (Eulenburg) and by ourselves. A marked increase 
of the sweat production, which in rare cases is only unilateral, is often associated 
with the feeling of heat. On the other hand, one of our patients complained of a 
constant dryness in the mouth. 

Of symptoms which are referred to other organs we must first consider some dis- 
turbances on the part of the respiration. The respiration is usually moderately 
accelerated, and many patients complain of dyspnoea and of a feeling of oppression 
in the chest. In one case we saw at times deep spasmodic inspirations ; in other 
cases a peculiar dry, " nervous cough " appears. There are also symptoms on the 
part of the digestive organs. In some patients there are attacks of violent diar- 
rhoea, and in one woman we saw paroxysms of severe vomiting. Finally we must 
mention certain disturbances in the skin : vitiligo has often been observed, and 
also chloasma-like pigment-spots and urticaria. A very rare but dangerous occur- 
rence, of which we ourselves have seen a very striking example, is an apparently 
spontaneous gangrene of the extremities. In our case, which ended fatally, the 
gangrene affected the right leg. Not the slightest anomaly could be made out 
in the vessels at the autopsy. This gangrene in exophthalmic goitre recalls decid- 
edly the so-called " spontaneous symmetrical gangrene " (vide supra), for which 
we also must assume a neurotic origin. 

The general nutrition of the patient usually does not suffer much, but a certain 
degree of anaemia and emaciation is often present. Some cases, especially if the 
symptoms of exophthalmic goitre develop rather rapidly and intensely, may be 
associated with considerable emaciation and a very pronounced general weak- 
ness, and in rare cases even with an actual atrophy of the muscles of the arm 
or leg. 

Pathological Anatomy and Pathogenesis.— Although all the symptoms of 
exophthalmic goitre point to an affection of the nervous system as a cause of the 
disease, as we see from the symptomatology, the results of pathological investiga- 
tions are still very meager. There is a class of cases in which changes in the sym-' 
pathetic, and especially in the lowest cervical ganglion, are said to have been pres- 
ent ; but the pathological significance of the discovery is not placed beyond all 
doubt ; and in other cases nothing abnormal at all could be found in the sympa- 
thetic. The theory that all the symptoms of exophthalmic goitre are derived 
from a disturbance of the sympathetic also meets many difficulties and contradic- 
tions. If we regard only the three cardinal symptoms, we can bring the accelera- 
tion of the pulse, and perhaps the exophthalmus, into harmony with the theory of 
irritation of the sympathetic ; but not the goitre, which is due to a dilatation of the 
vessels. The theory of a paralysis of the sympathetic explains the goitre, and also 
the exophthalmus — if we assume as the cause of the latter a dilatation of the vessels 



EXOPHTHALMIC GOITRE. 



563 



in the back of the orbit — but again the acceleration of the pulse remains unex- 
plained. The attempt at explanation becomes still more complicated if we also con- 
sider the rarer symptoms of exophthalmic goitre. We believe, then, that we can not 
form a satisfactory theory of the disease from the single hypothesis of disturbances 
of the sympathetic, and that we must content ourselves provisionally with reckon- 
ing exophthalmic goitre among the general neuroses without known anatomical 
cause. The experiments by Filehne, interesting in themselves, in- which symp- 
toms similar to those of exophthalmic goitre were produced by dividing the resti- 
form bodies in young puppies, have had up to the present time no bearing upon 
human pathology. 

Course and Diagnosis. — The course of the disease is in most cases very chronic, 
and may extend over years and years, but there are also more acute cases with a 
rapid development of all the symptoms and a comparatively unfavorable course. 
We may often see considerable variation in the intensity of the symptoms. In 
general, the cases beginning in youth give a more unfavorable prognosis than 
those arising in later years. Recoveries have certainly been observed, but they 
are at all events rare. The disease sometimes terminates fatally with the signs 
of general marasmus, but more frequently from complications in the heart or 
lungs. We would note especially, however, that mild, and to some extent rudi- 
mentary, cases of the disease are not rare, and that these in no way endanger life ; 
and even in severe cases we sometimes see marked improvement, or at least an 
arrest of the disease. The diagnosis of undeveloped cases is difficult at times, since 
the three cardinal symptoms are not always by any means fully developed. We 
must then pay careful and especial attention to the other symptoms of the disease, 
chiefly to the general nervous irritability, the tremor, the subjective feeling of 
heat, and the tendency to sweating. In well-developed cases, however, the diag- 
nosis is almost always to be made with certainty and without difficulty. 

Treatment. — In the first place we must consider the general treatment of the 
patient. Physical and mental rest, good food, and the avoidance of all stimulants 
— like alcohol or strong coffee — a country residence, and the cautious use of 
cold-water cures, especially sponging, maj r cause an actual improvement of the 
condition. For anaemic patients we prescribe iron, alone or in combination with 
small doses of arsenic. The springs at Franzensbad, Schwalbach, Pyrmont, Elster, 
and Cudowa, are also sometimes attended with good results. 

Of other remedies, electricity is first to be mentioned, especially the application of 
galvanism to the neck — the so-called galvanization of the sympathetic at the 
inner border of the sterno-mastoid. Accordingly as we regard the condition as a 
paralysis or as an irritation of the sympathetic, we shall try chiefly the action of 
the kathode or of the anode. Strong currents are always to be avoided. With 
galvanization of the sympathetic we may judiciously combine galvanization of the 
spinal cord. The slowing of the pulse, which sometimes appears at once, is strik- 
ing (irritation of the vagus ?). Among internal remedies we may recommend 
atropine or tincture of belladonna, and ergot or ergotine. We believe we have 
repeatedly seen good results from the latter. In a symptomatic point of view, 
digitalis has often been prescribed, but usually without any good result. The use 
of iodine preparations against the goitre is also almost always unavailing. With 
great exophthalmus the eyes must be protected from external injuries. 

In some cases the extirpation of the goitre has been practiced, and favorable 
results have been claimed for it ; but we doubt whether these cases were really 
exophthalmic goitre. In genuine typical cases we would scarcely determine to 
advise the operation. 



564 



THE DISEASES OF THE SPINAL COED. 



III. — The Diseases of the Spinal Cord. 



CHAPTER I. 
DISEASES OF THE SPINAL MENINGES. 

1. Acute Inflammations of the Spinal Meninges. 

JEtiology and Pathology. — Isolated acute inflammation of the spinal meninges 
is very rarely primary, so far as we know, but inflammatory processes in the 
neighborhood quite frequently involve the meninges, or a spinal meningitis 
occurs as one symptom of a general cerebro-spinal meningitis. This latter con- 
dition is seen chiefly in the idiopathic, generally epidemic, cerebro-spinal menin- 
gitis, which is a specific infectious disease, and has already been described in 
detail in a previous chapter. A tubercular spinal meningitis is also very often 
combined with tubercular inflammation of the cerebral meninges, but, since the 
symptoms of the latter are usually in the foreground of the picture, we will treat 
of tubercular cerebro-spinal meningitis in the section on diseases of the cerebral 
meninges. Secondary cerebro-spinal meningitis is sometimes seen in the course 
of certain other infectious diseases, and is then probably to be regarded as a 
special localization of the specific poison of the disease. This is the explanation 
of the occurrence of acute spinal and cerebral meningitis as a sequel of croupous 
pneumonia, and also of its occurrence in pyaemic and septic diseases, and, very rare- 
ly, in typhoid and the acute exanthemata. We must mention, finally, the occur- 
rence of a purulent cerebro-spinal meningitis as a sequel of empyema, pulmonary 
gangrene, etc., which, although very rare, we have repeatedly noticed. In these 
cases the infection of the meninges also results from the primary foci of disease, 
but the channel of infection is not yet exactly known. Perhaps the intercostal 
nerves are the media of communication. 

In all the cases so far mentioned we have chiefly an inflammation of the pia 
mater, a so-called lepto meningitis ; the dura mater is not implicated in the dis- 
ease at all, or only to a slight degree. The condition is different in those inflam- 
matory processes which gradually invade the meninges from the neighboring 
parts outside the cord. Thus we very often see circumscribed inflammations on 
the outer surface of the dura (pachymeningitis) in caries of the vertebrae, and 
these inflammations often invade the inner surface of the dura, or more rarely 
reach the pia mater. Acute purulent peripachymeningitis is a very rare disease ; 
it is a purulent inflammation of the connective tissue between the dura mater 
and the vertebral column, which in almost all cases is of secondary origin. "We 
have seen a very characteristic case of this sort in the course of a puerperal 
pyaemia. The inflammation had spread from a purulent inflammation of the pel- 
vic cellular tissue, through the foramina of the vertebral canal, and had finally 
set up a purulent inflammation on the outer surface of the dura extending up 
to the cervical cord. We meet with an affection of the pia mater from an exten- 
sion of the inflammation, chiefly in diseases of the spinal cord, since the pia takes 
part in the process to a greater or less extent in many cases of myelitis. 

We do not know with certainty whether other influences, especially injuries 



DISEASES OF THE SPINAL MENINGES. 



565 



and exposure to cold, can lead directly, as has often been claimed, to inflammation 
of the spinal meninges. 

We need to say but little in regard to the pathological anatomy of acute spinal 
meningitis. The changes in purulent inflammation of the pia mater have been 
described in the chapter on epidemic meningitis. Precisely the same conditions 
are found in the other forms of acute leptomeningitis. The changes in pachy- 
meningitis are completely analogous. The dura mater is traversed by dilated 
vessels, and therefore is reddened ; it is also thickened, and on its internal or ex- 
ternal surface {pachymeningitis interna or externa, or peripachymeningitis) 
there is usually found a purulent or a sero-purulent exudation. 

Symptoms.— An accurate distinction between acute inflammations of the pia 
mater and those of the dura mater can not be made clinically. The symptoms 
of the disease include the symptoms of any primary disease present, the general 
symptoms, like fever, etc., and in addition the necessary consequences which the 
presence of a disturbance of the meningeal circulation and of the meningeal 
exudation exerts on the cord and nerve-roots. These consequences are due both 
to a mechanical compression of the parts named, and often probably to an inva- 
sion of the substance of the cord itself by the inflammation. To these is added 
the frequent combination of spinal symptoms with the symptoms of a co-existing 
cerebral meningitis. 

Those symptoms which occur in acute spinal meningitis, and are especially 
referred to it, are, all of them, already known to us from the description of 
epidemic meningitis (see page 93). Recapitulating them briefly, we may mention 
chiefly the very severe pain in the back, the great sensitiveness of the vertebral 
column, and its stiffness. To these may be added usually symptoms of irritation 
on the part of the nerve-roots : excentric pains in the trunk and the extremities, 
hyperesthesia of the skin and of the deeper parts, symptoms of direct or reflex 
motor irritation, muscular tension, contractions, etc. The cutaneous and tendon 
reflexes are often, but not always, much diminished or abolished in consequence 
of the lesion of the nerve-roots. There are at times disturbances in the passage of 
urine and faeces. If, in the later course of the disease, there are actual paralysis and 
anaesthesia, they are usually a sign of a more marked implication of the cord itself. 

Diagnosis. — From the symptoms named we can, in many cases, make a diag- 
nosis of spinal meningitis. Of course a meningitis is found often enough on the 
autopsy-table, whose symptoms during life were completely obscured by other 
severe general symptoms, while, on the other hand, with severe constitutional 
symptoms the symptoms of meningitis may be illusory, as in typhoid or pyaemia. 
Fuller information as to the seat and the extent of the inflammation is afforded 
by considering the most painful parts of the vertebral column, the predominance 
of pain and cutaneous hyperaesthesia in the arms (cervical region) or legs (lumbar 
region), etc. When the meningitis involves the upper portion of the cord and the 
medulla there may also be disturbances of respiration, symptoms in the pupils, 
and anomalies in the innervation of the heart. We can decide as to the form of 
the meningitis, whether purulent or tubercular, only by a consideration of the 
history, the other morbid symptoms, and the course of the disease. 

Prognosis. — We have seen an undoubted recovery, in severe cases, only in epi- 
demic cerebro-spinal meningitis, and in the sporadic cases of idiopathic meningitis, 
which are probably identical in aetiology. In all other cases reported with a favor- 
able termination the diagnosis may be doubted, for in general the rule is certain 
that, in extensive acute purulent leptomeningitis and pachymeningitis, the prog- 
nosis is almost absolutely unfavorable, whether it be secondary to another infec- 
tious disease or arise from propagation from some neighboring focus of inflamma- 
tion. We may, perhaps, make an exception of certain mild, circumscribed cases, 



566 



THE DISEASES OF THE SPINAL CORD. 



which do not come to suppuration, but these are always uncertain in regard to 
diagnosis. 

Treatment. — In regard to treatment we must refer entirely to what has been 
said under epidemic and tubercular meningitis. 

2. Chronic Spinal Leptomeningitis. 

Although chronic leptomeningitis (usually wrongly termed chronic spinal 
meningitis) once played quite a large part in the diagnosis and pathology of dis- 
eases of the spinal cord, we must at present assert that its occurrence as an inde- 
pendent disease may justly be doubted. Almost all the cases reported come from 
a time when the diagnosis of many diseases of the cord itself was still perfectly 
impossible, and when the thickenings and opacities of the meninges were much 
more striking at the autopsy than the far more essential changes in the sub- 
stance of the cord itself, which could not be made out with the naked eye, but 
only by a careful microscopic examination. At any rate, we may say that a case 
of primary chronic leptomeningitis, which can be surely and convincingly proved 
clinically and anatomically, does not exist, and that our present clinical experi- 
ence, also, by no means favors the assumption of the existence of mild and curable 
forms of it. Among many cases of spinal disease we shall scarcely be induced 
even to assume the probability of the existence of primary chronic meningitis. It 
goes without saying that we can not dispute the possibility of its occurrence, 
although even for this we can scarcely find an analogy. 

The case is different with secondary chronic leptomeningitis. This, in the first 
place, in rare cases, is the termination of an acute meningitis. Secondary lepto- 
meningitis may be certainly made out, especially in epidemic meningitis. We 
also find chronic meningitis frequently as a secondary affection in primary dis- 
eases of the cord and the vertebrae. Thus, for example, in old cases of chronic 
spinal disease, associated with atrophy, like locomotor ataxia, progressive muscu- 
lar atrophy, etc., the pia is almost always quite opaque, thickened, and often 
united to the cord and the dura by very many firm adhesions, while a cloudy 
sero-gelatinous exudation is found in the meshes of the arachnoid. All these 
anomalies, however, are of a secondary nature, and have no clinical significance, 
for the same changes, though rarely so marked, are quite often found in old people, 
where they are analogous to the equally frequent opacities of the cerebral men- 
inges, the pleuritic adhesions, etc., and where, during life, they have not caused 
the slightest symptom of spinal disease. 

The symptoms which have been set down as characteristic of leptomeningitis 
correspond precisely to those of acute meningitis, except, of course, that they are 
relatively less intense, and that the course of the disease is more protracted. Pain 
and stiffness in the back and neck, abnormal painful sensations and paresthesia 
in the extremities, a girdle sensation, and finally paresis, anaesthesia, and vesical 
disturbances, are the leading features of the type of disease as constructed, in whose 
fabrication there have been, at any rate, many confusions with myelitis, spondy- 
litis, beginning locomotor ataxia, multiple neuritis, etc. 

It is clear that under such circumstances no special rules for the treatment of 
chronic spinal meningitis can be given. Given a case, we would try local applica- 
tions to the vertebral column ; painting with iodine ; dry, or, exceptionally, in 
strong patients, wet cups; also protracted tepid baths, 90° to 95° (26°-28° R.), or 
cautious cold-water treatment ; and finally the use of the galvanic current. Of 
internal remedies, iodide of potassium would be most indicated. We may refer 
to the description of the treatment of myelitis in regard to all further details. 



DISEASES OF THE SPINAL MENINGES. 



567 



3. Pachymeningitis Cervicalis Hypertrophica. 

Pachymeningitis cervicalis hypertrophica was first fully described, as a spe- 
cial form of disease, by Charcot in 1871, and later by his pupil Joffroy. Little is 
known as to its origin ; it has been attributed to exposure to cold and the abuse of 
alcohol. 

Anatomically, the disease is characterized by a chronic and often very con- 
siderable thickening of the dura, almost always, as it seems, in the cervical portion 
of the cord, while the pia takes but a comparatively small part in the affection. 
The dura may attain a thickness of six or seven millimetres, and usually appears 
composed of a number of concentric layers. Histologically, the hypertrophy con- 
sists of a new growth of dense connective tissue. The clinical symptoms of the 
disease arise from the fact that, first, the penetrating nerve-roots, and later on the 
cord itself, undergo a considerable mechanical compression. If this is of high 
degree and persistent, there are, as a necessary result, secondary degenerations of 
the motor nerves and muscles, and a secondary descending degeneration of the 
pyramidal tract in the cord. 

The clinical symptoms are easily understood from this. The disease almost 
always begins with severe pain, which shoots from the neck into the occiput and 
the arms. Beside this, there are paresthesia and a numb feeling in the arms and 
hands. Rarely there is an eruption of herpes. All these symptoms depend upon 
the irritation of the posterior roots. 

After this first period of the disease {periode douloureuse of Charcot) has 
lasted some two or three months, the second period begins— the period of paralysis. 
An atrophic paralysis in the up- 
per extremities gradually develops, 
mainly as a result of the compres- 
sion of the anterior motor roots. 
This affects, in a remarkable man- 
ner, chiefly the distribution of the 
ulnar and median nerves, while the 
distribution of the radial on both 
sides usually remains free. The 
hand, therefore, assumes a charac- 
teristic position (Fig. 80), as a result 

of the contracture of the antagO- Fig. 80.— Position of the hand in pachymeningitis cervi- 
nistic extensors. The paralyzed calis hypertrophica. (From Charcot.) 

muscles rapidly become atrophic 

and show a marked reaction of degeneration. In this stage there may also be 
partial anaesthesia of the skin. 

If the compression of the cord advances, the motor fibers for the lower extremi- 
ties, which pass through the cervical cord, must necessarily at last be involved 
sympathetically — the third, period of the disease. The result of this is a spastic 
paralysis of the lower extremities — that is, a paresis or paralysis with increased 
tendon reflexes, but of course without muscular atrophy, because the trophic cen- 
ters for the muscles of the legs, in the anterior cornua of the lumbar cord, remain 
perfectly intact. The compression of the cervical cord, however, may finally lead 
also to anaesthesia of the lower extremities, to paralysis of the bladder, and bed- 
sores, under which symptoms death ensues ; but, on the other hand, it must be 
mentioned that probably cases of recovery, or at least of actual improvement in 
pachymeningitis cervicalis hypertrophica, may occur even after it has lasted for 
years. 

The diagnosis of the disease is based first upon the fact that the affection 




568 



THE DISEASES OF THE SPINAL COED. 



begins with pains in the arms, and upon the later appearance of the characteristic 
paralyses. It may easily be confused with tumors in the cervical cord and with 
cervical spondylitis. Amyotrophic lateral sclerosis is distinguished, however, by the 
absence of disturbances of sensibility, by the final appearance of atrophy in the 
lower extremities, by the bulbar symptoms, and by the fact that the functions 
of the bladder remain intact. 

Treatment can do little directly, and must be chiefly symptomatic. Baths, 
iodide of potassium, and electricity are most used. Joffroy recommends the use 
of the hot iron to the neck. 

4. HEMORRHAGE INTO THE SPINAL MENINGES. 

(Hcematorrhachis. Meningeal Apoplexy. Pachymeningitis spinalis hcemorrhagica interna?) 

Large haemorrhages into and between the spinal meninges are of rare occur- 
rence. They arise chiefly from traumatic influences, from concussion or frac- 
ture of the vertebral column, or from direct injuries of the meninges, like stabs 
or gun-shot wounds. In a few cases great physical exertion may also lead to a 
meningeal apoplexy. Diseases of the vertebrae, caries, and carcinoma, may also 
lead to a haemorrhage from the erosion of a vessel. The frequent little meningeal 
haemorrhages, which appear as a complication of meningitis, in haemorrhagic dis- 
eases, in the course of severe general infectious diseases, septic infections, typhoid, 
and small-pox, and as a result of severe general convulsions, very rarely have any 
clinical significance. Finally, it may be mentioned that aneurism of the aorta 
or its branches may rupture into the vertebral canal. 

The clinical symptoms of meningeal haemorrhage are almost always sudden 
and "apoplectiform," but are unattended by any disturbance of consciousness. 
Their intensity depends entirely upon the degree of compression which the nerve- 
roots and the cord undergo from the effused blood. The symptoms of irritation 
usually predominate — severe pain in the back, paraesthesia, and neuralgic pains in 
the extremities ; and also symptoms in the motor distribution, tension, tremors, and 
contractures of the muscles. "With large haemorrhages, symptoms of paralysis, 
partial anaesthesia, disturbances of the bladder, etc., may ensue. Therefore the 
different types of the disease, depending upon the seat of the haemorrhage, follow 
the same general rules which are to be considered in judging of the seat of any 
other affection of the cord {vide infra). On the whole, the diagnosis of meningeal 
haemorrhage can but rarely be made with any certainty, unless suggestive aetiologi- 
cal factors precede and the symptoms and manner of beginning are especially 
characteristic. 

The course is quite favorable in many cases if the blood is rapidly reabsorbed, 
but sometimes a permanent disturbance of function is left. 

In regard to treatment, complete rest and the energetic local use of ice are 
chiefly to be recommended, and also local blood-letting — dry cups, or leeches, where 
there are severe initial symptoms of irritation. If permanent disturbances are left, 
they should be treated by the ordinary methods — iodide of potassium, baths, and 
electricity. 

We must here speak of pachymeningitis interna hemorrhagica as a special 
form of disease, which usually occurs at the same time with haematoma of the 
cerebral dura mater {vide infra), and is precisely analogous to it in its aetiology 
and pathological anatomy. Encapsulated collections of blood are found on the 
inner surface of the dura ; these may have quite a considerable circumference, 
and contain blood already disintegrated, detritus, haematoidin crystals, etc., since 
they are usually of old standing. Beside this, there are also the signs of a fibrin- 
ous inflammation — as in the cerebral dura — which, according to the opinion of 



DISTURBANCES OF CIRCULATION, HEMORRHAGES, ETC. 569 



most observers, is the primary process, so that the haemorrhages into the newly 
formed false membrane are secondary. The symptoms of the affection, which has 
been observed chiefly in the chronic insane (general paralytics) and drunkards, are 
rarely pronounced, and consist chiefly of pain in the back, stiffness of the vertebrae, 
and some signs of compression on the part of the nerve-roots and the cord ; but 
we can very rarely make a sure diagnosis. 



CHAPTER H. 

DISTURBANCES OF CIRCULATION, HEMORRHAGES, FUNCTIONAL 
DISTURBANCES, AND TRAUMATIC LESIONS OF THE SPINAL 
CORD. 

1. Disturbances of Circulation. — Our knowledge as to the occurrence and as to 
the clinical significance of pure disturbances of circulation in the spinal cord is 
very slight. All that is stated in regard to it, in the descriptions of the pathology 
of the spinal cord, corresponds much more to theoretical hypotheses than to the 
actual objective facts. 

It goes without saying that a complete anaemia of the spinal cord must destroy 
its function ; this fact is best illustrated by the well-known experiment of Stenson : 
if we compress the abdominal aorta of an animal, and thus cut off the blood-sup- 
ply to the lumbar cord almost completely, a paralysis of the posterior portion of 
the body very rapidly ensues. Some precisely analogous observations have been 
made in man in the rare cases of obstruction of the aorta by emboli or thrombi. 
Pronounced spinal symptoms in general anaemia, which may be referred to a co- 
existing anaemia of the cord, are rare, and at any rate are of much less clinical 
prominence than the important results of a co-existing cerebral anaemia (vide 
infra). In only a few cases has paraplegia been seen after a great general loss of 
blood, as after metrorrhagia or intestinal haemorrhage. 

Any statement which may be made as to the occurrence of hyperaemia of the 
spinal cord is still more uncertain. We do not know whether active hyperaemia 
of the cord has in itself any clinical significance. The hyperaemia from stasis, in 
general disturbances of the circulation, in which certainly the spinal cord often 
takes part, causes no especially marked symptoms. 

2. Haemorrhage into the Substance of the Spinal Cord— Spinal Apoplexy— 
Haematomyelia. — Primary haemorrhage into the spinal cord is as rare as haemor- 
rhage into the brain is frequent. In some cases it may arise from traumatic influ- 
ences, but in others we are disposed to assume a primary disease of the spinal 
vessels. Perhaps there are occasionally aneurismal dilatations in the cord, similar 
to those found in the smaller vessels in the brain, and these may give rise to 
haemorrhage. Finally, the sudden onset of spinal paralysis has been seen after 
great physical exertion, and this perhaps is due to a spinal apoplexy. The small 
spinal haemorrhages, which are seen as a complication in tumors of the cord, and 
in inflammatory affections like myelitis, epidemic meningitis, etc., and in the 
general haemorrhagic diathesis, as in scurvy or severe general infectious diseases, 
but rarely have any special significance. 

Anatomical experience in regard to primary spinal apoplexy is still extremely 
slight, but the conditions met with do not differ materially, at any rate, from simi- 
lar processes in other organs. If the haemorrhage is abundant, we find the sub- 
stance of the cord destroyed to a great extent. The apoplectic center usually 
extends principally in the long axis of the cord. The blood is still fluid in fresh 



570 



THE DISEASES OF THE SPINAL COED. 



cases. Later on it undergoes all those changes which are fully described in the 
chapter on cerebral apoplexy. 

The symptoms of spinal apoplexy must in the first place depend entirely upon 
the seat and extent of the haemorrhage. The sudden, apoplectiform beginning of 
the symptoms is always characteristic. Usually in a very short time a more or 
less complete paralysis, with a severe pain in the back, comes on ; the paralysis 
being usually in the lower extremities, or rarely in the muscles of the trunk and 
the upper extremities also. There are usually at the same time anaesthesia and 
paralysis of the bladder ; but in this respect, as also in the condition of the reflexes, 
there are of course many variations according to the seat of the haemorrhage. 
We need not go into a precise description of the details, since they will follow of 
themselves from the general rules in regard to the localization of affections of 
the cord, which will be described in the chapter on myelitis. 

The course of haemorrhage of the cord may in many cases be comparatively 
favorable. If the blood is absorbed, and no essential paths of conduction are per- 
manently destroyed, the symptoms of paralysis gradually pass away, and recovery, 
or at least improvement and an arrest of the symptoms follow. In many cases, 
of course, the severe type of spinal paralysis develops, with bed-sores, cystitis, etc., 
and this, after a longer or shorter time, leads to death. 

We must always be very guarded in making a diagnosis of spinal haemorrhage. 
We can do so with some probability only when the symptoms begin in a pro- 
nounced apoplectiform manner, and when sure aetiological factors are to be made 
out ; but we should never forget that many forms of multiple neuritis (vide 
supra), acute myelitis, and even chronic spinal affections, may also show a 
remarkably sudden onset, or at least may suddenly become worse. The distinc- 
tion between genuine spinal apoplexy and meningeal haemorrhage can hardly 
ever be made with certainty. 

Treatment. — If we have the rare opportunity to be able to interfere at the 
beginning of the symptoms, we should prescribe a perfectly quiet position in bed, 
local use of ice, and eventually ergotine. Later on the treatment should be 
directed according to the methods generally in use in spinal paralysis. 

3. Functional Disturbances. — In practice we very often see cases of disease 
where the patient complains of a set of symptoms which are in all probability of 
spinal origin ; but since all the objective signs of a severe spinal affection are 
entirely absent, and since the whole development and further course of these cases 
oppose the theory of a coarse anatomical disturbance in the cord, we have a right 
to regard them as mere " functional disturbances," and thus to express their rela- 
tion to certain injurious aetiological influences, and their comparative freedom 
from danger. We know nothing definite at all as to whether the symptoms are 
based upon unknown disturbances in the nervous mechanism itself, or whether 
circulatory disturbances, on a basis of abnormal vaso-motor influences, play a part 
here ; but the types- of disease met with clinically are very characteristic, are usu- 
ally easy to be recognized, and, on account of their frequency, have the greatest 
practical significance. As a rule, the spinal symptoms are joined to certain cere- 
bral symptoms, since the morbid phenomena present are an expression of a disturb- 
ance of the whole central nervous system. The type of disease which is briefly 
described in what follows, for which the names of spinal irritation or spinal neu- 
rasthenia are most in use, is often, then, only a complication of a general neuras- 
thenia, to the description of which we must therefore refer for the details. 

The aetiology of the disease is often easy to discover. We have to do with 
patients upon whom one or more of those injurious influences have acted, which 
have an undoubted influence in the development of almost all the neuroses : 
severe and persistent emotional excitement, mental and physical over-exertion, 



DISTURBANCES OF CIRCULATION, HEMORRHAGES, ETC. 571 



improper methods of living, toxic influences, like alcohol and nicotine, sexual 
excesses, like onanism, etc. Beside these there is very often a hereditary predis- 
position, a congenital weak resistance of the nervous system, which is often 
increased hy a poor state of the general nutrition. Finally, a hypochondriacal 
disposition is of great aetiological significance, as it causes not only an abnormally 
increased attention to the symptoms, but also an abnormal hyperesthesia to all 
subjective sensations. The constant anxiety about the dreaded results of any 
excesses committed is often much more injurious than the excesses themselves. 
Hypochondriacal dread, too, usually plays the largest part in the neurasthenic 
conditions frequent among physicians. 

The symptoms of the morbid conditions in question usually begin gradually. 
The patient begins to complain of weakness and fatigue in walking, and also very 
often of pains in the back and loins, and not infrequently in the extremities also. 
In spite of the vivid description which the patients give of their pain, they usually 
have to admit, if questioned about it closely, that the intensity of the pain is 
really not very great. Beside the pain there are usually many forms of paraes- 
thesia — numbness, formication, cold feelings, etc. The more the patient knows, or 
at least believes he knows, of the symptomatology of spinal diseases from reading 
and from associating with other patients, the more detailed are his complaints. 
Disturbances of the bladder are usually present only in a slight degree, but still 
they do occur. They often depend merely upon the disturbance of the involuntary 
reflex mechanism, due to the added factor of increased voluntary attention. There 
are very often sexual disturbances, which are usually to be referred to former 
excesses, especially to onanism or to the hypochondriacal condition of the 
patient. 

If we make a physical examination of the patient we can not discover definite 
signs of a spinal affection. In some of the cases we find an increased sensitive- 
ness of the vertebrae on pressure, which may be limited to a few definite spots, 
a symptom to which the name of " spinal irritation " is often given ; but we 
often fail to find this tenderness of the vertebrae. Nothing abnormal is to be dis- 
covered in the pupils or the reflexes. The tendon reflexes are sometimes quite 
lively and sometimes weak. The sensibility is objectively perfectly normal ; 
neither can we discover actual paresis or atrophy of the muscles. Vaso-motor 
disturbances, however, are often seen : abnormal coldness, pallor or redness of 
the hands, tendency to sweating, etc. The manifold cerebral symptoms, that are 
usually present at the same time, will be mentioned in the description of neuras- 
thenia. The condition of the general nutrition in many patients remains un- 
changed, but, of course, some become pale, thin, and weak. 

The diagnosis of functional disturbances of the spinal cord is usually not diffi- 
cult, as we have said, and may often be made from the history, from the patient's 
whole outward behavior, and from the manner of his complaints ; but we can 
not lay too much stress upon the injunction that a careful physical examination 
should always be made, in order to avoid confusion with an incipient serious dis- 
ease. We shall repeatedly call attention in what follows to the symptoms which 
must chiefly be observed for this purpose. 

In regard to prognosis and treatment we will refer to what is said in the 
chapter on neurasthenia. 

4. Traumatic Lesions of the Spinal Cord.— In spite of the protected position of 
the spinal cord, it is often the seat of severe acute traumatic lesions. Fractures 
and dislocations of the vertebrae are the most frequent, and these may give rise 
to considerable injury of the spinal cord by the dislocation of the vertebrae, or 
by the projection of a fragment of bone. In many cases the cord is injured, not 
by the affection of the bones directly, but by the occurrence of traumatic haemor- 



572 



THE DISEASES OF THE SPINAL COED. 



rhage. Gun-shot wounds of the cord are quite frequent, in which the bullet either 
penetrates the cord itself or produces injury of the vertebrae and haemorrhage, 
which involve the cord indirectly. Stabs and incised wounds of the cord have 
been repeatedly seen. The point of a knife or sword may penetrate the spinal 
canal through the intervertebral disks and cause a partial section or at least a con- 
tusion of the cord. As in all other traumatic lesions of the cord, a secondary 
" traumatic inflammation " (vide infra), with its results, may be added to the direct 
injury in such cases. 

We need not go into all the details of the pathology and symptomatology of 
the traumatic lesions of the spinal cord, since the number of special conditions 
is, of course, almost inexhaustible; but it is usually not particularly difficult to 
judge of a given case, if we follow the rules which generally obtain in the pathol- 
ogy of the cord. We can easily tell when the cord is involved in injuries in its 
vicinity by the appearance of pronounced motor and sensory disturbances, which, 
however, differ very much according to the seat and the extent of the affection of 
the cord. There is usually at first a pronounced and often complete motor paraly- 
sis of the lower extremities, and sometimes, when the cervical vertebrae are injured, 
of the upper extremities also. There is also anaesthesia, differing very much, of 
course, in extent and intensity in the different cases; and there is very often vesi- 
cal and rectal paralysis. In many severe cases the secretion of urine seems at 
first much diminished or wholly wanting. If the spinal roots are affected there 
are severe shooting pains and paraesthesia. The reflexes are usually diminished 
at first, but, later, if the injury be above the reflex arc, they are increased; but if 
the arc itself be broken, they are permanently absent. In severe cases we often 
see in men a more or less complete and persistent erection of the penis, which is 
probably due to a direct or reflex irritation of the nerves of erection. In injuries 
of the cervical cord we often see a great and general increase of temperature, up 
to 110° or 112° (43°-44° C), especially in severe and rapidly fatal cases ; this is of 
physiological interest, and agrees with the results of experiments. On the other 
hand, there are also, especially in injuries of the dorsal cord, as it seems, great falls 
of temperature, down to 90° to 86° (32°-30° C). 

The further course of the affection differs very much. In the worst cases death 
ensues in a few hours or days. In other cases the patients recover from the first 
" shock," but permanent paralysis remains, which may sooner or later lead to death 
from the ensuing sequelae, cystitis and bed-sores ; but we often see partial improve- 
ment and a cessation of all the symptoms. Although certain functional disturb- 
ances remain permanently, life is not further endangered. Finally, in one class 
of comparatively mild cases, there may be a complete recovery. 

The treatment of the primary affections belongs to the domain of surgery; 
especially any attempt to trephine the vertebral column, in order, if possible, to 
relieve the existing pressure on the cord by reducing the dislocation of the verte- 
brae or the splinters of bone. In most cases we have to confine ourselves to putting 
the patient in a proper position on a water-bed, and guarding as carefully as pos- 
sible against bed-sores and cystitis. Locally, the constant application of ice is 
most to be recommended. We can expect but little from local blood-letting, 
inunctions with mercurial ointment, etc. If the first acute stage passes off favor- 
ably, the treatment of any paralytic symptoms remaining follows the ordinary 
rules (baths and electricity). 

5. Concussion of the Spine— Commotio Spinalis— Railway Spine.— As a result 
of severe concussions of the whole body we sometimes see a group of symptoms 
essentially spinal, the cause of which is supposed to be fine changes in the cord, 
provoked by its concussion, whose nature is, of course, still entirely unknown to 
us. It goes without saying that we can not use the term 1,1 commotio spinalis " 



DISTURBANCES OF CIRCULATION, HEMORRHAGES, ETC. 573 



for those cases where there is a coarse traumatic lesion, like haemorrhage, or injury 
to the vertebrae. 

The symptoms of spinal concussion may arise after any form of concussion of 
the body, but their comparatively frequent occurrence after railway accidents, 
" railway spine," is of special interest, since such cases, in passengers and in con- 
ductors and other railway employees, often involve the practical questions of acci- 
dent insurance and damages. 

The development of the symptoms in spinal concussion does not always occur 
in the same way. In one class of cases the severest symptoms come on immedi- 
ately after the injury ; but these symptoms are not to be referred exclusively to the 
concussion of the cord, but usually to an implication of the brain also. There is 
often a mor»e or less complete loss of consciousness, a paralysis of all the extremi- 
ties, and general collapse, with a small pulse, cool skin and dyspnoea, retention of 
urine, vomiting, etc. Such cases may end fatally in a few hours, without any 
actual coarse lesion of the nervous system which can be found on autopsy ; but, in 
other cases, the first severe onset passes off, and there remains a set of subjective 
and objective disturbances, which do not pass away for some time, and which 
may sometimes last for years. The chief symptom is usually a general motor 
weakness. Many patients can walk quite well alone, but get tired very easily, 
while others require support, and walk slowly and stiffly, with short steps and 
dragging of the feet. There is also the same general weakness in the hands, but 
there is never paralysis either of single muscles or groups of muscles. The condi- 
tion of the muscular nutrition is usually good, and the electrical excitability is 
normal, or merely reduced a little quantitatively. In regard to the sensibility, the 
patient usually complains of pain and parsesthesia. The pain is situated in the 
back, and often in different parts of the trunk (girdle pain) and the extremities. 
The parsesthesia consists of a feeling of numbness in the tips of the fingers, and 
of formication in the legs. The vertebral column, and sometimes other parts of 
the body, are often quite sensitive to pressure. We very often find a distinct 
objective diminution of sensibility, which frequently involves the whole surface 
of the body. The tactile sensibility is usually not abolished, but dulled, and the 
sensibility to pain is much diminished. In one case we saw an almost complete 
ana3sthesia of the sense of temperature, especially in the legs. Thomsen and 
Oppenheim, among others, have lately called attention to such anaesthesias in dif- 
ferent parts of the body, and also to disturbances in the distribution of the nerves 
of special sense, especially to contraction of the field of vision. The reflexes are 
often abnormal, but they differ in different cases. We have found the cutaneous 
reflexes, with the exception of the abdominal and cremaster reflexes, usually dimin- 
ished, and the tendon reflexes decidedly increased ; but the latter may also be 
weak or entirely absent. Micturition is sometimes unaffected, but in other cases 
it is quite difficult. Cerebral symptoms are either absent, or the patient com- 
plains of headache, attacks of fainting, tinnitus, specks before the eyes, and dizzi- 
ness. We often find quite a marked nervous irritability, and general mental 
depression. 

The symptoms described may last for months or years, as we have said. In 
many cases, especially with proper care and treatment, there is finally a marked 
improvement or complete recovery. In a second class of cases the condition is dif- 
ferent. In these the consequences of the spinal concussion at first seem to be 
slight, so that the victim believes that he has gotten off without much injury ; 
but new spinal symptoms begin several days or even weeks after the concussion, 
and these gradually increase to the type of a severe spinal disease. Pains, disturb- 
ances in the gait, pronounced paresis and anaesthesia of the legs, and anomalies in 
the functions of the bladder and sexual organs, are present and are often com- 



574: 



THE DISEASES OF THE SPINAL CORD. 



bined with bulbar symptoms, like disturbances of speech ; and cerebral symptoms, 
like sleeplessness, a depressed, anxious disposition, loss of memory, and nervous 
irritability. The further course is protracted. Sometimes improvement or even 
recovery appears later on, but in other cases the constantly increasing general 
weakness and emaciation, or the occurrence of complications, lead to an unfavor- 
able termination. The anatomical conditions in these cases are not yet precisely 
known. Probably there are always coarse anatomical changes, chronic inflam- 
matory processes in the meninges and cord, which have developed as a result of 
the injury. 

The diagnosis of spinal concussion is not without difficulty, since, on the one 
hand, it is often hard to distinguish merely functional disturbances from actual 
anatomical changes in the vertebral column and the cord, and, on the other, we 
must often bear in mind the possibility of a simulation, or at least an exaggeration, 
of the morbid symptoms. In regard to this we can decide only by the most careful 
examination, with special attention to those symptoms which are the most purely 
objective, especially the reflexes, etc. The circumstance seems to us, however, to 
be of great significance for the proper pathological estimation of many mild cases 
of spinal concussion, that the group of symptoms that develops is often of a 
pure neurasthenic and hypochondriacal or pronounced hysterical nature. From 
the injury, and the added action of the fright associated with it, and from the fear 
of the possible severe consequences of such an accident, a condition is often pro- 
voked in the patient which corresponds precisely to the mild degrees of spinal 
neurasthenia above described. This interpretation of the cases is especially to 
be borne in mind in those cases where the complete absence of results upon 
physical examination leads to the suspicion of a simulation of the morbid symp- 
toms. 

The treatment of spinal concussion is in fresh cases directed against the pri- 
mary symptoms of the concussion — the "shock." The body must be put in an 
easy position ; if the pulse be weak and the respiration imperfect, stimulants must 
be given — injections of ether or camphor, and wine or strong coffee. Cutaneous 
irritants externally, mustard plasters, rubbing, and eventually faradization of the 
respiratory muscles, are also to be employed. 

If the patient recovers, and severe spinal symptoms remain, or if they develop 
soon after, beside keeping up the hygienic treatment of rest and good food, we 
should employ, first of all, cautious galvanization along the vertebral column with 
ascending currents, combined with peripheral galvanization and faradization, and 
also cautious cold-water treatment, especially cold sponging ; among internal 
remedies we may give iodide of potassium, ergotine, and strychnine. We should 
generally advise against the employment of thermal baths, although the carbonic- 
acid iron baths at Cudowa, Elster, Schwalbach, Homburg, and Rippoldsau, have 
won an especial reputation in the treatment of spinal concussion. 

6. Diseases of the Spinal Cord after a sudden Reduction of the Atmospheric 
Pressure [Caisson Disease], — In bridge-builders and others, who have worked for 
hours under water in the so-called " caissons," under an external pressure of two 
or three atmospheres, we sometimes see the appearance of peculiar symptoms after 
leaving the caisson — that is, on the sudden reduction of the atmospheric pressure. 
Beside the frequent mild symptoms of pain in the ears and hasmorrhage from 
the ears, articular and muscular pains in the back and the extremities, slowing of 
the pulse and vomiting, there are also severe disturbances of motility and sensi- 
bility, which point unequivocally to an affection of the spinal cord. Usually the 
lower half of the body is alone affected. The legs are more or less completely 
paralyzed, the skin is usually anaesthetic up to the trunk, and there is generally 
retention of urine. The patient sometimes recovers in a few weeks, but in other 



THE PEESSUEE PAEALYSES OF THE SPINAL COED. 575 



cases the condition terminates fatally in a comparatively short time — in a few 
weeks or months. The first special anatomical investigations in question (Ley- 
den, F. Schultze) gave in such cases a disseminated but extensive affection in the 
dorsal cord, chiefly in the posterior columns and the posterior portions of the 
lateral columns. The nervous tissue in the diseased parts was completely destroyed, 
and instead of it was found detritus and a collection of large, round, finely granu- 
lar cells (fatty granular cells ?). Haemorrhages into the cord, which might per- 
haps be expected, have up to the present time not been found. 

Nothing definite is known as to the precise process in this form of spinal dis- 
ease. Leyden suspected that there was a development of gas from the blood 
which caused a rupture of the surrounding tissue, under the influence of the rap- 
idly diminished barometric pressure, as Hoppe-Seyler and P. Bert have discovered 
by experiment ; but the circumscribed limitation of the affection to the dorsal 
cord, and the lack of any signs of vascular haemorrhage, speak against this theory. 

The treatment is the same as in acute myelitis. 



CHAPTEE III. 

THE PRESSURE PARALYSES OF THE SPINAL CORD. 

(Slow Compression of the Spinal Cord, especially in Caries and Carcinoma of the Vertebra.) 

iEtiology*. — Many pathological processes which develop in the vicinity of the 
spinal cord may exert a gradually increasing pressure upon it, and thus, on the 
one hand, inhibit the conduction of nervous irritation, and, on the other, cause 
coarse mechanical injuries in the substance of the cord. The seat of such affec- 
tions is in the first place in the membranes of the spinal cord. In the chapter 
on meningitis we have already mentioned the compressing action of the masses of 
inflammatory exudation on the nerve-roots and the cord, and we have learned to 
recognize, especially in pachymeningitis cervicalis hypertrophica, a characteristic 
example of a gradually increasing compression of the cervical cord. Precisely 
similar conditions are found in the rare meningeal tumors, whose special pathol- 
ogy will be described in connection with the tumors of the cord itself. 

By far the most frequent pressure paralyses of the spinal cord, and hence the 
most important practically, are caused by certain diseases of the vertebras, and 
first of all by chronic caries of the vertebrae (spondylitis, Pott's disease, spondy- 
larthrocace).* There is no longer any doubt at present that certainly the greatest 
part, if not all, of the cases of vertebral caries are of tubercular origin, that verte- 
bral caries is a local tuberculosis of the vertebrae. Although these facts were 
formerly rendered very probable by the histological conditions of the process, and 
by its frequent relation to other unquestionable tubercular diseases, like phthisis, 
miliary tuberculosis, and tubercular meningitis, they have of late been confirmed 
beyond a doubt by the discovery, which can usually be made, of tubercle bacilli in 
the cheesy nodules of the vertebral caries. Tubercular spondylitis occurs at 
almost any age ; it is rare only in old people. It often develops in children, but 
it is almost as frequent in adults. The aetiological significance of injuries, like a 
fall or a blow, which are often mentioned by the patients themselves or their 
parents, is in most cases doubtful ; but we can very often succeed in finding agtio- 



* In the kyphoscolioses of the vertebral column, not due to spondylitis, there are practically never 
any symptoms of compression in the cord, even in very pronounced cases. In these cases the cord 
manifestly shows quite a great adaptability. 



576 



THE DISEASES OF THE SPINAL CORD. 



logical factors for the onset of tubercular disease in general — the tubercular habit, 
hereditary tendency, or tubercular disease elsewhere, like phthisis, pleurisy, other 
affections of the bones, etc. 

Cancer of the vertebrae, as well as caries, leads to pressure paralyses of the 
spinal cord ; but it is relatively much rarer than caries, it develops chiefly in older 
persons, and it occurs both as a primary new growth and also secondary to cancer 
of other organs — like the breast, the stomach, or the oesophagus. 

We must mention here briefly, as very rare causes of compression of the spinal 
cord, aneurism of the aorta, which gradually erodes the vertebrae, echinococci in 
the vertebral canal, exostoses of the vertebrae, and syphilitic new growths. 

Pathological Anatomy. — Vertebral caries is most common in the dorsal portion 
of the vertebral column (dorsal spondylitis), somewhat rarer in the cervical portion 
(cervical spondylitis), and rarest in the lumbar portion (lumbar spondylitis) and 
in the sacrum (sacral spondylitis). It usually extends over several adjacent verte- 
brae, or more rarely two separate foci of disease are seen. The process itself, the 
details of which can not be discussed here, probably always begins in the spongy 
substance of the bodies of the vertebrae. We see here, on section, in incipient 
cases, roundish, pale reddish, or yellowish nodules, which consist of newly formed 
fungous tissue — that is, tubercular granulation - tissue. The bony substances 
become more and more destroyed by the invasion of the new growth, which itself 
shows the characteristic tendency of all tubercular new growths to cheesy degen- 
eration. Thus there is often an extensive destruction of the bodies of the verte- 
brae, which later on also involves the vertebral processes, the intervertebral disks, 
and the other articular connections between the different vertebrae. 

There are essentially two factors to be considered in regard to the question 
which chiefly interests us here — that is, in regard to the occurrence of compression 
of the spinal cord. In the first place, it is clear that the complete or partial 
destruction of the bodies of one or even more vertebrae, and of their articular con- 
nections, can not remain without influence upon the posi- 
tion of the other adjacent vertebrae. In fact, we very often 
see dislocations of the vertebrae as a result of it, usually by 
the pushing backward of the partly destroyed vertebrae by 
the movements of the vertebrae above and below the dis- 
eased portion on one another (see Fig. 81). There arises, 
on the one hand, a contraction of the vertebral canal, and 
with it often a very considerable limitation of the space 
for the cord; and, on the other hand, that characteristic 
projection of the spinous processes in the region of the 
diseased portion of the vertebral column which forms the 
so-called Pott's boss — the angular kyphosis. In very slight 
degrees of the disease there is only a slight projection of 
one or more spinous processes, but in other cases it grad- 
ually becomes an extensive deformity of the vertebral 
column, which strikes us at the first glance. It goes with- 
out saying that, under some circumstances, the Pott's boss 
may be entirely absent in vertebral caries. 

The second factor, which is often to be considered in the mechanism of com- 
pression of the cord, is the formation of foci of cheesy pus on the posterior surface 
of the bodies of the vertebrae. Since the inflammatory tubercular > new growth 
involves the periosteum, there are often formed here large collections of cheesy pus, 
which are situated beneath the periosteum, raise it, and push it out far into the 
vertebral canal. In other cases, the tubercular new growth still further directly 
involves the outer surface of the dura, and forms here extensive cheesy masses, 




Fig. 81.— Schematic repre- 
sentation of vertebral 
displacement in spon- 
dylitis. The point of 
compression of the 
cord, at the level of the 
second dorsal vertebra, 
is at C. 



THE PRESSURE PARALYSES OF THE SPINAL CORD. 577 



which, of course may also cause a compression of the cord. The inner surface of 
the dura at the corresponding parts is usually markedly injected, hut a direct 
invasion of the pia hy the tubercular process through the dura is rare. 

If now a considerable contraction of the vertebral canal has arisen from dislo- 
cation of the vertebrae, or from the projection inward of the cheesy purulent 
masses into the canal, the necessary mechanical consequences in the spinal cord 
itself are usually to be recognized with ease. The cord appears smaller at the 
point of compression. If the narrow part corresponds to a bend in the vertebral 
column, we can very often see a marked angle of bending on the anterior surface 
of the cord. The consistency of the cord at the part affected, the extent of which 
seldom exceeds a few centimetres, is usually diminished ; the cord is soft and may 
be easily bent. In old cases only do we find the cord itself harder than normal 
and sclerosed {vide infra). It is very remarkable, however, that often, as we have 
repeatedly seen, marked symptoms of compression may be present during life with- 
out finding any coarse mechanical lesion of the cord in the cadaver, so that the 
cord may show an almost perfectly normal appearance. As in the peripheral 
nerves, so in the spinal cord, a moderate pressure is manifestly enough to excite a 
partial break in the conduction, without being at the same time necessarily associ- 
ated with an actual mechanical destruction of nervous elements. On careful 
microscopic examination of the cord, we find in such cases, in spite of the existence 
of a complete paraplegia during life, that most of the nerve-fibers are still com- 
pletely preserved, and that there are only here and there a few lacunae, corre- 
sponding to single fibers which have been destroyed. This discovery is especially 
interesting because it makes us understand the possibility of recovery, even in 
apparently severe cases {vide infra). 

Even where we can find considerable histological changes in the spinal cord, 
however, where the softness of the cord points to a coarse lesion of it, and where 
the microscope shows the destruction of a great part of the normal tissue at the 
point of compression, all these changes are merely the necessary results of the 
purely mechanical pressure on the spinal cord. As we must maintain, against the 
theory generally received at present, on the ground of many of our own investi- 
gations, we have not the slightest reason to refer the occurrence of paralysis in 
spondylitis to a secondary myelitis. Such a " compression myelitis " — that is, an 
inflammation of the spinal cord arising from the pressure as such — is to be rejected 
from general pathological reasons ; and the microscopic examination of the cord 
also shows nothing which points to an inflammation, or which may not be 
entirely the result of mechanical compression. If we take a portion from the 
soft place of compression for fresh examination, we find sometimes many, some- 
times only a few, granular cells, according to the amount of disintegrated nerve- 
medulla, the remains of which are taken up by the white blood-corpuscles — the 
wandering cells. If we make stained cross-sections of the hardened cord, we see 
under the microscope no signs of vascular changes, of hyperaemia, of accumula- 
tion of cells about the vessels, and only exceptionally a little traumatic haemor- 
rhage ; but we do find, beside many still preserved nerve-fibers, other fibers, which 
are involved in the disintegration or are already destroyed. Yery commonly the 
changes are distributed in the form of nodules. We find groups of greatly 
swollen axis-cylinders, which have wholly, or almost wholly, lost their medullary 
sheaths, and in other places we notice already the signs of their disintegration, or 
the already empty lacunae in the meshes of the neuroglia. If the destruction of 
the nervous tissue has advanced to a certain degree, there is in the later stages, as 
in all analogous processes, a secondary implication of the neuroglia. Now fol- 
lows an increase of the interstitial connective tissue. Its proliferations, which 
take the place of the destroyed nervous tissue, seem diffuse — at first loose, but later 
37 



578 



THE DISEASES OF THE SPINAL COED. 



firm and fibrillary. Thus it happens that in old cases we find nothing at the 
point of compression but a loss of nerve-fibers in the cord, and instead of it there 
is a firm fibrous tissue. All the changes mentioned are always much more devel- 
oped in the white matter of the cord than in the gray. 

Finally, in all cases of a more protracted compression of the cord we find an 
ascending and descending secondary degeneration of certain systems of fibers in 
the cord {vide infra). 

We need not go more fully into the details of compression of the cord from 
other causes, since the results, as far as they are of a purely mechanical nature, 
are precisely the same. In cancer of the vertebrae there may also be dislocations 
of the vertebral column after the destruction of some of the vertebrae, but usually 
the compression depends upon the direct growth of the newly formed tissue into 
the dura. In these cases the compression of the nerve-roots in the intervertebral 
foramina is also of importance. 

Clinical History. — Many cases of spondylitis run their course without involving 
the cord, or at least involving it only in quite a subordinate fashion. In other 
cases the symptoms of disease of the vertebrae exist for a long time alone, until at 
last, slowly or suddenly, the signs of compression of the cord are added to them. 
Finally, in a third group of cases, the vertebral disease is so latent that nothing 
but the spinal symptoms is prominent in the type of the disease, and the disease 
of the vertebrae may easily be entirely overlooked. 

Usually the symptoms of the developing primary disease, the affection of the 
vertebrae, precede the appearance of the first spinal symptoms by some time. The 
patient feels a dull pain at a definite part of the spine, which is iucreased by 
movements of the trunk, by bending or straightening up. Many patients notice 
the stiffness of the vertebral column of themselves, and sometimes even a begin- 
ning deformity. The first spinal symptoms usually consist in painful sensations, 
which are not confined to the place of the disease, but shoot out approximately 
along the course of the nerve-paths. These pains, which are due chiefly to an 
irritation of the nerve-roots caused by the compression, extend, according to the 
seat of the affection, into the shoulders and arms, into the lateral portions of the 
trunk, or into the lower extremities. They are sometimes very severe, and then 
they usually have a pronounced neuralgiform character, or they may be more dull 
and dragging. Beside the special pains, there are also many forms of paraesthe- 
sia, like formication and cold feelings. 

The disturbances of motility begin to appear at the same time with these symp- 
toms or soon after them. A stiffness and weakness arise which impede the gait, 
usually not in both legs at once, but first in one and then in the other. This 
paresis increases rapidly or slowly, and may finally go on to a complete motor 
paralysis. If the seat of the affection is in the dorsal vertebrae, as it usually is, or 
if it is in the lumbar vertebrae, the paralysis affects the lower extremities only, 
and the arms, of course, remain • intact ; but in cervical spondylitis the arms are 
usually first and chiefly affected. Only on great compression of the cervical cord 
is the conduction of the fibers passing through it for the lower extremities 
impaired, and then there are also disturbances of function in these. 

Disturbances of sensibility are often found, independently of the pains and 
paraesthesiae above mentioned, but in many cases of pressure paralysis they are 
present in only a comparatively slight degree. It seems that the sensory nerves 
resist pressure more than the motor nerves, just as in the pressure paralyses of 
peripheral nerves ; but possibly their position in the gray matter of the posterior 
cornua protects them better from mechanical attack than is the case, for example, 
with the motor fibers in the pyramidal tract (see Figs. 65 and 66). The fact is 
that often, even in complete motor paraplegia, there is little if any diminution of 



THE PRESSURE PARALYSES OF THE SPINAL CORD. 579 



sensibility, and that marked anaesthesia is rare, and is seen only in the last stages 
of the disease. We find most frequently an equally slight blunting of sensibility 
to all forms of sensation, especially to the sense of pain. The different parts of 
the skin not infrequently act differently, so that we find portions with quite nor- 
mal sensibility, as well as very anaesthetic portions. 

The condition of the reflexes is interesting. If the seat of the compression is 
above the reflex arc, which we must assume to be in the lumbar cord for the 
reflexes of the lower extremities, we should expect that the reflexes would persist, 
and in many cases even be increased, corresponding to the decline in the inhibi- 
tory influences coming from above. The latter takes place invariably with the ten- 
don reflexes, which are always increased in the lower extremities in the pressure 
paralyses arising from the cervical or dorsal cord. The increase of the tendon 
reflexes may reach so great a degree as to show in the lower extremities the pro- 
nounced type of spastic paralysis {vide infra). The limbs are then found in a 
rigid tonic extension, they can only with difficulty be flexed passively on account 
of the muscular resistance, and they show a very vigorous ankle clonus, sometimes 
degenerating into a general tremor of the leg, and also marked patellar reflex, 
adductor reflex, etc. ; but even in flaccid paraplegia the tendon reflexes may be 
quite vigorous. In cervical spondylitis the tendon and periosteal reflexes in the 
arms are also increased sometimes, but in other cases, if the reflex arc be injured, 
they are absent. Where the seat of the compression is above the lumbar cord, the 
cutaneous reflexes sometimes show considerable vigor, but their increase is much 
less frequently as marked as is the increase of the tendon reflexes. In severe 
pressure paralyses in the dorsal cord the cutaneous reflexes are even frequently 
diminished. They are probably never entirely absent, but one must understand 
testing them, and must employ long-continued cutaneous irritation, like pinching 
and pricking, in different parts of the skin in order to provoke them. 

Trophic disturbances are often found in the paralyzed parts. If there are 
severe symptoms of sensory irritation there may sometimes be eruptions of her- 
pes, corresponding to the course of the nerves. More frequently there are chronic 
disturbances in the nutrition of the skin in severe and long-continued cases. It 
becomes dry, the epidermis scales off, and the nails become brittle. Bed-sores form 
very easily in severe cases on the sacrum, on the buttocks, on the inner side of 
the knees, and on the heels, especially when the patient has insufficient care. The 
muscles retain their normal volume and their normal electrical excitability in 
many cases as long as their trophic center remains uninjured ; but sometimes, 
even when the point of compression is above the lumbar cord, there is a great 
atrophy of the muscles of the legs, although the electrical reaction of the nerves 
is normal, or at most a little reduced in quantity. If the lesion involves the lum- 
bar cord itself, or the fibers of the cauda equina, in caries of the sacrum, there 
must of course be an atrophic paralysis in the legs, with reaction of degenera- 
tion. There may also be an atrophic paralysis in the arms in cervical spondylitis. 

Disturbances of the rectum and bladder occur in almost all severe cases of 
pressure paralysis. The difficulty of micturition is often an early symptom of the 
disease ; later on there is complete retention of urine, and, in the more advanced 
stages of the disease, there is usually incontinence. With this the danger of the 
development of cystitis becomes very great. The bowels are usually controlled, 
but sometimes there is also incontinence of faeces. 

Thus we see, under some circumstances, in compression of the cord the whole 
group of symptoms arising which are the necessary consequence of the break 
in conduction in the spinal cord, and which we shall likewise meet again in vari- 
ous other spinal affections, especially in myelitis and in tumors. The intensity 
and choice of the symptoms must, of course, vary very much in the different 



580 



THE DISEASES OF THE SPINAL COED. 



cases. If the compression is quite slight, there are only mild symptoms of sensory 
irritation and slight paresis. One of the earliest and most constant signs of a 
compression of the cord, in the dorsal or cervical region, is a decided increase 
of the patellar reflex. We sometimes find it at a time when there is scarcely 
a single other spinal symptom present. If the compression increases, the paresis 
becomes more marked, the disturbance of sensibility is greater, and vesical 
disturbances arise, until finally the complete type of an entire transverse interrup- 
tion of conduction in the cord is developed ; but the latter is but rarely the case, 
since, as we have said, the conduction of sensory impressions is usually not 
wholly abolished. The time required for the development of the symptoms of 
spinal compression differs very much. They sometimes attain a considerable 
height in a short time, and sometimes they develop only after a course of 
months. Variations in the intensity of the symptoms are frequent, and they 
point perhaps to a corresponding variation in the severity of the compression. 

In regard to the result of pressure paralyses, it, of course, depends first upon 
the nature of the primary disease. In tumors, especially in cancer of the verte- 
brae, recovery is not to be thought of, but spondylitic processes without doubt can 
recover, which is by no means in contradiction to their character as a local tuber- 
cular process. In this connection the fact is of great practical importance that 
even the pressure paralyses may be completely restored, as far as the cause of the 
compression can be removed by the absorption of inflammatory and tubercular 
new growths, so that a complete and permanent recovery may take place even 
after the paralysis has lasted for some months, or a year, or even a year and a half. 
Such recoveries have been seen in great numbers by others and also by ourselves. 

Although, according to this, the prognosis in a part of the cases of pressure 
paralysis from spondylitis is comparatively good, still many other cases terminate 
unfavorably. The cause of this lies either in the occurrence of dangerous sequelae 
of the paralysis, like bed-sores, cystitis, or pyelo-nephritis, with fever and increasing 
general weakness ; or in the development of other tubercular diseases, especially 
phthisis, or more rarely miliary tuberculosis or tubercular meningitis, which 
proves fatal. 

Diagnosis. — The frequency of the pressure paralyses of the spinal cord admon- 
ishes us to examine the vertebral column carefully in every case of spinal disease, 
especially if the case can not be put under one of the special types of systemic dis- 
eases {vide infra) . We should look especially for the stiffness of special parts of 
the vertebral column on movements of the head or trunk, and also for the pro- 
nounced tenderness of single vertebrae to pressure, and, finally, as a most impor- 
tant and most certain sign, for the deformity of the vertebral column, the marked 
projection of a single spinous process, or the formation of an evident angular 
kyphosis. If we find such a Pott's boss the diagnosis is easy, and we can then 
at any rate refer the existing spinal symptoms to a compression of the cord caused 
by a disease of the vertebrae. 

The diagnosis is more difficult if the signs of an affection of the vertebrae are 
not evident. It must once for all be stated that vertebral caries does not inva- 
riably and necessarily result in a manifest Pott's boss, and that even the tenderness 
of the vertebrae to j)ressure is sometimes very slight in spondylitis. In such cases 
the examination of the vertebral column must be repeated more frequently, since 
even slight anomalies obtain a diagnostic value if constantly present ; and the whole 
course of the disease is also to be considered. The most characteristic features of 
a compression of the cord are its beginning with symptoms of sensory irritation, 
the preponderance of symptoms of motor paralysis with comparatively little dis- 
turbance of sensibility, and finally the frequent asymmetry of the symptoms on 
the two sides, which may even recall the type of the so-called " unilateral lesion " 



ACUTE AND CHRONIC MYELITIS. 



581 



of the spinal cord {vide infra). Sometimes the cause of the spinal symptoms is 
at first obscure, and later on in the disease a marked anomaly of the vertebral 
column develops. 

If the diagnosis of an affection of the vertebrae is certain, the next question is 
as to the nature of it, especially whether we have to do with a spondylitis, or with 
a cancer of the vertebrae. Since spondylitis is by far the more frequent disease, 
we must always think of that first, especially in young people, and where we have 
the formation of a pronounced angular kyphosis. In cancer of the vertebrae the 
coarser changes in the form of the vertebral column are generally less marked. 
This develops usually in older people, after the age of forty, and is manifested by 
the great intensity of the initial symptoms of sensory irritation. The " paraplegia 
dolorosa" the paralysis of the lower extremities associated with severe pains, is 
the most characteristic symptom of cancer of the vertebrae. The discovery of a 
primary nodule of cancer, as in the breast, or, as we ourselves have seen, the 
appearance of a swelling of the inguinal glands, may serve to supx>ort the diag- 
nosis. Finally, a certain stress is to be laid on the well-known general habit of 
patients with cancer, and on the peculiar cancerous cachexia. 

The place of compression is, in the majority of cases, to be recognized by the 
evident localization of the disease of the vertebrae. In other respects the same 
rules hold for localization which we shall discuss more fully in the description of 
myelitis in the following chapter. 

Treatment. — In regard to the special treatment of spondylitis, especially the 
orthopaedic treatment, we must refer to the text- books of surgery. In general, we 
have not thus far gained the impression that a particularly favorable influence 
can be exerted on the symptoms of spinal compression by contrivances for exten- 
sion of the vertebral column. These are often injudicious where there is para- 
plegia, since they increase the pain and make it harder to guard against bed-sores. 
We would not deny, however, that in many cases certain supports for the verte- 
bral column, and contrivances for extension, may be used to advantage. Perma- 
nent rest in bed is, at any rate, always of the greatest importance. Local applica- 
tions to the vertebral column are much used — dry cups, painting with iodine, and 
especially the hot iron. The use of the latter in spondylitis has even to-day warm 
advocates, and, in fact, deserves to be tried, the procedure with Paquelin's thermo- 
cautery being especially easy ; we make some three or four eschars on each side of 
the diseased vertebrae. 

Among other remedies we may mention stabile galvanization at the point of 
pressure, and the electrical treatment of the paralyzed extremities ; also the use of 
baths, especially salt baths, and, finally, the internal use of compounds of iodine — 
iodide of potassium and iodide of iron. In regard to the symptomatic treatment 
we will refer to the following chapter. 



CHAPTER IV. 

ACUTE AND CHRONIC MYELITIS. 

{Diffuse Myelitis. Trcmsverse Myelitis) 

Preliminary Remarks. — The pathological processes in the spinal cord known 
to us at the present time may be divided into two groups. In the first group we 
find this peculiarity, that the pathological changes are confined, with a remarkable 
constancy, to certain definite parts of the spinal cord, so that consequently the 
clinical symptoms of the disease may be quite exactly defined. > To this group 



582 



THE DISEASES OF THE SPINAL COED. 



belongs tlie disease known as anterior poliomyelitis (iroXios, gray), which is local- 
ized almost exclusively in the anterior cornua of the gray matter of the spinal 
cord, and also a class of affections, like locomotor ataxia, amyotrophic lateral scle- 
rosis, etc. , in which perfectly definite fasciculi in the cord are diseased. From the 
comparison of the anatomical lesions in these cases w T ith our other knowledge as 
to the structure and functions of the spinal cord, it has been shown that the dis- 
eased portions occupy a distinct position, even in their anatomical and physiologi- 
cal relations. Hence we are justified in terming these affections of the cord sys- 
temic diseases. We can not at present give a correct explanation of the remarkable 
fact that such isolated diseases may occur in parts of the cord which have perfectly 
definite functions, in " systems of fibers." We must imagine that the factors which 
cause the disease, in such cases, do not exert their influence upon the whole cord, 
but only upon the fibers and cells of a definite system ; an idea which finds a fitting 
analogy in the action of many poisons, like curare, strychnine, lead, etc. 

Beside the systemic diseases there is a second group of affections of the cord in 
which there is not, by any means, such a limitation of the process to definite por- 
tions of the cord. In these cases the disease extends more or less widely over the 
cross-section or the length of the cord, and forms either one large focus, or several 
single smaller foci, separate from one another. To this group, to the unsystemic, 
diffuse diseases of the spinal cord, belong the haemorrhages and traumatic lesions 
already described, and the new growths, the acute and chronic " inflammations " 
of the cord (diffuse myelitis), multiple sclerosis, etc. 

Since in the diffuse diseases of the spinal cord all those portions may be 
affected whose isolated affections form the systemic diseases, of course all the 
clinical symptoms of the latter may also be found in the diffuse affections ; for the 
individual symptoms of spinal disease, as such, never depend upon the form of the 
pathological process, but only upon its situation, and upon the irritation or inter- 
ruption of conduction in certain nerve-tracts caused by it. The diagnosis of spinal 
diseases, therefore, is, in the first place, always a topical diagnosis. We seek to 
recognize, from the functional disturbances prominent in the different cases, the 
place in the cord in which the affection must be situated, which has as a conse- 
quence these disturbances. By comparing all the existing morbid symptoms, and 
by attending to the functions which are still normal, we can decide whether 
the affection is limited in a systemic fashion to a special physiological region, or 
whether it extends in a diffuse, irregular fashion over a greater portion of the 
cord. In the former case we usually have no difficulty in finding a connection 
with the different well-known typical forms of disease ; in the latter case we can at 
least decide the main point, as to the extent and seat of the disease, and then, from 
the whole course and the combination of the morbid symptoms, we can also draw 
our conclusions, as far as it is possible, as to the form of the affection. 

After these general remarks we will pass on to the description of myelitis. 

JEtiology. — Hardly anything certain is known as to the causes of diffuse 
myelitis, in the same way as little is known in regard to the aetiology of diseases of 
the spinal cord in general. We often see the disease develop in men previously 
healthy, without being able to discover any influence which may act as a cause of 
the disease. In those cases, too, where we may at least ascribe a possible setiolog- 
ical significance to certain conditions, we are still completely in the dark as to the 
manner in which they act. 

The factors which seem to be most frequently related to the development of 
myelitis are as follows : Exposure to cold, especially repeated wettings, and work- 
ing in the open air under unfavorable conditions ; bodily fatigue and over-exer- 
tion, especially when combined with the factors first named, as in the hardships 
of war, etc. ; sexual excesses and violent emotions. But the significance of the two 



ACUTE AND CHRONIC MYELITIS. 



583 



causes last mentioned, for the origin of organic disease in the cord, is, however, 
extremely doubtful. 

The occasional appearance of spinal disease after certain acute infectious dis- 
eases, like typhoid, small-pox, or puerperal affections, favors the possibility of 
infectious causes; but these cases are very rare in comparison with the great 
number of primary cases of myelitis, and their anatomy is also but little known. 
Syphilis probably has a greater importance, although our knowledge on this 
point is not so broad that we can give a definite description of " syphilis of the 
spinal cord " ; but, at any rate, it is quite striking that in the history of patients 
with diffuse myelitis, especially in myelitis in the upper dorsal region, we quite 
often get, as it seems to us, an account of a former syphilitic infection. Of course, 
in any individual case, the actual connection between the two diseases can hardly 
ever be proved with certainty. 

It is proved with regard to purulent spinal meningitis that inflammations of 
neighboring organs may invade the spinal cord. In most of the other cases which 
are usually cited in regard to this point, we have to do with confusions between 
lesions of the cord from mechanical pressure and actual myelitis, as we have 
explained in detail in the previous chapter on compression of the cord. Hence 
we consider it unjustifiable to speak of a " traumatic myelitis " except in very rare 
cases. If spinal symptoms develop after an injury, we usually have to do either 
with the type of symptoms described above under spinal concussion, or with genu- 
ine traumatic lesions of the vertebrae, or sometimes perhaps with traumatic haemor- 
rhages, etc., which always excite disturbances in the functions of the spinal cord 
by mechanical conditions alone. Finally, in regard to the theory of an " ascend- 
ing neuritis " — that is, the supposed extension of an inflammation from the nerves 
to the cord — it is a hypothesis that is still very much in need of further confirma- 
tion. 

Pathological Anatomy. — Macroscopic examination of the cord in its fresh con- 
dition shows no marked pathological changes except in a small number of cases. 
At the first glance, the spinal cord often seems almost completely normal, even if 
there have been severe spinal symptoms during life, and sometimes the opacities 
and adhesions of the pia, which often strike us at first, have no practical importance. 
If we test the consistency of the cord carefully by touching it, of course a change 
in it often strikes the practiced examiner, since the cord over a definite extent is 
either softer and more flexible, or, on the other hand, harder and firmer. If we 
now make a number of cross-sections through the cord, we notice that the sub- 
stance of the cord rises up more on section, that the outline of the gray matter is 
less distinct, and especially that the white matter is of a reddish-gray color, and 
that sometimes there is also a reddish, hyperaemic coloring of the gray matter. In 
some cases we can recognize small capillary haemorrhages with the naked eye, 
but the macroscopic examination of the fresh cord is never sufficient for the pre- 
cise determination of the extent and intensity of the disease. 

The changes are much more plainly visible if we harden the cord in chromic 
acid, or Miiller's fluid,* for at least eight or ten weeks. All the normal parts of 
the white matter of the cord assume a dark-green color from the acid, which is 
really due to the staining of the medullary sheaths. The diseased portions, in 
which the medullary sheaths are mainly if not entirely absent, are thus often 
very sharply distinguished from the healthy, dark-green portions. Since similar 
differences in color between healthy and diseased tissue are also noticed in the 
gray matter, although less sharply defined, the cross-section of the cord, well 



[* The formula for Miiller's fluid is as follows: Two and a half parts of potassic bichromate, one 
part of sodic sulphate, and one hundred parts of water. — Trans.] 



584 



THE DISEASES OF THE SPINAL CORD. 



hardened in chromic acid, usually gives quite a correct idea of the extent of the 
disease. 

We obtain more precise disclosures, however, as to the form of the anatomical 
changes by microscopical examination. When made on the fresh, unhardened 
cord, it affords little information. The presence of numerous granular cells {vide 
infra) in fresh teased-out preparations is the only thing that is important, since 
they show with certainty the existence of a pathological change. If, however, we 
make fine cross-sections of the hardened cord, and stain them with carmine or 
some similar staining fluid, even the naked eye notices at first a marked difference 
between the diseased and the healthy tissue, since the former, which is almost 
always richer in connective tissue, has a much darker staining, and thus is distin- 
guished from the brighter normal tissue. The microscopic examination now shows 
that in the diseased parts the normal nerve-tissue has been almost wholly or at 
least partly destroyed. Only occasionally do we see nerve-fibers of normal appear- 
ance remaining here and there. In other places the fibers that are still visible 
are smaller and atrophied, and the axis-cylinders have in part lost their medullary 
sheaths, or are swollen. The changes in the ganglion-cells are harder to follow, 
but in more advanced cases they also show marked signs of destruction ; they are 
contracted, rounder, and have lost their processes. The increase of the connective 
tissue corresponds to the destruction of the nerve-substance. The meshes of the 
neuroglia extend and swell, so that the space formed by the destruction of the 
nerve-tissue is in great measure taken up by connective tissue. The older the 
process, the firmer and more fibrous is the connective tissue. The nuclei of the 
neuroglia increase in number, and we often find a very great increase in those 
peculiar, flat, connective-tissue cells with many processes, first described by Dei- 
ters, and named after him, the so-called "Deiters' spider-cells." The fatty granu- 
lar cells are also easily recognized in hardened preparations, so long as they are 
not treated with alcohol. They lie in the interstices between the meshes of the 
neuroglia, and are especially numerous about the vessels. They are to be regarded 
either as white blood-corpuscles, or as endothelial cells from the sheaths of the 
vessels, which have taken up the fat from the disintegrated nerve-substance. If, 
therefore, the process is still fresh, or if it is still advancing, the fatty granular 
globules are to be met with in great numbers, while in old, sclerosed nodules, only 
a few of them, or scarcely any, are to be found. The changes in the vessels are 
usually very striking. They are often dilated and congested. Here and there 
there may be haemorrhages. The vascular walls are thickened, especially in old 
cases, and sometimes have become peculiarly homogeneous — " hyaline degenera- 
tion " ; and a large accumulation of nuclei may be found about the vessels. The 
so-called corpora amylacea are sometimes present in great numbers, and some- 
times they are only scanty. Their significance and their genesis are still unknown. 

The extent of the whole process varies very much in different cases. We 
usually find one main focus of myelitis, which extends in a diffuse manner 
over the greatest part of the transverse section of the spinal cord, and may reach 
upward and downward for a space of five to ten centimetres or more. The dor- 
sal portion of the cord is most frequently affected (dorsal myelitis), the upper half 
being usually most involved, but in some cases the lower half is chiefly affected. 
Nearly the whole of the dorsal cord is often the seat of a diffuse inflammatory 
affection, which, of course, differs in extent at different levels. In other cases the 
chief focus of disease is in the cervical cord (cervical myelitis), while it is most rare 
in the lumbar cord (lumbar myelitis). We often find small, distinct foci in the 
vicinity of the main fccus. In all severe cases there develops later on a systemic 
ascending and descending secondary degeneration {vide infra). 

We have intentionally avoided any division of the process into different stages, 



ACUTE AND CHEONIC MYELITIS. 



585 



because, according to our present knowledge, this can be only artificial. As a 
general rule, the cases where the cord is soft and has more of a reddish-gray color, 
where the fatty granular cells are still abundant, and the meshes of the neuroglia 
are not yet fibrous, may be considered as belonging to the comparatively more 
acute and fresher stages; while in the older cases the cord has become firmer, 
" sclerosed," in the affected part, through the formation of a denser fibrillary con- 
nective tissue, and it has more of a gray appearance ; but we can not draw a sharp 
distinction between acute and chronic myelitis in regard to their pathological 
anatomy. Genuine transverse myelitis always shows a chronic course, and many 
cases deserve the name of " acute myelitis " in their clinical aspect only in so far 
as the beginning of the morbid symptoms is acute and rapid. We may entirely 
disregard the proper abscess of the cord, because it is so rare that it very seldom 
comes into question as an independent disease. It is still undecided whether there 
is a softening of the cord analogous to the foci of softening in the brain — that is, 
as a result of an obstruction of the vessels by a thrombus or embolus. At any 
rate, an actual softening of the cord is quite rare — that is, a change of the substance 
of the cord into a soft pulp, which contains nothing but the remains of the nerve- 
tissue and some fatty granular cells. We have seen ourselves only one such case, 
in the lower dorsal region, which lasted two years as a chronic transverse myelitis, 
and ended fatally. 

The Individual Symptoms of Myelitis.— The course of transverse myelitis differs 
so much in the different cases that it is impossible to give a picture of the disease 
which will be generally applicable. According as one or another part of the cord 
is involved, the clinical symptoms will affect chiefly the sensibility or the motility, 
the trophic functions or the reflexes, and will be present hi the upper or the lower 
extremities, or in both at once. The following description will, therefore, be 
devoted first to the single symptoms, and will give the inferences which, accord- 
ing to the present state of our knowledge, may be drawn from their presence as to 
the seat and the extent of the anatomical process. 

1. Symptoms of Motor Paralysis are not only the chief symptoms, as a rule, 
in well-developed myelitis, but are often the first sign of the beginning of the dis- 
ease. The patient feels at first only a slight weakness in one or both legs ; he gets 
tired more easily in walking, and begins to " drag " his legs after him. The motor 
weakness gradually becomes greater and increases to complete paralysis. The 
patient is then bed-ridden, and, finally, can not make the least active movement 
with his legs. The symptoms of paralysis in the arms are analogous. 

Since the chief paths for the conduction of voluntary motion are situated, as 
we have seen, in the lateral columns of the spinal cord, and especially in the 
lateral pyramidal tract, we conclude, in every spinal disease where symptoms of 
paralysis are present, that there is an interruption of tins tract — that is, an 
implication of the posterior portions of the lateral columns. Since in transverse 
myelitis the whole cross-section of the cord is more or less involved, the paralysis 
also extends to the two halves of the body : motor paraplegia is the characteristic 
form of paralysis for transverse myelitis. Paraplegia of the lower extremities 
may of course arise wherever the myelitis is situated, whether in the lumbar, 
dorsal, or cervical region ; but the upper extremities necessarily remain entirely 
free in every dorsal or lumbar myelitis. The occurrence of paretic symptoms here, 
and the final development of a brachial paraplegia, point with certainty to an 
implication of the cervical region, to a cervical myelitis. If the symptoms of 
paralysis are not alike in the two corresponding extremities, but are more marked 
on one side than on the other, the anatomical affection must also be more intense 
on that side of the cord than on the opposite side. 

2. Symptoms op Motor Irritation of various sorts are often seen, both at the 



586 



THE DISEASES OF THE SPINAL COED. 



beginning and during the whole course of myelitis. Single twitchings come on 
spontaneously in the limbs, which are at the same time paralyzed, or at least 
paretic, and these twitchings are short and rapid or slow and persistent. The 
thighs are drawn up on the abdomen, or there are severe spasms of the extensors. 
The interpretation of these symptoms is not always easy. It is often particularly 
hard to decide whether they are the result of a direct irritation of motor fibers 
in the cord, or whether they represent reflexes (vide infra). The value of the 
symptoms of motor irritation for the localization of the disease is accordingly 
slight, but, of course, in these cases we must chiefly consider the motor tracts in 
the lateral columns. 

Ataxia and intention tremor are comparatively rare, but are most frequent in 
the upper extremities. They are also seen in the stage of convalescence in acute 
cases. 

3. Disturbances of Sensibility.— The disturbances of sensibility usually 
appear to a marked degree only in the later stages of the disease. At the outset 
we usually notice merely mild symptoms of sensory irritation, like formication, 
prickling, numbness, a woolly feeling, etc., while severe pain is hardly ever 
present in transverse myelitis, and hence it always points to some affection of the 
vertebrae or the meninges. Slight diminution of sensibility is often to be made 
out early on careful examination, but, in many cases, the sensibility remains for a 
long time wholly, or almost wholly, intact, either because the localization of the 
disease spares the sensory portions of the cord, or because the sensory paths of 
conduction are more resistant, or can act vicariously for one another to a higher 
degree. In the further course of the disease, however, there are almost always 
more marked disturbances of sensibility : at first a simple diminution in the sensi- 
tiveness of the skin, sometimes partial paralyses of sensation, analgesia, paralysis 
of the sense of pressure, and finally frequently a complete anaesthesia. On the 
other hand, we see in many cases a striking hyperesthesia to pain, like a pin-prick. 

From the presence of marked disturbances of sensibility we can conclude with 
certainty that there is an affection of the posterior columns, and especially of the 
posterior cornua of the gray matter. With marked anaesthesia the latter are 
always involved. It is still very doubtful whether the statement made by Schiff, 
that the conduction of painful sensations is chiefly in the gray matter, and the 
conduction of tactile sensations is chiefly in the white matter, holds in man. The 
pathological facts, as we have said before, also give no support at all to the theory 
that there are sensory fibers in the lateral columns in man. 

The disturbance of sensibility gives important service in estimating the height 
at which the affection in the cord is situated. If we search on the trunk for the 
line where the cutaneous sensibility becomes normal, we may place the upper 
boundary of the myelitis, as far as it disturbs the sensibility, at approximately the 
same level. In myelitis in the lumbar region the disturbance of sensibility 
reaches to the umbilicus, or even a little higher ; in myelitis in the lower dorsal 
region it reaches about to the lower end of the sternum ; in myelitis in the upper 
dorsal region to the level of the axillae ; and in cervical myelitis the sensibility of 
the upper extremities is also impaired, but complete anaesthesia is very rare. 

4. Cutaneous Reflexes.— As is well known, the reflex arcs in the cord are 
found at about the same level as the centripetal sensory and the centrifugal motor 
fibers. They are also connected with fibers which come from above, and to which 
must be ascribed the property of reflex inhibition. If these fibers above the reflex 
arc are put into a state of irritation, the reflex is thereby impaired ; but if the con- 
duction is broken in these fibers, the reflex activity appears increased, the reflex 
comes on at a weaker irritation, and the contraction is more vigorous. If the 
reflex arc itself is broken at any point, the reflex must disappear. 



ACUTE AND CHEONIC MYELITIS. 



587 



The data from the examination of the patient may generally be harmonized with 
this scheme, although, of course, the reality probably shows more complicated 
conditions. In extensive lumbar myelitis, by which the reflex path in the lum- 
bar cord is broken, the cutaneous reflexes in the lower extremities must be dimin- 
ished or absent. In these cases the loss of sensibility runs about parallel to 
the diminution of the reflexes. In dorsal and cervical myelitis, however, the 
reflex arc in the lumbar cord remains unimpaired, but the conduction of sensory 
impressions to the brain may very well be interrupted. In these cases the cuta- 
neous reflexes are retained, even when there is anaesthesia ; or, if the reflex inhibi- 
tory influences are removed, they are decidedly increased. The cutaneous reflexes 
in the legs, however, may be diminished, even in disease above the lumbar cord, 
in which case we must imagine a loss of irritability in the fibers which take part 
in the reflex, or an irritation of the reflex inhibitory fibers. The cremaster reflex 
has its reflex arc about at the point of exit of the first lumbar nerves ; diseases of 
the cord at this point must therefore, under some circumstances, cause a disappear- 
ance of the reflex. Of the abdominal reflexes the upper, epigastric, corresponds 
about to the level of the fourth to the seventh dorsal nerves, and the lower 
abdominal reflex proper to the lower portion of the dorsal cord. 

5. Tendon Keflexes. — The same rules generally hold in judging of the ten- 
don reflexes as are to be considered in judging of the condition of the cutaneous 
reflexes. We know comparatively little of the course of the reflex arc of the 
patellar reflex in the lumbar cord. It lies about at the levels of exit of the second 
to the fourth lumbar nerves. We know, also, that the reflex fails as soon as the 
middle part of the posterior columns (see the chapter on locomotor ataxia) or the 
anterior cornua of the gray matter of the lumbar cord are much diseased. The 
Achilles' tendon reflex, or the ankle clonus, has its reflex arc at the level of the 
first sacral nerves. It is always absent in extensive disease of the posterior col- 
umns and of the gray matter in the corresponding portion of the lumbar cord, so 
that, beside the other symptoms, the absence of the tendon reflexes in the lower 
extremities is one of the most important points for the diagnosis of a myelitis of 
the lumbar cord. In almost all inflammations above the lumbar cord — that is, in 
dorsal and cervical myelitis — there is, however, a very decided increase of the 
tendon reflexes, the result, as we must suppose, of the loss of the reflex inhibitory 
influences. We have a certain right to assume that the fibers which influence 
the condition of the tendon reflexes run chiefly in the lateral columns of the 
spinal cord, but that they are not identical with the fibers of the lateral pyramidal 
tracts which serve for voluntary motion (see the chapter on spastic spinal paraly- 
sis). We may therefore assert that, with a considerable increase of the tendon 
reflexes in the lower extremities, the seat of the myelitis must be above the 
lumbar cord — that is, in the cervical or dorsal cord — and that in these cases we 
have to suppose that the lateral columns are chiefly implicated. In cervical mye- 
litis the tendon reflexes in the upper extremities are often considerably increased. 

We have already said, on page 512 et seq., what is necessary in regard to the 
different signs of the increased tendon reflexes, the exaggerated patellar reflex, 
ankle clonus, the periosteal reflexes, etc. The peculiar character which the 
paralysis of the legs assumes from a considerable increase of the tendon reflexes 
at the same time will be described more fully in the chapter on " spastic spinal 
paralysis " (vide irfrd). 

6. Disturbances in the Bladder and Eectum. — Disturbances in micturition 
are one of the commonest symptoms of myelitis. The first manifestation is usu- 
ally a difficulty in micturition ; the patient has to strain and to wait longer before 
urinating. There may finally be a complete retention of urine from paralysis of 
the detrusor urinse. In the later stages of the disease, however, there is usually a 



588 



THE DISEASES OF THE SPINAL COED. 



paralysis of the sphincter vesicas, and consequently incontinence of urine. The 
disturbances of the bladder give no points for the localization of myelitis, since 
they may occur with disease at any level of the spinal cord ; but we believe we 
are right in assuming that they always permit us to decide that the posterior 
columns of the cord are involved. 

The clinical significance of disturbances of the bladder in myelitis, and in 
many other diseases of the cord, apart from the great distress and discomfort for 
the patient, lies in the fact that they very often — almost always in severe cases — 
give rise to the development of cystitis. In retention of urine the use of the 
catheter, by which inflammatory irritants are often brought into the bladder, in 
spite of all attempts at disinfection, leads to decomposition of the urine and to cys- 
titis ; but where there is also incontinence, the imperfect closure of the sphincter 
and the constant presence of stagnating and decomposing urine in the urethra are 
the causes of the entrance of these irritants into the bladder. If cystitis has 
developed, it may be followed under some circumstances by pyelitis and puru- 
lent pyelo-nephritis (vide infra), which conditions are often the immediate cause 
of death from the sequelae connected with them, like fever, which is sometimes 
associated with chills, general weakness, and emaciation. 

Defecation is also disturbed in many cases of myelitis. There is usually con- 
stipation at first, which may depend either upon weakness of the intestinal peri- 
stalsis, or upon paresis of the abdominal muscles. Sometimes the constipation 
reaches such a degree that the bowels move only at intervals of one or two weeks. 
In many severe cases there is finally incontinence of faeces, as a result of iDaralysis 
of the sphincter ani. We can give no details as to the localization of the nerve- 
tracts in the cord which take part in defecation. 

We have yet to note that micturition and defecation are often aroused reflexly 
in an abnormal fashion where there is increased reflex irritability. On irritation 
of the skin over the thighs, the perineum, the gluteal region, etc., there is often 
an involuntary contraction of the bladder, associated with loss of urine. 

In conclusion, we may mention, as an addendum, that the sexual functions are 
often considerably disturbed in many cases of myelitis, and finally may be wholly 
lost. The tracts involved here lie probably chiefly in the upper lumbar cord, but 
then precise localization (posterior columns ?) is still unknown. 

7. Trophic Disturbances. — The trophic condition of the paralyzed muscles 
affords extremely important points for diagnosis. In cervical and dorsal myelitis 
the trophic centers in the lumbar cord for the muscles of the legs remain intact ; 
the paralyzed muscles, therefore, retain essentially their normal volume, and espe- 
cially their normal electrical excitability. Even in such cases the muscles are 
sometimes flabbier and of lesser girth than under normal conditions, but this 
depends partly on the decline in the general nutrition, and partly perhaps on the 
lack of movement, the "atrophy of inactivity." Only occasionally do we find 
more marked muscular atrophy, but it is of a simple character and not degenera- 
tive, and hence without reaction of degeneration ; but if we find in myelitis a 
genuine degenerative atrophy, with reaction of degeneration in the muscles of the 
lower extremities, we can from this draw a definite conclusion that the anterior 
gray cornua or the fibers of the anterior roots in the lumbar cord are affected (see 
page 507). In an analogous fashion degenerative atrophy with reaction of degen- 
eration in the muscles of the upper extremities points to an affection of the ante- 
rior gray matter in the cervical cord. 

Trophic disturbances in the skin are also frequent, but they have no definite 
diagnostic significance. We often find the skin dry, hard, with a scaly epidermis, 
and the nails thickened and brittle. Exceptionally there are eruptions of herpes, 
urticaria, etc. Vaso-motor disturbances also occur. Sometimes the paralyzed 



ACUTE AND CHRONIC MYELITIS. 



5S9 



extremities show a mottled, cyanotic reddening, and feel cold. Slight oedema is 
quite frequently present in the paralyzed parts. Disturbances of the sweat secre- 
tion are not infrequent. We find either that it is absent or that there is a great 
increase in it, so that the paralyzed parts are constantly moist. ' All these symp- 
toms have no value at present for the special topical diagnosis. 

The frequent occurrence of bed-sores in the sacral region, over the glutei, or 
more rarely on the feet or the inner side of the knees, is of great practical impor- 
tance. Although trophic and vaso-motor influences may play a part in their 
origin, still their ultimate cause is always to be found in external conditions, 
pressure, unclean] iness, etc. The more faulty the care of the patient is, the easier 
bed-sores arise. With completely paralyzed and anaesthetic patients, with incon- 
tinence of urine and faeces, of course they sometimes can not be wholly and per- 
manently avoided, even with the most careful management. The extent to 
which a bed-sore may reach is sometimes absolutely frightful. A large part of 
the sacrum may be laid bare, after the overlying soft parts and the periosteum 
have become gangrenous and been thrown off. 

8. Disturbances in the Region op the Cerebral Nerves are entirely absent 
in most cases of transverse myelitis. In rare cases of cervical myelitis the process 
may gradually extend upward and give rise to bulbar symptoms. We sometimes 
see changes in the pupils also in cervical myelitis, such as inequality and spinal 
myosis ; and finally myelitis has been repeatedly found combined with an optic 
neuritis. 

Different Forms of Myelitis, Course of the Disease, and Diagnosis.— The whole 
picture of transverse myelitis in its different forms may be constructed from the 
symptoms described in detail in the preceding paragraphs. We can usually deter- 
mine without difficulty, at least approximately, the seat and extent of the disease. 
If we group the chief symptoms of the different forms of myelitis together, they 
are as follows : 

Cervical Myelitis. — Paraplegia of the legs, combined with more or less exten- 
sive disturbances in the upper extremities, and eventually disturbances of sensi- 
bility over a like extent. At times atrophy of single muscular regions in the 
arms. Muscles of the legs not materially atrophied. Increased tendon reflexes 
and spastic symptoms in the legs and often in the arms. Cutaneous reflexes in 
the legs retained, and sometimes even increased. Disturbances of the bladder 
and rectum. Sometimes changes in the pupils. 

Dorsal Myelitis. — Upper extremities free. Motor, and eventually sensory 
paraplegia of the legs, without degenerative atrophy. Increased tendon reflexes, 
especially strong in myelitis in the upper dorsal cord ; cutaneous reflexes retained, 
rarely increased. Disturbances of the bladder and rectum. 

Lumbar Myelitis. — Upper extremities free. Motor, and eventually sensory 
paraplegia of the legs. Cutaneous and tendon reflexes in the legs diminished or 
absent. Under some circumstances degenerative muscular atrophy, with reaction 
of degeneration. Disturbances of the bladder and rectum. 

The whole course of myelitis is almost always chronic. We consider it impos- 
sible, as we have said, to make a sharp distinction between acute and chronic 
myelitis. Many cases, of course, show quite a rapid beginning, so that severe 
spinal symptoms develop in a few weeks. Such cases may be termed acute mye- 
litis, but their further course is almost always chronic. Many cases begin very 
gradually from the outset, and only after years lead to complete paraplegia. 

As a rule, the disease begins with motor symptoms, either in one leg or in both 
at about the same time. The paresis gradually increases more and more, spastic 
symptoms set in, and symptoms of sensory irritation, like formication, and also 
disturbances of the bladder, etc. The sensibility is sometimes a little blunted 



590 



THE DISEASES OF THE SPINAL CORD. 



quite early ; but it is almost always retained for a longer time than the motility. 
Only in the last stages is complete anesthesia common. The whole duration of 
the disease is seldom under a year, and it often lasts two or three years, or even 
longer. Remissions, apparent halts, and improvements are not infrequent, and 
the condition often becomes rapidly worse. Recoveries are not impossible, but 
they are rare at any rate. We know of no case that recovered where the diag- 
nosis could be made with certainty. The cases reported where a recovery is 
claimed are usually cases of pressure paralysis, multiple neuritis, poliomyelitis, 
etc. The fatal termination is the result of the general weakness which finally 
sets in ; or it comes from cystitis or pyelo-nephritis, both of which are often com- 
bined with pyasmic conditions ; or from extensive bed-sores ; or finally from some 
complications, like tuberculosis or acute diseases. 

The diagnosis of diffuse transverse myelitis is always made by considering the 
whole group of symptoms prominent in the individual case. The possibility 
of a compression of the cord must be excluded by a careful examination of the 
vertebral column, and by consideration of the course of the disease. We must 
also be sure that the existing symptoms do not correspond to a definite typical dis- 
ease, or a systemic disease, but that they can agree only with the assumption of an 
extensive diffuse disease at a certain point in the cord, to be made out accurately 
according to the symptoms. The further distinction, as to whether this diffuse 
disease is a myelitis, can of course hardly ever be made with absolute certainty, 
since diffuse new growths and the formation of cavities in the spinal cord must 
cause precisely the same symptoms. In these cases the decision can be made only 
by considering the whole course of the disease, and by the physician's individual 
acuteness in diagnosis. It is also still impossible at present to formulate with 
certainty the differential diagnosis between diffuse myelitis and certain combined 
fascicular or systemic diseases of the spinal cord (vide infra). 

Treatment. — Although our therapeutic endeavors may rarely hope for a per- 
manent and complete success, still in many cases the treatment can relieve the 
suffering and delay the end. 

We can try to meet the causal indication in cases where the history or the 
examination shows syphilis. Even if the connection between this and myelitis 
can not be assumed with certainty, which is usually the case, still we must always 
try inunction thoroughly, using half a drachm to a drachm (grm. 2-5) of 
mercurial ointment a day. We give twenty to thirty grains (grm. 1*5-2) of iodide 
of potassium daily at the same time. We sometimes see decided improvement 
from this ; but in some cases, of course, the result is uncertain, or the treatment 
seems to exert even an unfavorable influence upon the disease. In the latter case 
we must stop it at once. 

Of the other methods of treatment the chief are electricity, baths, and cold- 
water cures. We alternate with these. New attempts at cure raise the patient's 
courage and hope afresh. 

Electricity may give improvement in many cases, but of course it causes recov- 
ery only exceptionally, at most. In severe and hopeless cases, however, it is at 
least the best means of consoling the patient. The constant current has the great- 
est therapeutic value. We use large electrodes placed on the vertebral column, 
and pass not too strong a stabile or slowly labile current through the cord for about 
four or five minutes, chiefly through the region where we suppose the seat of the 
disease to be. We usually take the ascending current, and alternate with the two 
poles on the diseased part. We should avoid changes and great variations hi the 
current. We associate with this peripheral galvanization, and often faradization of 
the muscles and nerves of the paralyzed extremities. Single symptoms sometimes 
deserve special attention — faradization of the skin in anaesthesia, galvanization of 



ACUTE AND CHRONIC MYELITIS. 



591 



the bladder in vesical weakness, etc. The sittings should take place daily or every 
other day. If we would be successful, the treatment must be kept up persistently 
for months. 

The treatment of myelitis by baths, if prudently used, may also be of evident 
service. Even simple tub-baths, such as can be had in almost every household, 
do good service under some circumstances. The chief rules are never to make the 
baths too warm — about 85° or 90° at most (24°-26° R.) — to limit them at first to ten 
or fifteen minutes, and to give them at first not oftener than three or four times 
a week. If the baths are well borne, they can be employed daily. We should 
be most cautious in incipient and still advancing cases. The best action of the 
simple warm bath is seen in chronic myelitis with predominant spastic symptoms. 
In these cases the duration of the baths may be increased to an hour or more. 
Sometimes those baths work still better than simple water to which certain sub- 
stances are added, especially salt baths, which are made by the addition of five or 
ten pounds of common salt (Stassfurt salt), or four to six pounds of brine salt, or 
one to three quarts of brine to the water. By bringing carbonic acid into the 
water by a perforated tube in the floor of the tub, we can easily make " artificial 
Rehme baths," which were formerly often used with good success in the clinique 
here in Leipsic. 

If we can send patients in easy circumstances to a health resort, the carbonic- 
acid thermal salt springs at Rehme and Nauheim are most suitable for this pur- 
pose, and also sometimes mud-baths like Marienbad and Elster, and the thermal 
baths of Ragatz, Teplitz, Wildbad, Gastein, or Wiesbaden. 

A methodical cold-water treatment sometimes gives quite good results ; but in 
these cases we should wholly avoid all the more heroic treatment like douches, 
violent rubbing, and very cold baths, and prefer only short, cool, full or half baths, 
or mild cold sponging. Hydrotherapeutics are usually combined with electricity. 

We can expect but little success from internal treatment, but it can not be dis- 
pensed with in practice. Ergotine, strychnine (also given subcutaneously), iodide 
of potassium, and nitrate of silver, are most to be recommended. 

The general hygienic and symptomatic treatment is very important. If the 
first symptoms of a beginning spinal disease show themselves, we should urgently 
advise the patient to take the best possible physical care of himself, and recom- 
mend mental rest. The diet should be strengthening but easily digestible. Large 
amounts of spirits, much smoking, much tea and coffee, etc., are to be avoided. If 
the patient becomes bedridden, we must first employ the utmost care to get a good 
bed in order to guard against bed-sores. In severe cases, especially where there 
are disturbances of sensibility, a water-cushion is most desirable. The patient's 
position must also be frequently changed, and the sacral region must often be 
washed and rubbed. Every incipient bed-sore must be very carefully treated by 
Peruvian balsam ointment (1 to 30) or iodoform, in order to prevent its spreading. 
When the bed-sore is very extensive, the continuous bath is the best remedy. 

If there is retention of urine and the patient has to be catheterized, the most 
extreme care must be employed in cleaning and disinfecting the catheter, or else 
cystitis will develop in a few days. If it does, it is best in severe cases to wash out 
the bladder regularly with acetate of lead (1 to 1000) and like remedies. In milder 
cases we may try chlorate of potassium internally, fifty to seventy -five grains a 
day (grm. 3-5), astringents, or balsams. If there is complete incontinence it is 
advisable to introduce a permanent catheter (sonde a demeure) into the bladder — 
that is, a Nelaton's catheter which lies in the bladder, and is fastened to the thighs 
by strips of plaster. The urine runs away through a rubber tube, and we avoid 
the constant wetting of the skin and linen. 

Constipation must be met according to the general rules. We should be as 



592 



THE DISEASES OF THE SPINAL COED. 



sparing as possible with cathartics at first, and try to make an appropriate diet and 
enemata suffice. If there is severe pain, subcutaneous injections of morphine are 
unavoidable, but we always delay this as long as possible, although finally we let 
the dose of morphine be unlimited in hopeless cases. 



CHAPTEE V. 

MULTIPLE SCLEROSIS OF THE BRAIN AND SPINAL CORD. 

{Disseminated Nodular Sclerosis. Sclerose en plaques?) 

iEtiology and Pathology. — Multiple sclerosis of the central nervous system is a 
special chronic form of disease, whose anatomical basis consists in the develop- 
ment of numerous disseminated " sclerotic nodules " {vide infra) in the brain and 
cord. We know practically nothing as to its aetiology, for the significance of 
exposure to cold, over-exertion, and mental emotions, sometimes given as causes 
of the disease, is wholly doubtful. It is also still undecided whether syphilis plays 
any part in the aetiology of multiple sclerosis. A hereditary predisposition seems 
to be prominent in some cases. The affection occurs chiefly in youth, somewhere 
between the ages of eighteen and thirty-five, but we have ourselves seen one case, 
which came to an autopsy, in a man of sixty. The disease also occurs in children. 
No material distinction has been made out in regard to sex. 

In regard to the development of the different sclerotic nodules, nothing definite 
has been established at present in regard to their genesis. Various reasons lead us 
to favor the theory that the disease depends upon anomalies in the vessels, but the 
proof of this can not yet be given. The nodules are in part easy to recognize with 
the naked eye, from their gray color, and we can also feel an increased resistance. 
They are scattered over the whole central nervous system. Their favorite seats in 
the brain are the centrum ovale, the walls of the lateral ventricles, and the corpus 
callosum ; the nodules are also quite abundant in the pons, less frequent in the 
medulla, and very abundant and variously distributed in the cord (see Figs. 82 and 
83), and chiefly in its white substance. Examined microscopically, the nodules 
consist of an abundant, reticulated, fibrillary connective tissue, which is traversed 
only by comparatively few nerve-fibers that are preserved. In the vessels we 
notice first an increase in nuclei, and later usually a thickening of the walls. 
Fatty granular cells are always present in fresh cases. Charcot first made the 
statement that the axis-cylinders are preserved in the nodules for a remarkably 
long time, even after the destruction of the medullary sheaths. Perhaps this is 
connected with the fact that secondary degeneration in the cord is strikingly 
absent. 

Clinical History. — From the variations which the number and the localization 
of the nodules show, it may be understood from the outset that a type of the dis- 
ease which represents all cases can not exist ; but a comparison of a number of 
cases taken together always shows so characteristic a group of symptoms that the 
diagnosis can often be made with quite great certainty. We will first describe 
this typical form of disease, for the knowledge of which we must thank Charcot 
chiefly, and to that we will add some remarks upon the cases which differ from 
this type {'''formes frustes"), which are by no means very rare. 

The symptom of the typical cases of nodular sclerosis which we must first 
mention is tremor. This has been the reason why multiple sclerosis has formerly 
been repeatedly confounded with paralysis agitans, although the tremor in the two 



MULTIPLE SCLEROSIS OF THE BRAIN AND SPINAL CORD. 593 




diseases shows entirely different peculiarities. In distinction from the constant 
rhythmical oscillations of the limbs in paralysis agitans (vide infra), the tremor 
in multiple sclerosis comes on only with intended movements,- " intention tremor,' 1 
and usually does not show a perfectly regular rhythmical character, but is 
unequal and jerking, although the intended direction of the motion is, on the 
whole, always retained. The tremor is most marked in the upper extremi- 
ties, as shown if the patient tries to take hold of a certain 
object, to bring a glass of water to his mouth, to bring the tips 
of the forefingers together, etc. ; but the tremor also occurs in 
the head, in the trunk, and in the lower extremities. When 
the patient is perfectly quiet the tremor ceases entirely. Only 
a few exceptions to this rule have been known. If the pa- 
tient is mentally excited, the tremor usually becomes more 
marked. We know nothing as to its peculiar cause. It is 
also still doubtful whether, as many think, the tremor always 
depends upon the presence of cerebral nodules, or whether it 
may also be caused by nodules in the spinal cord. 

Two other symptoms, which often occur in nodular sclero- 
sis, are, to a certain degree, analogous to the tremor — a peculiar 
disturbance of speech, and nystagmus. The disturbance of 
speech depends upon disturbances in the motor innervation of 
the organs of speech, the tongue and larynx, and may proba- 
bly be referred to the presence of sclerotic nodules in the pons 
and medulla. The speech is slow, " scanning," obscure, and 
finally sometimes almost incomprehensible. The equality in 
the pitch is often very striking. We often notice tremulous 
movements in the tongue and the lips on speaking. Nystag- 
mus shows itself in the form of slight and usually lateral 
twitchings of the eyeballs on fixation, ©r on intended ocular 
movements. 









Fig. 82.— Example of 
disease of the cord 
in multiple sclero- 
sis. The dark por- 
tions are the parts 




Fig. 83.— Distribution of the sclerosed nodules on the 
surface of the pons. (From Leube.) 



Other motor disturbances are usually present beside the symptoms thus far 
described. 

In many cases the crude strength of the muscles is for a long time completely 



594 



THE DISEASES OF THE SPINAL COED. 



normal, but in other cases there is marked paresis, which sometimes increases to 
complete paralysis. The " spastic symptoms, 1 ' however, are far more characteristic 
and more frequent (see the chapter on " spastic spinal paralysis "). These depend, 
in great part at least, upon the very considerable increase in the tendon reflexes, 
which is almost always present. In the upper extremities the spastic symptoms 
are less prominent, but even here we almost always find very vigorous tendon 
and periosteal reflexes on striking the lower ends of the bones of the forearm or 
the tendon of the biceps or triceps. In the lower extremities we see not only 
marked patellar reflex and a very intense and persistent ankle clonus (formerly 
given the unsuitable name of " spinal epilepsy ") but very often a pronounced tonic 
rigidity of the two legs. Passive motion is difficult, and the gait is completely 
spastic. If there is at the same time a marked paresis in the legs, the gait, although 
stiff, is also dragging — a paretic-spastic gait. The disturbances of sensibility are 
usually remarkably subordinate in multiple sclerosis. Only rarely do we find a 
blunting of sensation, and quite exceptionally marked anaesthesia. The cutaneous 
reflexes usually remain completely normal. Of the disturbances of the organs of 
the special senses we have still to mention that optic atrophy has often been seen 
associated with considerable disturbance of vision, like amblyopia or achroma- 
topsia, or even with complete blindness. Optic neuritis with a subsequent atrophy 
also occurs, especially in the temporal halves of the papillae, according to Gnauck. 
Finally, we sometimes see anomalies in the innervation of the ocular muscles, and 
diplopia caused by these anomalies. 

In one class of cases there are certain cerebral symptoms which may be impor- 
tant with regard to diagnosis. In the course of the disease there often appears a 
certain mental weakness, an imbecility, which sometimes increases to marked 
dementia. Conditions of melancholy or exaltation are much rarer. We must 
also mention the occurrence of apoplectiform attacks. After slight prodromal 
symptoms, like headache and vertigo, loss of consciousness and hemiplegia come 
on quite suddenly. With this the face is usually red, the pulse is frequent, and 
the temperature may rise to 104° or 106° (40°-41° C). After a day or two the con- 
sciousness gradually returns, and the hemiplegia soon disappears. Epileptiform 
attacks are much rarer. We saw these repeatedly in a typical case ; they were 
mainly unilateral, and were followed by a hemiplegia which soon passed away. 
The precise cause of these attacks is still wholly unknown. Vertigo or giddiness 
is a frequent cerebral symptom, which may develop even in the earlier stages of 
the disease, and often comes on paroxysmally. 

Symptoms on the part of the bladder, the rectum, or the genital organs, are 
usually entirely absent in the typical cases, or they appear only toward the close 
of the disease. Trophic disturbances, like muscular atrophy, are also rare. 

In regard to the general course of typica] cases, the disease develops very slowly 
and gradually. Motor symptoms, tremor, paresis, and disturbances in gait, usually 
appear in the lower extremities first. The patient often complains at the same 
time of occasional headache and vertigo. The speech gradually becomes more 
indistinct, the intelligence weaker, and the other symptoms of the disease described 
above develop. The affection almost always lasts for years and years. Variations, 
cessations, and remissions are common. We often see the condition rapidly grow 
worse, especially after the above-mentioned apoplectiform attacks. The last stage 
is characterized by the gradually increasing disturbance of the general nutrition, 
and, finally, by paralysis and bed-sores. Death ensues from intercurrent diseases, 
or from the increasing weakness, or sometimes in an apoplectiform attack. 

Anomalous Cases. — Beside the typical form of multiple sclerosis described, 
there are often, as we have said, cases that vary from the type. We will mention 
briefly the following possibilities : 



MULTIPLE SCLEROSIS OF THE BRAIN AND SPINAL CORD. 595 



1. The disease may be very latent. We saw one case in which, for a long time, 
the only symptom was a complaint of slight headache and vertigo. Finally, there 
was a transitory apoplectiform attack, several months later an epileptiform attack, 
and a few days after that death took place. The autopsy showed a completely 
developed multiple sclerosis. 

2. Sometimes the disease appears under the exact type of a chronic myelitis. 
The cerebral nodules cause no symptoms, they are present, perhaps, only in small 
numbers, and the spinal nodules cause a gradually increasing paraplegia of the 
legs, with vesical disturbance, loss of sensibility, etc. We have notes of two cases 
of multiple sclerosis, with autopsies, in which, during life, the diagnosis of a simple 
transverse myelitis had been made. 

3. Cases have been repeatedly known where multiple sclerosis has appeared 
under almost the exact type of a spastic spinal paralysis (vide infra). In these 
cases many nodules were situated in the lateral columns of the cord. If the spas- 
tic symptoms are combined with muscular atrophy (nodules in the anterior gray 
cornua), the disease may even simulate the type of an amyotrophic lateral scle- 
rosis, with at times co-existing bulbar symptoms (vide infra). If multiple sclerosis 
be localized to an unusual extent in the pons and medulla, the symptoms of a 
chronic bulbar paralysis may be prominent. 

4. Symptoms like those of locomotor ataxia, pain and ataxia, are less frequently 
of chief prominence. Combinations of multiple sclerosis and gray degeneration 
of the posterior columns have, however, also been observed. 

5. It sometimes happens that multiple sclerosis is the reason for a slowly devel- 
oping hemiplegia, which may then be falsely regarded as cerebral, while the 
autopsy shows several nodules in the corresponding side of the cord and pons. 

6. In many cases the mental disturbance, dementia, is so prominent that there 
is the pronounced picture of paralytic dementia (general paralysis), with disturb- 
ances of speech, etc. 

7. Finally, we must mention here that Westphal has of late described some 
very chronic cases which have closely resembled multiple sclerosis in their type, 
although the autopsy usually showed no discoverable anatomical lesion of the 
nervous system at all. In these cases the symptoms consisted chiefly of muscular 
paresis, tremor on voluntary motion, paretic-spastic gait, disturbance of speech, 
difficulty in moving the eyes, rigid expression of the face, and of the presence of 
the so-called paradoxical contraction in the muscles of the legs (see page 514). A 
hereditary predisposition to nervous disease was probably of significance in their 
aetiology. Westphal proposes to call such cases provisionally " pseudo-sclerosis. " 

The diagnosis of multiple sclerosis in atypical cases is sometimes quite impossi- 
ble, or at best it can be made with a fair amount of probability only when some, 
at least, of the characteristic symptoms of the disease are present beside the anom- 
alous symptoms. The circumstance, indeed, that the anomalous cases will not 
properly fit the molds of any other form of disease, should make us think of the 
possibility of a multiple sclerosis ; for in these anomalous cases, of course, there 
may be all possible combinations of symptoms. 

The diagnosis is usually not difficult in the typical cases. The intention tre- 
mor, the spastic symptoms, the disturbance of speech, the nystagmus, the gradual 
manifestation of mental weakness, and eventually the apoplectiform attacks, are 
the most valuable signs in diagnosis. The distinction from paralysis agitans 
(vide infra) is almost always easy, if we remember that in this latter disease, in dis- 
tinction from all others, the tremor is chiefly during rest, and the oscillations are 
much more equal. The diagnosis of " pseudo-sclerosis " can scarcely be made with 
certainty at present. 

The prognosis of multiple sclerosis is utterly unfavorable. A case of recovery 



596 



THE DISEASES OF THE SPINAL COED. 



has never yet been seen with certainty. The disease may, of course, last for a 
very long time, as was said above. 

The treatment adopts the same remedies as have been mentioned in the descrip- 
tion of chronic myelitis. The galvanic current, tepid baths and sponging, and 
perhaps the internal use of nitrate of silver, may give the best promise of a tem- 
porary benefit. 



CHAPTER VI. 

LOCOMOTOR ATAXIA.* 

(Tabes Dorsalis. Gray Degeneration of the Posterior Columns. Atazie locomotrice progressive.) 

We give at present the old name of tabes dorsalis, " consumption of the spinal 
cord," to a perfectly definite chronic disease of the central nervous system, whose 
chief anatomical basis is regarded as a typical degeneration of the posterior col- 
umns of the spinal cord. The disease has not been accurately known for a very 
long time. The first description, which, of course, is defective in many respects, 
is found in a work of W. Horn in 1827. We must thank especially the investiga- 
tions of Romberg in Germany, in 1851, and of Duchenne in France, in 1858, for a 
more comprehensive knowledge of the disease, and for a precise distinction between 
it and the other chronic diseases of the spinal cord. 

iEtiology.— But little that is definite is known as to the cause of locomotor 
ataxia. Hereditary conditions play a very slight part in genuine cases, and even 
a general " neuropathic taint " can only rarely be made out in ataxic patients. 
Much weight in regard to aetiology was formerly laid upon previous exposure to 
cold. It can not be denied that in many cases the first symptoms of the disease 
follow some pronounced exposure to wet or cold ; but much more frequently 
nothing of the sort can be made out. The case is similar with regard to physical 
and mental over-exertion, which were formerly made answerable for the origin of 
many cases of locomotor ataxia. It is an utterly ungrounded assertion that sexual 
excesses may be the cause of locomotor ataxia. Some observers report that loco- 
motor ataxia may develop as a result of acute diseases or of injuries, like a broken 
leg, etc. In these rare cases, too, it is hard to confirm the connection. The ear- 
lier teaching that locomotor ataxia develops after " suppression of the foot-sweat " 
is manifestly due to a confusion of cause and effect. The absence of foot-sweat is 
not the cause, but a symptom of incipient locomotor ataxia. 

We must, however, mention one setiological factor, which has of late been 
made very prominent, especially by Fournier in France and Erb in Germany — 
syphilis. 

In spite of the vigorous contradiction which this theory has met with from 
another school, the probability of the connection between locomotor ataxia and a 
previous syphilitic infection seems to us to become constantly greater on more 
accurate investigation. Of course this theory can at first be supported only by 
statistics. Erb was able to find a history of syphilis, with secondary symptoms, in 
about 62 per cent, of his patients; and Fournier, in 103 cases, found syphilitic 
antecedents as many as 94 times. Our own observations agree exactly with Erb's 

[* The Germans very properly follow Komberg, the earliest investigator of this disease, in calling 
it tabes dorsalis. Although we prefer this name, we do not feel justified in departing from the estab- 
lished usage in this country, and therefore we have in most places substituted the name in common 
use — locomotor ataxia. In a few instances the context has demanded the retention of the name tabes. 
—Trans.] 



LOCOMOTOR ATAXIA. 



597 



data, since 61 per cent, of our patients stated definitely that they had formerly 
suffered from syphilis. If we also reckon the cases where the patients admit a 
former sore but no secondary symptoms, the percentage becomes much greater — 
90 per cent. In general it is worthy of note that, as a rule, in most cases of loco- 
motor ataxia, the previous syphilis has not had a great intensity. Only quite 
infrequently do we find tertiary syphilitic symptoms as well as locomotor ataxia ; 
we have seen, for example, severe ulcers of the skin, gummous periostitis, etc. 
The time between the infection and the beginning of the first symptoms of loco- 
motor ataxia varies very much ; it may be from two to twenty years. 

Although we thus recognize the great probability of the connection between 
locomotor ataxia and syphilis, we can not, on the other hand, conceal the fact 
that the perception of the precise nature of this connection causes no slight dif- 
ficulty at present. The anatomical changes in locomotor ataxia {vide infra) do 
not correspond at all to the other well-known anatomical products of constitu- 
tional syphilis, gummous new-growths ; and thus they require an entirely sepa- 
rate classification. We are most disposed to assume that a chemical poison is 
formed by the action of the syphilitic infection, which has a special deleterious 
action on the affected system of fibers, these fibers being usually centripetal. 
Whether the same disturbance of nutrition as in ordinary locomotor ataxia can 
not also be provoked by other agents like ergotine, can at present neither be 
affirmed nor denied. At least provisionally it can not be questioned that there 
are also cases of ataxia where we can not discover a former syphilitic infection. 
We might state here, in opposition to statements that several authors have made, 
that the theory that syphilis excites merely an increased predisposition to the dis- 
ease seems to us to say absolutely nothing. 

Finally, we must mention here the interesting fact discovered by Tuczek, that 
in chronic ergot poisoning — " ergotism " — symptoms may develop which are pre- 
cisely analogous to locomotor ataxia, and which depend upon a corresponding 
affection of the posterior columns of the cord that can be made out anatomically. 

Locomotor ataxia is chiefly a disease of middle life. Most of the cases begin at 
the age of thirty-five or forty-five. The disease is decidedly more frequent in the 
male sex than in the female ; but it is not especially rare in women, and here we 
can usually make out, with remarkable frequency, a previous syphilitic infection. 

Pathological Anatomy. — If we examine the spinal cord of a patient who has 
died in the advanced stage of locomotor ataxia, the smallness and thinness of the 
cord usually strike us first. The pia mater is thickened and opaque, especially on 
the posterior surface. We often see the posterior columns appearing through the 
pia as a gray band extending the whole length of the spinal cord. On cross-sec- 
tion we notice that the smallness of the cord is due chiefly to the atrophy of the 
posterior columns, which is often very considerable. These have wholly lost their 
normal backward prominence, and seem flat and sunken. From their pronounced 
gray color they are very plainly distinguished on cross-section from the rest of 
the white matter of the cord. The posterior cornua of the gray matter, and the 
posterior nerve-roots, show exceptionally a considerable atrophy, and appear very 
small and thin, and also of a gray color. 

Microscopic examination gives more exact information as to the extent and 
form of the degeneration. This shows that all portions of the posterior columns 
are not affected in like manner. The degeneration is always most intense in the 
lumbar cord ; here it affects chiefly the middle and posterior portions of the 
posterior columns, while the most anterior portion remains intact in all cases (see 
Fig. 84). In the dorsal cord the posterior columns are almost completely degen- 
erated. There are usually small normal areas still preserved in the posterior 
external and the most anterior portions. In the cervical cord (see Fig. 85) the 



598 



THE DISEASES OF THE SPINAL CORD. 



so-called columns of Goll are chiefly affected, together with the prolongation of 
the fibers from the root-zones of the lumbar cord, and also the " lateral root- 
areas," that is, those portions in the columns of Burdach where fibers enter 




Fig. 84. — Transverse section through the lumbar Fig. 85.— Transverse section through the cervical 
region in locomotor ataxia. The diseased region in locomotor ataxia. G. Columns of 

portions of the posterior columns are shaded. Goll. Wz. Root-zones. 

directly from the posterior nerve-roots, and from which fibers may be traced 
farther into the gray matter of the posterior cornua ; but the so-called posterior 
external areas, and also two little antero lateral areas, remain entirely, or at least 
for a long time, free from the disease. Figures 86 and 87 show how the first 
beginnings of the disease are localized in the posterior columns. These were 
drawn from preparations from a case examined by us in the very first stage of the 
disease. A system of very fine fibers, entering through the posterior roots, is also 
frequently affected, even very early. They branch outward immediately after 




Fig. 86. Fig. 87. 

Transverse section through the posterior columns of the cord in beginning locomotor ataxia. 
Fig. 86. Dorsal region. Fig. 87. Lumbar region. 

the entrance of the roots, and here occupy a small but very sharply defined 
territory at the point of the posterior cornua, between the posterior and lateral 
columns (Lissauer). 

We must state, with reference to the participation of the gray matter in the 
disease, that the posterior cornua, as we have already said, are also found consid- 
erably affected, which is explained mainly by the atrophy of the posterior root- 
fibers which enter them directly. It also can not appear strange that the medul- 
lated fibers, found in Clarke's columns, seem very much reduced in number, since 
they are also direct processes of the posterior root-fibers. The cells of the columns 
of Clarke remain normal. 

On the other hand, the peripheral processes of the posterior root-fibers are not 
wholly spared. At any rate, in advanced locomotor ataxia we can also make out 
in the larger peripheral nerve-trunks, like the sciatic, and probably still more in 
the finer branches of the sensory nerves, a number of degenerated fibers, at least 



LOCOMOTOR ATAXIA. 



599 



of centripetal fibers (Bejerine and others). At present we can make no definite 
statement as to which part of the conducting tract the degeneration here begins in, 
or how far primary and secondary atrophies are to be separated. 

It is most remarkable that the changes described are found in almost precisely 
the same manner in all cases, that the same portions of the spinal cord are always 
chiefly affected, while certain other portions constantly remain free ; that the dis- 
ease is very exactly limited, and is precisely symmetrical in the two halves of the 
cord. This condition is explained only by the assumption that in locomotor ataxia 
certain systems of fibers are always affected ; that is, fibers which belong together 
in their anatomical and physiological aspect. Since fibers of different functions 
are manifestly diseased, as the symptoms of locomotor ataxia show, we must 
regard the trouble, not as a simple affection, but as a combined systemic disease, 
the more so as we often find certain cerebral nerves, the optic, and part of the 
oculo-motor and other ocular nerves, affected at the same time {vide infra). 

The form of the disease consists of a primary degenerative atrophy of the 
nerve-fibers, and a corresponding secondary increase of the connective tissue. 
The gray color of the posterior columns is due to the loss of the medullary sheaths. 
Since the destruction of the nerve-fibers advances but very slowly, we never 
find more than a few fatty granular cells (see page 584). In old cases we find 
numerous corpora amylacea, whose origin and significance are still unknown. 
The thickening of the pia mater is a secondary and insignificant phenomenon. 

We will state below the little that we know as to the precise relations between 
the anatomical lesions and the clinical symptoms of locomotor ataxia, and we will 
also mention some other rarer anatomical changes in the disease. 

Clinical History. — A disease which has as its basis so definite and strictly lim- 
ited an anatomical change as is the case with locomotor ataxia, would also be 
expected to give a very characteristic clinical picture. This supposition is entirely 
correct, and there are few diseases which can be diagnosticated, even in their 
earliest stages, with as much certainty as locomotor ataxia. This fact is explained 
only by regarding locomotor ataxia as a systemic disease, in which certain systems 
of fibers are always affected, while others are as constantly spared by the disease. 
The difference between different cases of locomotor ataxia lies, therefore, less in 
the symptoms themselves than in their intensity, their duration, and the order 
of their occurrence. In this regard, however, the differences in the clinical 
pictures are extremely varied, so that, even with a comparatively great personal 
experience, we often see new combinations of symptoms and also peculiarities in 
their course. 

For the majority of cases we may sketch the following general description of 
the disease, in which it is better to divide the whole course into several stages ; 
but, of course, this division can have only a schematic value. 

Locomotor ataxia begins, as a rule, with a stage of initial symptoms, which 
develops very gradually and insidiously, and which may be of a very varying 
duration. The most characteristic symptoms of this stage are those of sensory 
irritation, most frequently in the form of the so-called lightning-like, " lancinat- 
ing " pains in the lower extremities. They are sometimes very severe, but at other 
times only of slight intensity, and are comparatively little noticed by the patient, 
who regards them as "rheumatism." Many patients have a feeling of numbness 
and tingling in the tips of the fingers, especially of the ring and little fingers, and 
there is often a pronounced girdle sensation in the trunk. In some cases, too, 
neuralgic and migraine-like pains in the head may appear in the early stages. 

Beside these symptoms of sensory irritation, which may often be for years the 
only symptoms of which the patient complains, two objective symptoms appear 
very early, which are of the greatest importance in the diagnosis of incipient loco- 



600 



THE DISEASES OF THE SPINAL CORD. 



motor ataxia: the disappearance of the patellar reflex, first discovered by Westphal, 
and the reflex immobility of the pupils (Argyll Robertson). The absence of the 
patellar reflex is the most constant of all the known symptoms of locomotor 
ataxia, and it is found so early that we can hardly ever decide with exactness 
upon the time of its occurrence. The reflex immobility of the pupil — that is, the 
failure of the pupil to contract to light, while the changes on accommodation 
may be perfectly retained — is, indeed, not so constant as the failure of the patellar 
reflex, but still it is quite frequent. If all three symptoms — lancinating pains, 
absence of patellar reflex, and immobility of the pupils — are present at the same 
time, the diagnosis of locomotor ataxia is absolutely certain, even if all other 
symptoms are wanting, because this peculiar combination of three such apparently 
heterogeneous symptoms is seen in this disease alone. 

Among the rarer initial symptoms we shall also learn to recognize diplopia, 
caused by paralysis of certain ocular muscles, loss of vision, from optic atrophy, 
and certain disturbances of cutaneous sensibility, like analgesia. Sometimes dis- 
turbances in micturition appear quite early, while in other cases, however, gastric 
crises {vide infra) are the first symptom which the patient notices. 

After this first stage of the disease has lasted for a very varying period, from 
a few months to two or five or even twenty years, the second stage begins ; this 
we usually term the ataxic stage of locomotor ataxia. 

The beginning of this stage is recognized by the appearance of disturbances of 
gait. The gait becomes more difficult and more uncertain, and there are certain 
peculiarities which we will describe more fully later. Careful examination shows 
that the disturbance in gait is due not to a paresis of the muscles, but to a 
disturbance of co-ordination, ataxia of the lower extremities. This symptom 
usually increases very slowly, until it reaches a degree where the patient can 
walk only with effort, and finally can not walk at all. There is often later, but 
almost always not for years, ataxia of the upper extremities. 

Beside the persisting symptoms of the first stage, there are often now more 
marked disturbances of sensibility, as well as ataxia. The patient has a feeling as 
if he were walking on wool, felt, or similar substances. If he closes his eyes there 
is great swaying of the whole body — "Romberg's symptom.' 1 Physical examina- 
tion of the sensibility often shows a marked loss of tactile sense, of sensibility to 
pain, or other disturbances {vide infra). A loss of muscular sense is especially 
frequent. The disturbances of micturition, like incontinence, gradually become 
more marked, and very often cystitis gradually develops. This stage may also 
last for years. Sometimes the disease seems to stand still, frequently even mani- 
fest improvement is seen, but then the condition becomes worse again. 

The third stage, the terminal stage of the disease, develops if the patient has 
not previously succumbed to an intercurrent disease. The symptoms are the 
same as in most of the other chronic diseases of the spinal cord. The patient 
gradually becomes more and more wretched and helpless, and finally is confined 
almost wholly to his bed. The ataxia is very marked, and sometimes even paresis 
develops, which may increase to an actual paralysis of the legs. In these cases, 
which are by no means frequent, we are right in calling the third stage of loco- 
motor ataxia the "paralytic stage." A severe pyelo-cystitis usually develops, 
bed-sores appear, and death finally frees the patient from his lamentable condition. 

We must now complete this briefly sketched picture of the disease by a more 
careful description of the single symptoms. 

1. Disturbances of Motility in the Extremities.— The typical motor symp- 
tom of developed locomotor ataxia is the disturbance of co-ordination, the ataxia 
(see page 510). This is almost always seen in the lower extremities first. If we 
have the patient describe a circle in the air with his foot, while lying on his back, 



LOCOMOTOE ATAXIA. 



601 



we notice the irregularity, the " excursion " of the movement. It is still better to 
tell the patient to touch the knee of one leg with the heel of the other foot. We 
see then that the leg moved is often carried beyond the point designated several 
times before it reaches it. The ataxia is often noticeable, even in throwing one 
leg over the other, as the leg raised makes much too great and too " throwing " a 
movement. 

The alteration of the gait is very characteristic — the ataxic gait, from which we 
can often perceive the patient's disease at the first glance. If the patient sits down 
and tries to get up again to walk, there is difficulty in rising. He separates 
his legs to find a firm point of support, he takes a stick to help himself if he 
can, and he often gets the proper balance to keep himself erect only after several 
attempts. The gait itself is straddling, and the legs are raised abnormally high 
and set down with a stamp. If we have the patient turn rapidly or make a 
proper military " about face, 1 ' the uncertainty of movement is still more marked. 
These methods of testing are therefore especially suitable for ascertaining the 
first beginnings of ataxia. Most patients always walk with a stick and control 
the movements of their legs by keeping their eyes fixed on the floor as they walk. 
This control is particularly necessary when the sensibility of the legs, especially 
the muscular sensibility, is diminished at the same time. 

The disturbances of sensibility are also the sole reason for Romberg's symptom 
mentioned above — namely, the swaying with the eyes shut, especially when the 
patient puts his feet together. This phenomenon has often been classed with 
ataxia, but it depends merely upon the defective control of the muscular move- 
ments, which are necessary to preserve the equilibrium, as a result of the impaired 
sensibility of the skin of the soles of the feet and that of the muscles themselves. 
If this control is supplied by the eyes, the swaying is insignificant, but it at once 
becomes more marked if the control by the eyes is lost. From a like reason it is 
much harder for most ataxics to walk in the dark than by daylight. 

If the ataxia is very marked, the patient can finally keep on his legs no longer. 
Walking is wholly impossible. The ataxia can then be made out very plainly 
from the different movements of the legs in bed. The throwing movement, the 
excess of innervation, is almost always most prominent. 

If ataxia of the upper extremities occurs in the course of the disease, it is easily 
recognized if the patient tries to takes hold of some definite object like his ears, 
or if he brings the tips of his two forefingers together from a certain distance, 
or if he does fine work with his hands, like writing or sewing. The movements 
are irregular and uncertain, and the excursions are marked. If there is at the 
same time any sensory disturbance in the arms, the anomaly in their move- 
ments is still greater with the eyes shut. 

There has been much written and much dispute as to the cause of the ataxia in 
tabes dorsalis, although at present we have not attained perfect clearness and 
unity. There are three principal theories, or, more properly, groups of theories, 
which have been advanced up to the present time to explain the ataxia. Accord- 
ing to the first theory (Jaccoud, Cyon, Benedikt), ataxia depends upon a disturb- 
ance in the reflex activity of the spinal cord. According to the second theory 
(Ley den and others), ataxia is the result of the sensory disturbance in tabes, 
"sensory ataxia" ; and finally, according to a third theory (Friedreich, Erb), in 
ataxia we have a lesion of definite " co-ordinatory fibers," which run centrifugally, 
and preside over the co-ordination of motion. The exact place where these fibers 
run is not definitely asserted. If Charcot places these fibers in the external por- 
tions of the posterior columns, in the "cuneate fasciculi," it does not agree 
with the above theory, because centrifugal fibers probably do not pass through 
this part at all. 



602 



THE DISEASES OF THE SPINAL COED. 



It would be an impossible task for us to try here to estimate these theories 
exactly and critically. The main reason why it is at present impossible to give 
an incontrovertible explanation of the occurrence of ataxia lies in the fact that 
we are not yet in a condition to know and to analyze exactly the process of normal 
co-ordination of motion ; for manifestly every theory as to the causes of ataxia 
must begin with the processes involved in the co-ordination of normal movements. 
If we try to get a clear idea of this, the most essential point seems to us to be that 
co-ordination of motion is not a congenital function, but a power of our organs of 
motion learned by practice. The movements of little children who are learning to 
walk are ataxic, and even in later life it often happens that we have to learn how 
to perform certain complicated and difficult movements. We can get no other 
idea of this learning how to co-ordinate, than that it takes place by the aid of the 
constant action of controlling and correcting impressions coming from the 
periphery — that is, centripetal — but we must bear in mind that these actions are 
mainly unconscious. The surer we become in the execution of the movements, 
the more the regulatory influence of the centripetal irritations falls into the back- 
ground, without ever wholly disappearing. In these cases we must not consider, 
by any means, merely the irritations which are brought to the central organs 
from the skin of the parts moved ; but we should consider, just as much or even 
more, those irritations which are due to the varying tension and position of the 
deeper parts, the muscles, the fasciae, the ligaments, and the articular surfaces. 
Even the special organs of sense, particularly the eye, under some circumstances, 
assist materially in regulating motion. 

According to this, a disturbance of co-ordination must take place when the 
regulating influences themselves either are absent or have lost their activity — that 
is, when the possibility of a successful transmission of these influences to the mo- 
tor apparatus is absent. We do not know exactly which of these two conditions 
is realized in locomotor ataxia. Perhaps both are concerned. Several circum- 
stances may be cited to favor the theory of a loss of centripetal irritations in loco- 
motor ataxia : the disturbances of sensibility that can often be made out, the 
absence of the tendon reflexes, the undoubtedly diminished muscular tonus, etc. 
All these symptoms are certainly not in themselves the causes of ataxia, but still 
they are noteworthy facts, because they generally point to the actual loss of cen- 
tripetal irritations. A second theory has perhaps still more support. Accord- 
ing to this, the transmission of the regulatory centripetal irritations to the motor 
apparatus is disturbed in locomotor ataxia. It harmonizes completely with the 
fact that the degree of ataxia in tabes does not run at all parallel to the disturb- 
ance of conscious sensibility. There are doubtless cases where there is a good 
deal of ataxia, while the sensibility — that is, the conscious perception of sensory 
impressions — is practically undisturbed. On the other hand, there are several cases 
recorded in literature in which, in spite of marked anaesthesia, there was no ataxia. 
In these cases the regulatory influence of the irritations from the anaesthetic parts 
was certainly absent, but it could be replaced by the control of the organs of the 
other senses, especially the eye ; for as long as the completely anaesthetic patient 
has his eyes open he can walk well, but as soon as he shuts his eyes he can no 
longer stand a moment, and falls at once. In these cases, then, a regulation of 
motion by the eyes is still possible ; there is no special ataxia. In genuine ataxia, 
motion remains uncoordinated in spite of the control sought from the sensations 
of sight ; which can be explained by the fact that the influences coming from the 
eyes, which regulate motion, are no longer of value, because their transmission to 
the motor apparatus has become impossible. Nevertheless, the eye has a certain 
unmistakable influence on the movements of ataxics. As soon as the patient 
shuts his eyes all the movements become much more uncertain and lack any con- 



LOCOMOTOR ATAXIA. 



603 



trol, so that the patient's judgment as to the degree of his movements, when there 
is at the same time cutaneous and muscular ansesthesia, is entirely lost. 

We may suppose that the point where the transmission of centripetal impres- 
sions to the motor apparatus for the purpose of co-ordination of motion takes place, 
is only in the gray matter, and that it takes place only by the interposition of 
the ganglion cells. We must thus assume that ataxia, so far as it depends upon 
any disturbance of transmission, must be due anatomically to a lesion of the gray 
matter (posterior cornua ?) ; although, of course, we do not exclude the idea that 
the loss of centripetal, unconscious irritations, independently of a lesion of the 
centripetal fibers running in the posterior roots into the cord itself, may have an 
influence upon the occurrence of ataxia. 

These brief glances at the conditions to be considered in the question as to the 
origin of ataxia may suffice to give the reader a preliminary survey of the most 
important points, and an incitement to further reflection upon this interesting 
subject. 

Ataxia is the chief motor disturbance in tabes. The crude strength of the 
muscles may be perfectly normal, and it is chiefly a service of Duchenne's to have 
made clear for the first time the principal distinction between ataxia and paraly- 
sis. He showed that ataxics, who can no longer walk a step alone, can neverthe- 
less exert the greatest strength with their legs. We have ourselves treated a 
teacher of gymnastics who, in spite of the most marked ataxia of the arms, had 
still so much strength in them that he could support himself in bed on his arms 
and keep his whole body, with his legs extended, in the air. 

It sometimes happens, however, that even the crude strength disappears in 
locomotor ataxia, and that the muscles become paretic. We have stated above 
that even a complete paraplegia may finally develop in the course of the disease. 
In these cases we find, on anatomical examination, that the process is no longer 
confined to the posterior columns, but that there is also a systemic degeneration of 
the lateral pyramidal motor tracts in the lumbar cord. 

We may add, finally, that slight symptoms of motor irritation, slight twitch- 
ings in the muscles, especially in the fingers, are not uncommon, but they are 
noticed only when the attention is especially directed to them. It is not certainly 
known how they arise ; in our opinion, they are of reflex origin. 

The condition of the muscles on passive motion is very characteristic. We 
notice in most cases a very striking flaccidity of the limbs, so that there is hardly 
any muscular resistance to be felt. We have to do, as it seems, with a diminution 
of muscular tonus, whose cause is not yet quite clear; but since there are many 
reasons for believing that the normal muscular tonus is of reflex origin, we are 
led to think of a connection between the absence of muscular tonus and the other 
reflex disturbances in locomotor ataxia, like the absence of the tendon reflexes. 

The electrical excitability of the nerves and muscles, as we may also note here, 
remains perfectly normal in uncomplicated locomotor ataxia. 

2. Disturbances of the Cutaneous and Muscular Sensibility. — As we 
have already said, locomotor ataxia begins, in the great majority of cases, with 
symptoms of sensory irritation, which usually persist in the later course of the 
disease also. Beside the simple parsesthesia — the feeling of tingling and numbness 
in the legs, and sometimes, too, a similar feeling which appears quite early in the 
upper extremities (especially often, as we have said, in the ulnar region) — the 
tabetic pains are remarkably characteristic of the disease. 

The intensity of the pains differs very much in different cases ; but we see a 
complete absence of them extremely rarely. The patient's attention is often 
first called to his slight and infrequent pains by direct questioning ; but in some 
cases the severe pains are a constant distress to him. The pains most character- 



604: 



THE DISEASES OF THE SPINAL CORD. 



istic of locomotor ataxia are the lightning-like, " lancinating " pains, which shoot 
like neuralgic pains for some distance along the course of the nerves. They often 
come on in very severe paroxysms, and are absent at other times. There are 
also boring, stabbing pains, which are fixed at one point and have their seat espe- 
cially in the vicinity of the joints ; and finally " constricting pains," which are 
felt most frequently in the back and loins. The well-known " girdle feeling " of 
ataxics — that is, the sensation of a band tightly encircling the trunk, or a tight, 
f s drawn-together " pressure on the lateral portions of the trunk — belongs to the 
latter form of symptoms of sensory irritation. This girdle feeling is manifestly 
due to irritative processes in the region of the lower dorsal or upper lumbar 
nerves. Since it is comparatively quite frequent, and often appears quite early, it 
also has a certain diagnostic significance. 

The tabetic pains also begin in the legs, corresponding to the almost constant 
beginning of the symptoms of the disease in the lower extremities ; but later on 
quite analogous pains sometimes appear in the arms, and in very advanced cases 
we have also observed pains in the region of the occipital nerves and of the 
trigeminus. On the other hand, neuralgic pains in the face, especially in the 
region of the frontal nerve, or in the occiput, or even migraine-like attacks, also 
occur, even in the initial stage of locomotor ataxia, as we have ourselves observed. 
In some cases the lancinating pains in locomotor ataxia may be accompanied by 
the appearance of an eruption of herpes — a condition which at any rate is extremely 
rare. 

Usually much later than the pains appears also a diminution of sensibility 
which can be made out objectively. As a rule, it may be stated that in most, but 
not in all, cases of locomotor ataxia, the sensibility does not remain normal; 
although more marked anaesthesia never appears until the more advanced stages 
of the disease. 

The form of the disturbances of sensibility varies extremely, and no disease 
furnishes so many opportunities for the study of interesting details in the region 
of anomalies of sensation as locomotor ataxia. Our knowledge of the occurrence 
of partial paralyses of sensation especially is very largely based on the examina- 
tion of ataxic patients. The tactile sense suffers in most cases of locomotor ataxia, 
but we can usually make out only a certain blunting of it. Only when the dis- 
ease is far advanced does the patient cease to feel a light touch on the skin. 
The sense of pain is also often abnormal. We sometimes see a pronounced anal- 
gesia, but in other cases there is a very decided sensibility to pain, in spite of a 
defective tactile sensibility. It is a very frequent symptom that, at a pin-prick, 
the patient has at first only a slight and not a painful sensation, and that a few 
seconds later, especially if the prick persist, he suddenly winces and says he feels a 
decided pain. With it there is usually a reflex contraction in the affected leg. 
We usually speak of this symptom as a" delayed conduction of painful sensa- 
tions " or " delayed reflex " ; but it seems to us that the symptom has not yet been 
analyzed carefully enough, and especially that it has not been properly separated 
from the after-sensations, which are also very common in locomotor ataxia. It 
often happens that after a single prick, ataxic patients report at varying intervals 
five or six or more painful after-sensations.* 

If the first sensation is not painful in these cases, it may happen that the 
patient may first say k< Now " at a prick, and soon after " Ow," when he first feels 



* If, while the patient's eyes are shut, we prick the leg and the arm or neck as nearly as possible 
at the same time, the prick on the leg would necessarily be felt much later than that on the arm, if there 
is a delayed conduction of sensory impressions from the leg ; but we have never as yet been able to 
make out this condition with certainty. 



LOCOMOTOE ATAXIA. 



605 



the pain (the "double sensation" of Naunyn, Eemak, and others). Fischer has 
termed a peculiar disturbance of sensibility occurring- in locomotor ataxia, poly- 
aesthesia : the patient asserts, when examined with an aesthesiometer, that he feels 
several (four or five) points, although he was touched with but one. 

Disturbances of the sense of pressure and that of temperature are also quite 
frequently found, especially as partial paralyses of sensation, when the sensibility 
is otherwise well preserved. On the other hand, the special sensations of tempera- 
ture may sometimes be quite well-defined, while in other respects there is quite a 
high degree of anaesthesia. 

The considerable anomalies of the muscular sense, which are often to be made 
out in more advanced cases, have a special interest (see page 479). If the patient 
shuts his eyes, he is often entirely unaware of the situation and position of his 
limbs. He makes a false report as to the direction and extent of passive motions.* 
If the muscular sense in the arms is disturbed, and we put the arms into any 
unusual position, the patient has considerable trouble in bringing the hands together 
with his eyes shut. He gropes about in the air with his arms until he accidentally 
touches one arm with the other hand, and then he feels down this to the hand. 
The action of ataxia and muscular anaesthesia are accordingly combined in these 
cases, but we can not possibly consider the former as a result of the latter ; for 
there are doubtless cases of ataxia — we have ourselves carefully examined such 
with regard to this question — in which the perception of motion and position is 
perfectly normal, in spite of the existence of ataxia. The disturbance of move- 
ments willed, by the loss of muscular sense, is noticed only when the eyes are 
shut. With the eyes open the control by the sense of sight supplies the lack of 
muscular sensibility. Pitres has lately described peculiar attacks of muscular 
rigidity, and attacks of a decided feeling of fatigue in the muscles, apparently 
coming on spontaneously in incipient locomotor ataxia (" crises de courbature 
musculaire "). 

Only in rare and far-advanced cases is there finally a complete anaesthesia of 
the lower, and exceptionally of the upper extremities. We then see also at times 
disturbances of sensibility in the region of the trigeminus, in the skin of the face. 
These disturbances are probably connected with a degeneration of the sensory 
ascending root of the trigeminus, which degeneration has already been observed 
several times at the autopsy (Westphal). 

3. Disturbances of the Eeflexes. — The cutaneous reflexes show no constant 
changes in locomotor ataxia. They are usually approximately normal, but some- 
times they are diminished, especially if there is at the same time a marked disturb- 
ance of sensibility. 

The absence of the tendon reflexes, especially of the patellar reflex, is, how- 
ever, an almost constant sign of locomotor ataxia, and is a sign of the highest diag- 
nostic value. As we have already said, the disappearance of this reflex is one of 
the earliest symptoms of the disease, and is therefore of the greatest significance 
in the diagnosis of initial ataxia. We must now state, however, in opposition to 
our statement in the first edition of this work, that we have ourselves seen some 
cases where all the other symptoms corresponded precisely to locomotor ataxia,f 
but where the patellar reflex remained normal, or was even somewhat increased. 
These, however, are only very rare exceptions, which do not disprove the rule, and 



* We can describe different letters and figures in the air with the patient's extremities, and try 
"whether they can be correctly recognized with the eyes shut. 

+ In such cases, however, we must always be extremely guarded in our diagnosis, and we must 
especially bear in mind the possibility of a confusion between locomotor ataxia and a multiple sclerosis 
which takes an unusual course. 



606 



THE DISEASES OF THE SPINAL COED, 



do not at all contradict our general views as to locomotor ataxia. In individual 
cases the affected fibers, which serve to set free the reflex, may be spared for a long 
time, just as any other characteristic symptom of the disease may, under some cir- 
cumstances, occasionally be absent. We do not know whether the patellar reflex 
may be preserved during the whole course of the disease, but at any rate no case 
of locomotor ataxia with the tendon reflexes preserved, which came to an autopsy, 
has ever yet been published. Concerning the precise anatomical cause of the dis- 
appearance of the patellar reflex, it can be due only to a degeneration in the cen- 
tripetal portion of the affected reflex arc — that is, only in the fibers which belong 
to the territory of the posterior roots. It is in accordance with this that a disease 
of the middle portion of the posterior columns in the lumbar cord (that is, the 
root-zones, see Pig. 87) always seems to be accompanied by a failure of the patellar 
reflex. The direct mechanical irritability of the muscles, especially of the quadri- 
ceps, is almost always retained in locomotor ataxia.* 

4. Disturbances in the Eye and the other Organs of Special Sense. — 
The authority for regarding locomotor ataxia as a combined systemic disease arises 
from the frequency with which certain cerebral symptoms, as well as the spinal, 
are found in it. 

The symptoms in the eyes deserve the first attention. We find disturbances in 
the pupils, of course not in all cases, but still in the great majority of them. The 
pupils are often very much contracted, " spinal myosis," and show no trace of con- 
traction to light, although the well-known changes in the pupils are very manifest 
upon any variation of the accommodation — dilatation of the pupils with approxi- 
mately parallel axes of vision on looking at distant objects, and contraction of the 
pupils with the most marked convergence of the eyeballs on fixing a near object. 
We give this phenomenon, whose precise anatomical cause is not yet known, the 
name of reflex immobility of the pupils with retained mobility on accommodation 
(Argyll Robertson pupils). It is not at all necessary, however, that there should 
also be a myosis, for we not very infrequently find the pupils quite dilated or 
unequal, although we find there is reflex immobility. As we have already said, 
the immobility of the pupils is often a very early symptom, so that it also has a 
diagnostic importance. 

The paralyses of the ocular muscles in locomotor ataxia are also very interest- 
ing. They are usually unilateral, but sometimes bilateral, and often appear even 
at the beginning of the disease, so that diplopia may be the first subjective symp- 
tom of which the patient complains. In every sudden oculo-motor or abducens 
paralysis, coming on without any other cause, we must think of the possibility 
of an incipient locomotor ataxia. It is remarkable that these paralyses in many 
cases disappear permanently and entirely after some time ; but sometimes they 
remain, as we have repeatedly seen, especially in a case with bilateral abducens 
and unilateral oculo-motor paralysis, and also in a case with almost complete 
bilateral oculo-motor paralysis. In the autopsies on such cases we find the 
trunks of the affected nerves and their nuclei markedly atrophic. It seems to 
us very probable, however, that the temporary ocular paralyses in ataxic patients 
depend upon changes in the peripheral nerves of the ocular muscles. 

The third complication in the eyes in locomotor ataxia is optic atrophy. It 
occurs in about ten or fifteen per cent, of all cases, and is usually an initial symp- 



* [From autopsies on cases of combined sclerosis, where the symptoms very closely resembled those 
of locomotor ataxia, but where the patellar reflex persisted until near the close of life, Westphal thinks 
that the patellar reflex disappears only when a special region in the posterior columns is involved in 
the disease. This region lies at the junction of the dorsal and lumbar cords, between the posterior 
cornu and a line running parallel with the posterior fissure, and starting from the angle seen in the 
posterior cornu at the site of the substantia gelatinosa. — Tkans.] 



LOCOMOTOR ATAXIA. 



607 



torn, at a time when the absence of the tendon reflexes, which may usually also 
be noticed, is the only thing", except this, to render the diagnosis of the disease 
possible. The patient complains of diminution of vision ; and the power to distin- 
guish colors, especially green, disappears quite early. On objective examination, 
we find, beside this anomaly in the color sense, usually a limitation of the field of 
vision, and the beginning gray degeneration of the optic nerve can easily be made 
out on ophthalmoscopic examination. The affection sometimes makes little halts 
and slight apparent improvements, but it usually ends with complete blindness. 
The optic atrophy more rarely first appears in the later stages of the disease, when 
all the other symptoms are already fully developed. 

Auditory disturbances are much rarer than those of sight, but they also occur. 
The cause, in at least a part of the cases, is an atrophy of the acoustic nerve. 
Symptoms are also frequently seen which resemble those of Meniere's disease- 
tinnitus, vertigo, and deafness. 

Changes in the senses of taste and smell have been observed only in a few 
cases. 

5. Disturbances in the Bladder, the Rectum, and the Sexual Organs.— 
Difficulty in emptying the bladder is an almost constant symptom in the later 
stages of locomotor ataxia. It sometimes, indeed, appears very early. The patient 
feels the desire to urinate more frequently, there is often a slight involuntary 
micturition, and at other times there is retention of urine, sometimes coming on 
quite suddenly, and in advanced stages there is often complete incontinence. A 
cystitis very often develops as a result of all these disturbances, which may be the 
starting-point of severe cysto-pyelitis and pyelo-nephritis, and thus be the cause 
of death. 

Persistent constipation is also a very frequent symptom of locomotor ataxia, 
the reason for which is, perhaps, to be sought in the defective reflex excitation of 
intestinal peristalsis. The constipation may, in many cases, give rise to great dis- 
tress to the patient, since it sometimes provokes very painful sensations in the 
loins and abdomen. The coccyodynia, which sometimes occurs in locomotor ataxia, 
has already been mentioned (see page 497). Incontinence of faeces occurs quite 
rarely in the last stages of the disease. 

A diminution in the sexual functions is found almost constantly in advanced 
cases. The loss in power is also often one of the initial symptoms. 

6. Symptoms in the Internal Organs. — We see, not very infrequently, in 
locomotor ataxia certain symptoms in the internal organs which are, in part, 
very characteristic, and which, at any rate, are based upon disturbances of inner- 
vation. The most important and the most frequent are the so-called "gastric 
crises." These almost always come on suddenly and paroxysmally, and consist of 
an extremely severe cardialgic pain, which is accompanied by violent vomiting. 
The patient also feels very wretched, and there is often at the same time palpita- 
tion, acceleration of the pulse, vertigo, etc. The attacks last about two or three 
days. Iii many patients they are repeated every few months. As we have said, 
the gastric crises may appear very early. We ourselves know cases where, in 
consequence of severe gastric crises, a severe gastric affection has been falsely 
diagnosticated, in the beginning of the disease. Attacks of diarrhoea, " intestinal 
crises," usually not associated with pain, have also been repeatedly observed. 

We term attacks of severe dyspnoea "laryngeal crises." These, probably, 
depend upon a (reflex ?) spasm of the glottis, and may attain a very alarming 
degree. They are also associated with a severe spasmodic nervous cough. Paraly- 
sis of the laryngeal muscles (crico-arytsenoids) has also been observed. We may 
assume changes in the vagus-accessory nucleus, or in the vagus or recurrent itself 
(Oppenheim), as the anatomical cause of all these symptoms. 



603 



THE DISEASES OF THE SPINAL CORD. 



In a few cases " renal crises " (" arises nephritiques ") have also been described. 
They consist of severe attacks of pain, like renal colic. French authors also 
describe " urethral crises " and " crises clitoridiennes" the paroxysmal appearance 
of voluptuous feelings with a vaginal secretion in women, in the beginning of the 
disease. 

We may mention, finally, that we sometimes see in ataxic patients a constant 
and very great frequency of the pulse, 100 to 120 a minute. We also frequently 
see the combination of locomotor ataxia with aortic insufficiency which has been 
mentioned by some authors. The precise connection between the two affections 
is still uncertain (syphilis ?). 

7. Trophic Disturbances. — In many cases of locomotor ataxia trophic dis- 
turbances are entirely absent. We have already spoken of the occasional appear- 
ance of an eruption of herpes, with severe lancinating pains. In some cases a 
marked exfoliation of the epidermis has been seen, and also a falling out of the 
hair and nails. Sometimes there are small haemorrhages, apparently spontaneous, 
into the skin or into the visible mucous membranes, especially into the conjunc- 
tiva, as we have seen in several cases. 

The peculiar joint affections which occur in locomotor ataxia, and were first 
accurately described by Charcot as " arthropathies tabetiques" have a greater 
interest. The affection is situated most frequently in the knee- and hip-joints, 
more rarely in the ankle- and shoulder-joints. It is usually bilateral, even if it be 
more marked on one side than on the other. We sometimes find abundant serous 
effusions, so that the knee-joint, in particular, may swell up in a monstrous fashion ; 
but we find especially a high degree of arthritis deformans, with marked atrophy of 
the ends of the bones, and with the formation of many osteophytes. Spontaneous 
dislocations and fractures also occur. An affection of the anterior gray cornua, 
which Charcot suspected to be a cause of the articular affection, could not be made 
out in a case examined by us anatomically. We do not believe that the theory of 
an exclusive " nervous-trophic disturbance " can explain the origin of the tabetic 
joint affections. Perhaps we have to do with syphilitic joint affections, and per- 
haps with those of some other more fortuitous (traumatic ?) origin, which are 
rather a complication than a symptom of locomotor ataxia. We believe, however, 
that the unusual intensity and the peculiar form of the anatomical lesion are, 
indeed, directly connected with locomotor ataxia, and are due chiefly to the anaes- 
thesia of the articular surfaces. We saw a case, a short time ago, where an affec- 
tion of the knee-joint developed in a comparatively very early stage of locomotor 
ataxia, which, up to that time, had not been diagnosticated at all. As the patient 
felt no pain at all in his knee, he nevertheless hunted most vigorously through a 
whole autumn, until finally an extremely severe swelling of the knee-joint and an 
actual dislocation of the leg ensued. 

The muscles preserve their normal state of nutrition, except as they take 
part in a general emaciation. Charcot described a case of a combination of loco- 
motor ataxia with genuine progressive muscular atrophy, in which the autopsy 
showed a degeneration of the anterior gray cornua in the spinal cord beside the 
atrophy of the posterior columns. The first report upon a unilateral atrophy of 
the tongue, which sometimes develops quite early in locomotor ataxia, is due to 
the same observer. Nothing definite is known at present as to the origin of this 
peculiar complication. 

In conclusion, it is worthy of note that cases of " mal perforant du pied " 
(ulcerations on the heels or between the toes) have been repeatedly observed in 
locomotor ataxia. 

8. Cerebral Symptoms. — Beside the frequent important disturbances on the 
part of certain cerebral nerves, like the optic and oculo-motor, which have already 



LOCOMOTOR ATAXIA. 



609 



been mentioned, we must mention here the relation between locomotor ataxia and 
progressive general paralysis (g. v.). On the one hand, the symptoms of loco- 
motor ataxia are often present in the course of general paralysis, so that the 
autopsy shows a typical degeneration of the posterior columns (Westphal) ; and, 
on the other hand, it also happens that the whole process begins with a locomotor 
ataxia, which may exist alone for years without any mental symptoms, and then 
only at the close do the symptoms of paralytic dementia, delusions of grandeur, 
dementia, etc., appear. 

The complication of locomotor ataxia with hemiplegia repeatedly occurs. The 
latter depends upon a cerebral haemorrhage or an embolic or thrombotic soften- 
ing, so that it is doubtful whether the two affections have a real connection or 
are merely a chance combination. It seems to us worthy of note that in two 
such cases we saw scarcely any contracture develop in the paralyzed limbs. 

Course and Prognosis. — Although most of the characteristic symptoms of loco- 
motor ataxia develop in almost all cases, still the order and the intensity of their 
onset vary greatly. We have already briefly described the general type of the 
disease which most frequently comes under observation, and many other pecu- 
liarities in its course have been mentioned from time to time. 

We have stated that the initial period is usually characterized, apart from the 
symptoms that can be made out only objectively, such as absence of the patellar 
reflex and reflex immobility of the pupils, by the lancinating pains ; that these may 
differ very much in intensity ; and that the duration of this first stage may vary 
between a few months and ten or twenty years. The optic atrophy, the ocular 
paralyses, gastric crises, vesical disturbances, etc., were mentioned as rarer initial 
symptoms. The passage from the first stage to the second — the stage of ataxia — is 
sometimes very gradual, but in some cases very rapid and sudden. We have 
repeatedly seen such changes, with a sudden change for the worse in the condi- 
tion. If the previous symptoms were slight, the patient dates his disease from 
this point, and says that he was quite suddenly broken down by some cause, and 
that since then he has not been able to walk at all, or else only with difficulty. 
In such cases there is often slow improvement following the sudden change for 
the worse in the condition, which, of course, is not permanent. 

No rules of general value can be given as to the further advance of the dis- 
ease, the invasion of the arms by the ataxia, or the occurrence of the rarer symp- 
toms, like the joint affections, etc. Almost every individual case affords its idio- 
syncrasies, since one group of symptoms is often especially prominent, while 
another is entirely absent, or developed only to a slight degree. On the whole, 
however, we can almost always make out a gradual, even if a very slow, advance 
in the disease. New symptoms appear, the old ones increase, the general condi- 
tion becomes worse, until finally the last stage of the disease comes on. 

Recovery from locomotor ataxia occurs only very rarely, if at all. The treat- 
ment of the affection may, indeed, cause improvement, delay the course of the 
disease, and alleviate single symptoms, but the prognosis is always to be regarded 
as unfavorable, although many patients, especially under favorable external con- 
ditions, may lead a tolerable existence for years. 

Diagnosis. — There is scarcely any other disease of the spinal cord whose diag- 
nosis can in most cases be made with so great certainty and such comparative 
ease as locomotor ataxia. Since locomotor ataxia is a combined systemic disease, 
it affords a definite combination of symptoms such as can occur under no other 
conditions. The diagnosis, therefore, is to be made not from any one single 
symptom, but only from the combination of all and from the whole course of the 
disease. 

The diagnosis of initial locomotor ataxia is especially important. In every case 
39 



610 



THE DISEASES OF THE SPINAL COED. 



of obstinate " rheumatic " pains, or similar pains in the lower extremities, we should 
think of the possibility of locomotor ataxia, and examine the tendon reflexes and the 
pupils. The combination of characteristic pains, absence of the patellar reflex on the 
two sides, and reflex immobility of the pupils, usually makes the diagnosis almost 
perfectly certain ; two of these symptoms, especially if the reflex immobility of the 
pupils be one, make it at least very probable. Ocular paralyses, temporary ptosis, 
or temporary diplopia, may be very important for the diagnosis. With these symp- 
toms, too, we should never forget to think of the possibility of locomotor ataxia, 
and to look for the other characteristic symptoms. Finally, we may recall the 
fact here that the disease may begin with an optic atrophy, and that early gastric 
crises may simulate a gastric affection, or early disturbance in micturition a vesi- 
cal trouble, until careful examination of the other symptoms explains the true 
nature of the disease. 

In the fully developed ataxic stage of tabes the diagnosis is almost always easy, 
and often can be made at the first glance. The history, the characteristic ataxic 
gait, the swaying with the eyes shut, the absence of the reflexes, etc., make the 
diagnosis certain. The diagnosis may be more difficult if we happen to see the 
patient for the first time in the final stage, when actual paralysis has set in, 
when a complicating hemiplegia has arisen, etc. In such cases we must lay 
stress on the development of the disease and find out what characteristic tabetic 
symptoms — pupillary symptoms, absence of patellar reflex, remains of ataxia, or 
pains — can now be discovered. With proper attention and knowledge of the case, 
the diagnosis can even then almost always be made correctly. 

Vertebral affections are to be mentioned first of the diseases which may be 
confused with locomotor ataxia. These also cause, under some circumstances, 
lancinating pains and an absence of the patellar reflex, as a result of compres- 
sion of the spmal roots ; but in these cases the later course of the disease is 
entirely different, apart from the changes in the vertebral column and the absence 
of other characteristic symptoms of locomotor ataxia. The same holds true of 
certain deep-seated tumors in the neighborhood of the spinal cord. We have 
already said that in rare cases a multiple sclerosis may afford similar symptoms 
to locomotor ataxia. In these cases the chief stress in regard to diagnosis is to be 
laid on the ensemble of symptoms and their development. It is of greater 
practical importance that certain toxic nervous diseases may have a great similar- 
ity to locomotor ataxia. Chronic alcoholic neuritis has already been spoken of in 
this connection (see page 550). In these cases, however, the reflex immobility of 
the pupils and the disturbances of the bladder are usually absent, while atrophic 
paralysis may develop later, which never happens in locomotor ataxia. The 
etiological factors are also, of course, to be taken into account. 

Finally, it may be mentioned here that we have twice seen a group of nerv- 
ous symptoms in workmen who have worked many years in tobacco factories, 
which resembled locomotor ataxia in so many points that we might term it " nico- 
tine tabes." The morbid symptoms, which resemble locomotor ataxia, consist of 
painful sensations, absence of the patellar reflex, contracted pupils with reflex 
immobility, and uncertainty of gait ; but the whole type of the disease is distin- 
guished from locomotor ataxia by a peculiar tremor, by a marked increase of the 
cutaneous reflexes, especially in the lower extremities, etc. 

Treatment. — The tedious course of locomotor ataxia demands that the physician 
have at hand a choice of remedies and methods of treatment which he can vary 
according to the predominating circumstances, either to obtain a certain amount 
of improvement by a new way of attacking the disease, or at least constantly to 
kindle the patient's hope and courage anew. 

If syphilis is a possible etiological factor, we regard it as entirely justifiable 



LOCOMOTOE ATAXIA. 



611 



to prescribe first an anti-syphilitic treatment : inunction of fifty to seventy-five 
grains (grm. 3-5) of mercurial ointment a day, with iodide of potassium inter- 
nally. In very many cases this, of course, does no brilliant service — at times the 
disease has even been noticed to grow worse under inunction — but sometimes we 
see distinct improvement. The earlier the treatment is begun, the more is to be 
expected of it. At any rate, we should try whether we can not check the further 
advance of the disease by a methodical and continuous anti-syphilitic treatment. 
When symptoms implying loss of function (Ausfallssymptome) have already 
appeared, we can not, of course, cause them to disappear, for iodine and mer- 
cury can not restore fibers in the posterior columns that have already been 
destroyed. 

If the anti-syphilitic treatment is not indicated, or has been unsuccessful, elec- 
tricity and balneo-therapeutics or hydro-therapeutics deserve the most confidence. 

The electrical treatment consists chiefly of the passage of the ascending con- 
stant current through the spinal cord. The currents must not be too strong, and 
the sittings should take place daily, or every other day. Erb recommends placing 
the medium-sized kathode in the vicinity of the sympathetic, and the large anode 
close to the spinous processes on the other side of the vertebral column, moving it 
at intervals from above downward. This procedure lasts about four or five min- 
utes for each side. We also obtain good results symptomatically wheu there are 
severe pains, vesical weakness, etc., by peripheral galvanization. If we find pain- 
ful points on the vertebral column, as is rarely the case, they should be especially 
treated with the stabile anode. Lately, the treatment recommended by Kumpf 
with the faradic brush has been used several times with good results. This con- 
sists in brushing the skin of the back and the extremities with a strong current 
for five or ten minutes. Every form of electrical treatment, in order to obtain 
results, must be kept up for months. 

Hydro-therapeutics, used rationally, have often resulted in considerable im- 
provement in locomotor ataxia, although they may cause much mischief. Hot 
baths, especially vapor-baths, are often followed by a rapid change for the worse 
— a fact which, unfortunately, we can often observe where vapor-baths have been 
prescribed for patients at the beginning of their disease "for rheumatism." Con- 
tinuous wet packs and severe rubbings are also often accompanied by unfavorable 
results. Tepid half or full baths, however, of 75° to 86° at most (20°-24° R), 
associated with gentle rubbing of the skin, often do good service. Wet com- 
presses, laid about the abdomen or the legs at night, often have a favorable influ- 
ence on the pains. In general, it is a good plan to send well-to-do patients in 
summer to a water-cure establishment which is conducted by an experienced 
director and well managed, but the necessary procedures may also be undertaken 
at home. 

Of the baths whose use is recommended in locomotor ataxia, Oeynhausen- 
Eehme has the greatest reputation, and the best results to show. Many ataxics, of 
course, come back from Eehme just as they went; but, in advising a bath, Eehme is 
always the first to be considered. We may refer to what was said on page 591 as 
to the establishment of artificial Eehme baths. The baths in Nauheim have a 
very similar composition. The indifferent thermal baths, Teplitz, Wildbad, and 
Eagaz, formerly much in favor, have at present lost their reputation in locomotor 
ataxia. Mud baths and iron baths — Pyrmont, Driburg, Cudowa, Elster, Franzens- 
bad — may sometimes act favorably. 

Beside the methods of treatment so far mentioned, there are still a number of 
internal remedies, the use of which seems sometimes to be of advantage. The 
chief one to be mentioned is nitrate of silver, first recommended by Wunderlich, 
one-sixth-of- a-grain pills (grm. 0*01), at first three, gradually increasing to six a 



612 



THE DISEASES OF THE SPINAL CORD. 



day, before meals ; and ergotine,* one-grain pills (grm. 0*05), three to six a day; 
we may also try iodide of potassium, phosphorus, arsenic, etc. All these remedies, 
especially the two first named, may be used for a long time, and, with interrup- 
tions, even for years. 

Finally, we must mention here nerve-stretching, usually stretching of the 
sciatics, which for a short time was practiced on many ataxic patients as a result 
of a somewhat too sanguine recommendation on the part of Langenbuch. Since, 
however, experience has taught us that nerve-stretching, in spite of some apparent 
successes, scarcely ever exerts a permanent favorable action, and is also not wholly 
without danger, the operation has been almost entirely given up in locomotor 
ataxia. It may still be tried in those cases where we have unusually severe attacks 
of pain in the region of definite nerves. 

Symptomatically, the same remedies are to be considered as were mentioned in 
the treatment of chronic myelitis. We try to alleviate the pains by narcotic 
embrocations and bandaging the legs. Ergotine, bromide of potassium, quinine, 
and salicylic acid sometimes procure temporary relief, but in bad cases morphine 
is indispensable. We try to remove the constipation by prescriptions as to diet, or 
by mild cathartics, like the bitter waters, tamarinds, and rhubarb, and by enemata. 
Morphine is the best remedy in the gastric and laryngeal crises. Cystitis and bed- 
sores must be treated according to the rules in general use. 

In regard to the patient's general manner of life, we must warn him against 
any physical or mental over-exertion, prescribe a prudent but strengthening diet, 
and enjoin good air, a country residence in summer, or perhaps the Alps or sea 
air. The earlier we get the patient under treatment, the more persevering and 
careful should we be in our treatment, because then we can still hope for success. 
In old and far-advanced cases we must confine ourselves to a purely symptomatic 
treatment. 

APPENDIX. 

HEREDITARY ATAXIA. FRIEDREICH'S FORM OF LOCOMOTOR ATAXIA. 

A peculiar and rare disease, which has a certain similarity to locomotor ataxia, 
was first described by Friedreich under the name of " hereditary ataxia. " The 
affection almost always occurs in several children of the same family, and develops 
in youth, somewhere between twelve and eighteen years of age. The female 
members of the family are decidedly more often affected than the male. A stage 
of initial pains is usually absent. The disease begins with a pronounced ataxia of 
the legs, which usually very soon passes to the arms. The tendon reflexes disap- 
pear in most cases, but the sensibility of the skin and muscles remains perfectly 
intact, a fact which may properly be an evidence for the independence of ataxic 
disturbances from anomalies of sensibility. The vesical functions also remain 
completely normal for a long time. Disturbances of vision have not been observed 
up to the present time, but in the further course of the disease a peculiar disturb- 
ance of speech arises, which is probably due to a disturbance of co-ordination in 
the muscular movements of the lips and tongue necessary in speaking. Fried- 
reich has also sought to interpret the nystagmus which appears by the hypothe- 
sis of an "ataxic nystagmus." The disease lasts for a very long time, for many 
years, and finally leads to complete paralysis, contractures, and atrophy of the 
paralyzed muscles. 

* There is only an apparent contradiction in the fact that, in spite of the occurrence of an " ergotine 
tabes " (vide supra), ergotine is also used as a remedy against tabes. It may very well be that the 
same remedy, which in large doses causes certain systems of fibers to atrophy, may in smaller doses 
have some favorable (irritating) action on them ; but we must always be cautious in the use of ergotine. 



AMYOTROPHIC LATERAL SCLEROSIS. 



613 



The anatomical examination of the spinal cord has so far shown in all cases a 
combined fascicular disease of the posterior and lateral columns. In the case 
reported by Kahler and Pick this disease could be demonstrated as a combined 
systemic disease. It affected the lateral pyramidal tracts, the lateral cerebellar 
tracts, the fundamental bundle of the posterior columns, and the columns of Goll. 
P. Schultze has lately taken the same views in regard to the anatomical lesion. 

The disease is incurable ; at least, all the attempts at treatment up to the pres- 
ent time have been unsuccessful. 



CHAPTER VII. 
AMYOTROPHIC LATERAL SCLEROSIS. 

Amyotrophic lateral sclerosis is a disease perfectly sharply denned both in its 
clinical and its pathological aspects, and in the majority of cases it may be diag- 
nosticated with great certainty, even during the patient's life. For the first accu- 
rate knowledge of it we must thank Charcot, who published in 1869, in company 
with Joffroy, his first observations upon such cases, and who in 1874 was able to 
give quite a complete description of the disease ; but an exact knowledge of amyo- 
trophic lateral sclerosis was first made possible by Flechsig's investigations upon 
the course of the paths of conduction in the spinal cord. According to these, it 
may be stated with perfect certainty that the affection is to be regarded as a sys- 
temic degeneration of the pyramidal tract throughout its whole extent, or at least 
in certain portions of it, combined with atrophy of certain nerve-nuclei in the 
medulla oblongata. It is still entirely unknown to us what causes bring on the 
disease of these nerve-fibers and the cells belonging to them. In individual cases 
we can not usually make out any definite serological factor at all. Severe physi- 
cal exertion is sometimes claimed to be a cause for the disease. It occurs chiefly 
in persons in youth and middle life, between twenty-five and forty-five. The 
male sex seems to be decidedly more prone to the disease than the female. 

Pathological Anatomy. — In the typical cases of amyotrophic lateral sclerosis, 
which come to autopsy in the last stage of the disease (initial cases have not yet 
been examined anatomically), we find in the spinal cord a perfectly sharply 
defined degeneration or " sclerosis " of both pyramidal tracts, and a considerable 
atrophy of the corresponding large ganglion-cells in the anterior gray cornua, 
especially in the external portion. The degeneration of the pyramidal tract is to 
be made out either in the two lateral columns alone, or, if there is an anterior 
pyramidal tract also, in one or both anterior columns (see page 504 and Figs. 65 
and 66). It occupies precisely the same area on cross-section of the cord as the 
region of the pyramidal tract ; the boundaries of which tract have been determined 
by the distribution of secondary descending degeneration {vide infra), and by 
the results of the history of development. Beginning in the lowest part of the 
lumbar cord, it may be traced upward to the pyramids of the medulla, and some- 
times, but not always, still farther through the pons and the crura to the internal 
capsule. In some cases examined lately by Charcot and Marie the degeneration 
extended even to the central convolutions, whose large motor ganglion-cells also 
showed a pronounced atrophy. Of the greatest clinical importance, however, is the 
already-mentioned co-existing disease of the motor ganglion-cells in the anterior 
cornua of the spinal cord and the disease of certain nerve-nuclei in the medulla 
oblongata, especially the hypoglossus nucleus, the vagus-accessory nucleus, etc. 
From these cells, which are inserted into the motor tract, the degeneration passes 



614 



THE DISEASES OF THE SPINAL CORD. 



on toward the periphery, in the affected nerve-trunks (hypoglossus, etc.), or in the 
anterior roots belonging to them. It is difficult to make out atrophied fibers in 
the peripheral nerves, and up to the present time they have not always been 
looked for with sufficient care, but it can scarcely be doubted but that the affected 
motor fibers, which are processes of the atrophied ganglion-cells, are likewise to 
be found in a condition of degeneration. Finally, the muscles show a consid- 
erable atrophy, as is plainly manifest even during the life-time of the patient. 
Their volume is much diminished ; many muscles (for details vide infra) finally 
almost wholly disappear, so that in their place there is little left but connective 
tissue and fat. In the other muscles we find, beside a number of normal fibers 
still preserved, many very small fibers, and also some which have lost their trans- 
verse striation and show a granular or fatty degeneration. The nuclei of the 
sarcolemma are usually increased, and the interstitial fat tissue is often, but not 
always, abundantly developed. 

We accordingly see that the anatomical basis of amyotrophic lateral sclerosis 
is a more or less completely isolated disease of the great motor cortico-muscular 
conducting tract from the center to the periphery. The process is to be regarded 
as a simple degenerative atrophy. Fiber after fiber becomes diseased and atro- 
phies. We do not know where the process begins, whether at one definite spot, 
whence it extends upward and downward, or whether the fibers throughout their 
whole extent, with the corresponding ganglion-cells and muscular fibers, are 
attacked at the same time. Perhaps different possibilities are to be regarded in 
these cases, which may explain the many variations in the clinical course. At 
any rate, the different portions of the system may become diseased in a varying 
order, and the further extension of the disease may vary in its rapidity. The 
spinal and the bulbar diseases are perfectly analogous to each other and are co- 
ordinated. Both affect portions of the same system ; one belongs to the muscles 
of the extremities, the other to the muscles of the face, tongue, etc. The nerve- 
nuclei in the medulla are to be regarded as precisely analogous to the anterior 
gray cornua. The destruction of the nerve-fibers is always the primary process, 
the increase of the interstitial connective tissue and the slight changes in the ves- 
sels are a secondary, accidental process. 

Beside the typical cases of amyotrophic lateral sclerosis, there are also, quite 
rarely, combined and transitional forms. Beside the degeneration of the pyram- 
idal tract, an affection of the posterior columns and a degeneration of the lateral 
cerebellar tract have also occasionally been found. 

Clinical History. — In all typical cases the clinical symptoms give a perfectly 
characteristic type of disease, limited strictly to the motor sphere, corresponding 
to the perfectly systemic anatomical lesions just described. 

The first signs of the disease almost always begin in the arm. The patient 
notices a difficulty in working, and becomes easily tired. The weakness of the 
arm gradually increases, and finally, usually some months later, involves the 
other arm. A wasting of certain muscles, which gradually increases and becomes 
more extensive, is now often noticed by the patient. About six months or a year 
later, symptoms appear in the lower extremities. The gait becomes stiff and 
uncertain, the patient gets tired more easily, and quite a marked tremor of the 
legs often comes on, apparently spontaneously. 

If we now examine the patient carefully, the type of the disease is usually 
perfectly plain. We notice, first in the upper extremities, a very pronounced 
and more or less extensive muscular atrophy. This is usually most marked 
where it begins — namely, at the thenar and hypothenar eminences. The inter- 
ossei are also plainly atrophied, and the muscles on the extensor side of the 
forearms. The flexors of the hand and the fingers remain intact longer. In 



AMYOTROPHIC LATERAL SCLEROSIS. 



615 



the upper arm the triceps and the deltoid are usually the most atrophied, and 
later, and to a less degree, the biceps and the muscles of the shoulder. We find 
a functional disturbance of the muscles — a paresis — corresponding to the degree 
of atrophy. The functional capacity depends upon how much muscle is left, and 
only with a complete disappearance of the muscle is there a complete loss of the 
corresponding motion, but a marked paresis can sometimes be noticed in muscles 
which are not yet much atrophied. The electrical excitability in the muscular 
fibers still preserved is normal. The strength of contraction of the muscle irri- 
tated by the faradic current is therefore proportional to the amount of muscular 
substance still present. In the much-atrophied muscles the effects of irritation 
are finally very slight, and then we can always make out a distinct reaction of 
degeneration in the degenerated muscular fibers that are still left, especially in 
the ball of the thumb. We can scarcely ever make out with certainty a loss of 
excitability in the nerve-trunk, probably because here a greater number of normal 
fibers are always preserved. 

The examination of the tendon reflexes is very important. They are invari- 
ably much increased, even from the early stages of the disease. We obtain 
vigorous reflex contractions from a gentle blow on the tendons of the biceps and 
the triceps, and on the lower ends of the bones of the forearm. These are of 
diagnostic importance, because they never occur in this way in ordinary " pro- 
gressive muscular atrophy" — that is, that disease in which the degeneration 
extends merely from the muscles to the motor ganglion-cells in the anterior 
cornua, while the lateral motor-tracts remain free {vide infra). In the later 
stages of the disease marked contractures in the arms and hands sometimes, but 
not always, develop. The sensibility of the skin and deeper parts, however, 
remains absolutely normal. 

The first morbid symptoms usually develop in the lower extremities some 
months later than in the arms. The pure spastic symptoms are here remarkably 
prominent, while the muscular atrophy is late in its development, and is but 
slight. The legs become stiff, and oppose considerable muscular resistance to 
attempts at passive motion, but the crude strength of the muscles is decidedly 
below the normal. There is an obvious paresis, although there is, as it seems, 
hardly ever a complete paralysis of the legs ; and the disturbance of motion, at 
any rate, is considerably increased by the spastic symptoms (see a later chapter). 
These symptoms depend mainly upon the great increase of the tendon reflexes. 
The patellar reflex is very vigorous, and we often find a marked and persistent 
ankle clonus. The patient can still walk quite a distance, but the gait is, of course, 
difficult and laborious. The patient walks with short, slow, dragging steps— the 
spastic-paretic gait. The sensibility also remains absolutely normal in the legs. 
The cutaneous reflexes show no striking changes. Disturbances in micturition 
are also entirely absent. The bowels may be somewhat costive, but are otherwise 
normal. 

After the condition has lasted for some time (a year or two) in this form — 
muscular atrophy and increased tendon reflexes in the upper extremities and 
spastic paresis in the lower — and has slowly grown worse, bulbar symptoms come 
on in the third and last stage of the disease. The speech gradually becomes more 
indistinct, and there is difficulty in swallowing. If we examine closely we find 
the lips atrophied, so that puckering the mouth, whistling, etc., are difficult. We 
also notice a decided atrophy of the tongue. Its surface is uneven, and we notice 
more or less marked fibrillary twitchings of single muscular bundles. The sensi- 
bility is also normal here. We sometimes find a vigorous masseter reflex on 
striking the lower jaw, analogous to the increased tendon reflexes in the extremi- 
ties. If the patient has trouble in taking food, from difficulty in swallowing, the 



616 



THE DISEASES OF THE SPINAL COED. 



state of the general nutrition soon becomes worse. Kespiratory disturbances are 
usually the final immediate cause of death, if an intercurrent disease, like inhala- 
tion pneumonia, etc., does not previously put an end to the patient's melancholy 
condition. 

The picture * of amyotrophic lateral sclerosis just sketched accords very well 
with the pathological lesions. As the degeneration affects the main motor tract 
exclusively, the clinical symptoms are also limited entirely to the domain of 
motility. The associated affection of the anterior gray cornua explains the occur- 
rence of muscular atrophy, while the degeneration of the lateral columns must 
be made answerable for the paresis, independent of the atrophy, and for the 
spastic symptoms. The increase of the tendon reflexes, whose reflex arc passes 
through the anterior cornua, forces us to suppose that the disease in the lateral 
columns precedes the degeneration in the anterior cornua, as this increase is seen 
especially in the lower extremities ; for manifestly there can be no longer any 
reflex in muscular fibers whose special ganglion-cells are already atrophied. The 
increased reflexes are seen only in muscles which are composed, at least in part, 
of normal fibers. The bulbar symptoms are dependent upon the degeneration of 
the nerve-nuclei in the medulla. 

The diagnosis of the disease is usually easily made. Its typical course, the 
muscular atrophy with co-existing increased tendon reflexes, the complete absence 
of sensory or vesical disturbances, and the final appearance of bulbar symptoms, 
are chiefly to be considered in diagnosis. Confusion may arise from the fact that 
tumors or myelitis may for a long time have a similar localization, as in the gray 
matter of the cervical cord, and therefore provoke analogous symptoms ; but in 
such cases the later course is almost always different, and thus a subsequent diag- 
nosis can be made correctly. 

The prognosis of amyotrophic lateral sclerosis must be regarded as absolutely 
unfavorable. The disease advances slowly, but unceasingly, and usually leads to 
death in a few years. Only in a few cases, occurring in early youth (Seelig- 
miiller), does the disease seem to come to a stand-still. 

We can, therefore, expect but slight results from treatment. At most we can 
perhaps check the advance of the disease by an electrical treatment, kept up with 
very great patience and perseverance. 



CHAPTEE VIII. 
PROGRESSIVE (SPINAL) MUSCULAR ATROPHY. 

Preliminary Remarks and Pathological Anatomy.— Few diseases of the spinal 

cord have undergone such different conceptions and significations in the course 
of time as progressive muscular atrophy. The reason for this lies chiefly in the 

* Leyden has disputed the propriety of regarding amyotrophic lateral sclerosis as a special form of 
disease, "because the same anatomical lesion also occurs in ordinary progressive bulbar paralysis {vide 
infra). He especially opposes Charcot's claim that the contractures in the arms and legs reported by 
him are characteristic of amyotrophic lateral sclerosis. The disease does not, in fact, depend upon 
the contractures, but upon the increase of the tendon reflexes, which was also present in Leyden's 
cases. We have ourselves made an autopsy on a case only a short time ago, in which the diagnosis 
of an amyotrophic lateral sclerosis was made merely from this symptom and the muscular atrophy, in 
spite of the absence of all special contractures, and the diagnosis was confirmed by the autopsy. 
For further details compare our remarks on the relations between amyotrophic lateral sclerosis and 
progressive muscular atrophy and bulbar paralysis in the chapter which treats especially of the latter 
disease (see the diseases of the medulla oblongata). 



PROGRESSIVE (SPINAL) MUSCULAR ATROPHY. 617 



fact that its main symptom, the progressive atrophy of the voluntary muscles, 
may be found in many totally distinct diseases, and hence has given rise to con- 
stant confusion and mistakes. If, at the present time, we read the older and even 
a part of the newer literature on this subject, we find everywhere a mixture of 
different cases, not at all of the same disease, and only the latest accurate clinical 
and anatomical methods of investigation have enabled us to bring at least some 
order out of this chaos. 

Except for a few earlier observations, Duchenne and Aran, in 1849 and 1850, 
gave the first good description of progressive muscular atrophy. The French 
observers, therefore, at present speak of the disease, in distinction from other 
similar affections, as "atrophie musculaire progressive, type Duchenne- Aran." 
A short time after, in 1855, Cruveilhier, on the ground of a positive lesion on 
autopsy, first pronounced the opinion that a disease of the gray matter in the 
spinal cord was to be regarded as the special anatomical cause of the disease. 
Since then a tedious dispute has been carried on, and even in part kept up to the 
present time, as to whether, in fact, the disease has its seat in the spinal cord, or 
rather in the muscles themselves — a dispute which was necessarily without results 
for a long time ; the more because the actual pathological basis was very scanty, 
and because the data of examinations completely contradicted one another, owing 
to the confusion between different forms of morbid processes which did not belong 
together at all. The spinal nature of the disease was proved especially by the inves- 
tigations of Lockhart Clarke, and Charcot, while in Germany Friedreich in par- 
ticular has of late asserted its myopathic origin. 

In our opinion there can no longer be any doubt * of the fact that there is 
a perfectly clearly defined disease, whose chief clinical symptom consists of a 
very slow but constantly progressing atrophy of the muscles, following a cer- 
tain type, while anatomical examination shows a degenerative atrophy, not only 
of the affected muscles, but also of the corresponding peripheral nerve-fibers, 
anterior root-fibers, and motor ganglion-cells in the anterior cornua of the spinal 
cord. We are, therefore, right in separating this disease, as a " spinal form of 
progressive muscular atrophy," from those cases where there is also the develop- 
ment of an independent progressive atrophy of the muscles, but where the affec- 
tion always remains to the last confined to the muscles, and never invades the 
motor nerves and the spinal cord. These last-named cases form the pure muscu- 
lar atrophies, which correspond to the types of the " hereditary or juvenile muscu- 
lar atrophy or pseudo-hypertrophy" (see the appendix to this chapter). The spi- 
nal form of progressive muscular atrophy, with which we have to do here, is 
undoubtedly nearly allied to " amyotrophic lateral sclerosis," described in the pre- 
vious chapter ; but although in the latter the whole pyramidal motor tract may be 
degenerated, and the lateral pyramidal tracts in the cord are in particular always 
affected, in " progressive muscular atrophy " the degeneration, as we have said, is 
confined to that portion of the motor conducting tract which extends from the 
ganglion-cells of the anterior cornua to the muscular fibers themselves. The 
further central prolongation of this tract, however — that is, the lateral pyramidal 
tract — remains perfectly normal. It is very improbable that this difference in the 
extent of the anatomical localization is the principal distinction between the two 
diseases named. In their eetiological relations the two diseases, and also progres- 
sive bulbar paralysis (vide infra), are identical. The clinical distinctions due to 
the different anatomical localization are, however, of sufficiently marked promi- 

* To the cases already published we can add a recent observation of our own, on a case of progres- 
sive muscular atrophy, involving the upper extremities chiefly, with almost complete atrophy of the 
ganglion-cells in the anterior cornua, although it was not followed by a corresponding co-existing 
degeneration of the lateral pyramidal tracts. 



618 



THE DISEASES OF THE SPINAL COED. 



nence to justify, at least provisionally, a special description of progressive muscular 
atrophy and of amyotrophic lateral sclerosis. 

The precise anatomical lesion in progressive (spinal) muscular atrophy is as 
follows : 

In the spinal cord, most marked usually in the cervical cord, we find the ante- 
rior gray cornua very small; the ganglion-cells have wholly or largely disap- 
peared, and those remaining are atrophied ; and the neuroglia is changed to a fine 
fibrous tissue, sometimes studded with spider-cells ; but the lateral columns, espe- 
cially the pyramidal tracts — that is, the portion of the motor conducting tract cen- 
tral to the ganglion-cells of the anterior cornua/ — are perfectly normal. The 
anterior roots and the affected motor fibers in the peripheral nerves are also atro- 
phied, although in the nerve-trunks the discovery of degenerated fibers mixed 
with many other normal fibers is not perfectly easy. In the muscles the atrophy 
is, of course, still more noticeable on a post-mortem examination than on examina- 
tion during life. The muscles most affected are reduced to small, pale, and flabby 
bundles, in which fat and connective tissue outweigh the proper muscular tissue. 
On histological examination, we find in many fibers a simple atrophy — that is, a 
very considerable diminution, but with the transverse striation still retained ; but 
in many other fibers we run across the signs of a degenerative atrophy — fatty and 
waxy degeneration of the muscular fibers, a splitting longitudinally or trans- 
versely, etc. The interstitial connective tissue is always increased, the muscular 
nuclei are increased in number, and we often find quite a deposit of fat between 
the fibers which are still preserved. 

So far the actual lesion. In comprehending it, the only difficulties arise from 
the questions as to the mode of development, and as to the reciprocal dependence 
of the different disturbances. Is the atrophy of the anterior cornua to be regarded 
as primary, and the atrophy of the nerves and muscles as a secondary descending 
degeneration ; or does the process begin in the muscles, and extend upward from 
them to the spinal cord; or, finally, do we have to do with an approximately 
simultaneous degeneration of the whole motor portion affected ? These are 
questions to which at present no definite answer can be given. Many reasons seem 
to us to favor the belief that the degenerative process begins in the last terminal 
branches of the motor nerves, and from these ascends gradually to the spinal cord. 
This, however, is not yet proved, and possibly the starting-point of the disease and 
its further extent may differ in different cases. 

iEtiology and Clinical History. — Progressive muscular atrophy is an extremely 
slow and chronic disease from the beginning. We often can not find any 
setiological factors which seem to favor its development, but in a good many cases 
the first symptoms follow an immoderate muscular exertion. Thus we see the 
first signs of muscular weakness corning on, for example, after continued thrash- 
ing, hard washing, and similar severe physical toil. A hereditary predisposition is 
reported as common by most observers, but it is at present certain that most cases 
of this " hereditary muscular atrophy " belong, not to the spinal, but to the 
myopathic form (vide infra). It also seems to us to be very probable that the 
number of most of the other aetiological factors reported is to be explained, for 
the most part, only by erroneously reckoning other forms of atrophic processes 
with genuine progressive muscular atrophy. We refer especially to the alleged 
origin of this disease from injuries, from acute diseases, like typhoid and diph- 
theria, or from syphilis. 

The disease begins, by far the most frequently, in the upper extremities, and 
especially, as it seems, in the right arm, but sometimes in the left, or in both arms 
at once. As a rule, it begins with an atrophy of the short muscles of the thumb 
and of the hypothenar eminence, which is accompanied by a corresponding dis- 



PROGRESSIVE (SPINAL) MUSCULAR ATROPHY. 619 



turbance of function. Any other symptoms, especially disturbances of sensibility, 
parsesthesia, or pain, are usually entirely absent. The atrophy usually affects the 
abductor pollicis brevis first, and then the opponeus and the adductor. We notice 
very early the characteristic sinking- in and flattening of the ball of the thumb, 
and the abnormal position of the thumb, which is persistently approximated to 
the second metacarpal bone — the " ape hand. " At the same time, or a little earlier 
or later, the interossei begin to atrophy, which is recognized by the sinking in of 
the interosseous spaces and the increasing incomplete extension of the terminal 
phalanges of the fingers. The atrophy of the lumbricales causes a visible flatten- 
ing of the hollow of the hand. If the disturbance in the function of the interossei 
has reached a certain degree, the same claw-like position of the fingers appears, as 
we have already learned to recognize in ulnar paralysis (see Fig. 77), due to the 
contracture of the antagonist of the interossei, the extensor communis digitorum. 

In the further progress of the disease the atrophy extends either to the muscles 
of the forearm, or, what is not at all rare, it jumps over these and attacks the 
muscles of the shoulder, usually the deltoid first. In the forearm it is usually the 
muscles on the extensor side which are first attacked, the abductor and extensor 
longus pollicis, and only later the supinators, flexors, etc. In the upper arm the 
deltoid almost always atrophies first, and then the biceps, while the triceps may 
remain intact for a comparatively long time. Sooner or later the muscles of the 
trunk are often added to the list, the trapezius first usually, then the pectorals, 
the rhomboidei, and the latissimus dorsi. The disturbance of function caused 
by the atrophy of all these muscles is readily apparent from what was said in 
the chapter on the different forms of paralysis. In advanced cases the arms hang 
down laxly by the two sides of the trunk. Only with the greatest difficulty, if it 
all, can the patient do anything with them, either dress or undress ; but he some- 
times learns to help himself, at least in some degree, by throwing movements, by 
bending his body to meet anything, by using his mouth in taking hold of things, 
etc. Quite rarely the atrophy finally attacks the muscles of the neck. The 
severest respiratory disturbances may be excited by an implication of the dia- 
phragm and the other muscles of respiration. 

The time which elapses before the gradual appearance of the more marked 
disturbances of function is almost always very long. Years may elapse before 
the atrophy extends from the little muscles of the hand to the other muscles of 
the arm. In the muscles of the legs the first signs of atrophy almost always 
develop very late if at all. The arms are often perfectly useless when the patient 
can still walk for hours. Of course there are some exceptions to this rule. In 
the arms themselves, too, the process does not always develop in the way described 
above. Thus we not very rarely see the affection begin in the scapular muscles or 
the deltoid, and from this point the atrophy involves the muscles of the hand or 
of the upper arm. The muscles of the trunk, the pectorals, and the muscles of 
the back, are much more rarely the starting-point of the disease, and in only a 
very few cases have we been able to make out that the disease began in the legs. 
It is worthy of note that in such abnormal cases the muscles first affected were 
sometimes, but not always, subjected to extraordinary demands in carrying loads, 
etc. 

Beside the atrophy, and the loss of function that runs parallel to it, we must 
mention some other changes in the muscles. The fibrillary muscular twitchings 
are often very striking. A constant tremor and wave of the muscle may be pro- 
voked by them. In some cases they are weak and only rarely noticed. They 
usually become vigorous if one irritates the muscle mechanically by a blow. 
The electrical excitability of the diseased muscles varies, inasmuch as it depends 
entirely upon the number of normal fibers still preserved in the muscle. Since 



620 



THE DISEASES OF THE SPINAL COED. 



the atrophy affects only one fiber after another, the faradic and galvanic excita- 
bility decrease gradually, and are lost completely only when the greatest part of 
the muscle is destroyed. On careful testing, we can then, however, almost always 
make out a decided reaction of degeneration in single muscles that are much dis- 
eased, especially in the form of the so-called partial reaction of degeneration : the 
excitability of the nerves is retained, but the contractions in the muscles them- 
selves seem very slow, and the anodic closure contractions (AnSZ) predominate 
(see page 521.) 

In many cases there is an increase of the fatty tissue at the same time with 
the atrophy of the muscular substance, which often makes it very hard to judge 
of the atrophy ; but the loss of function in the muscles, the diminished electrical 
excitability, and the peculiar soft feeling which atrophied muscles have when 
covered with fat, reveal the true condition of things. Other trophic disturbances 
in the skin are usually entirely absent, but they are sometimes seen. In a few 
cases a spontaneous pemphigoid formation of bullae has been observed, especially 
in the hands. The skin sometimes becomes thick and fissured, and the nails 
become brittle, grooved, and greatly curved. The coldness and cyanosis of the 
skin sometimes seen are due perhaps to vaso-motor disturbances, but at any rate 
we must also consider the disturbance of circulation which is due to the lack of 
muscular movements. 

The examination of the tendon reflexes is of great diagnostic importance. While 
they are invariably decidedly increased in the upper extremities in amyotrophic lat- 
eral sclerosis, they are entirely absent in genuine progressive muscular atrophy, a 
condition which is easily explained by the atrophy of the motor ganglion-cells 
belonging to the reflex arc, or by the atrophy of the centrifugal motor fibers. 
Since no degeneration of the lateral pyramidal tract precedes this atrophy, it goes 
without saying that the preceding increase of the tendon reflexes, characteristic 
of amyotrophic lateral sclerosis, is also absent. In the lower extremities the patel- 
lar reflex is retained as long as the disease spares the legs, but it is not increased. 
If the atrophy involves the legs, the patellar reflex is usually lost. 

In distinction from all these manifest disturbances in the motor region, the 
sensibility of the skin and deeper parts remains perfectly preserved. There are 
also never any anomalies in the functions of the sphincters of the bladder or 
rectum. 

In many cases the affection finally invades the muscular region innervated 
from the medulla; the symptoms of "progressive bulbar paralysis " {vide infra) 
are added to those of progressive muscular atrophy. This combination of spinal 
and bulbar disease appears, as we have previously shown, as a rule, in amyotro- 
phic lateral sclerosis, and even after the disease has lasted a comparatively short 
time. In genuine progressive muscular atrophy the bulbar symptoms usually 
develop, if at all, only after the disease has gone on for years. Then the speech 
begins to become indistinct, from the atrophy of the tongue, swallowing is difficult, 
and the patient finally succumbs to increasing inanition or to respiratory disturb- 
ances. In their principal characteristics the muscular atrophy of the extremities 
and the bulbar symptoms are precisely analogous phenomena, inasmuch as the 
nerve-nuclei in the medulla have precisely the same significance for the muscles 
of the tongue, the pharynx, and the face, as the anterior gray cornua of the cord 
have for the muscles of the trunk and the extremities. In many cases, however, 
bulbar symptoms do not develop at all, since the patients die before then of some 
intercurrent disease. 

Diagnosis. — The diagnosis of progressive muscular atrophy can easily be made 
if we confine ourselves strictly to the definition of the disease, and do not confuse 
it with other affections in which the muscular atrophy is only a symptom which 



PRIMAEY MYOPATHIC FORMS OF MUSCULAR ATROPHY. 621 



under some circumstances may have an entirely different origin : muscular atro- 
phies in extensive diffuse myelitis, in tumors, and in the formation of cavities in 
the cord, in multiple neuritis, as a result of articular affections (see the chapters 
on acute and chronic inflammations of the joints), etc. We should consider espe- 
cially the typical course of the affection in most cases of genuine progressive mus- 
cular atrophy, its beginning in the upper extremities, the small muscles of the 
hand, or more rarely the muscles of the shoulder and upper arm, its slow advance, 
the peculiar "individualization" of the atrophy— that is, the affection of some 
muscles while other neighboring muscles remain completely normal — and, finally, 
the absence of all disturbances of sensibility or of the sphincters. Progressive 
muscular atrophy is doubtless nearly allied to amyotrophic lateral sclerosis, but the 
latter is distinguished by its more rapid course, and especially by the increase of 
the tendon reflexes due to the affection of the lateral columns, and the correspond- 
ing appearance of spastic symptoms in the legs. The differential diagnosis between 
the spinal and the myopathic, juvenile muscular atrophy, will be described in the 
appendix to this chapter. 

The prognosis of progressive muscular atrophy is to be regarded as absolutely 
unfavorable. The disease appears comparatively benign only in its frequently 
very slow advance, since it may last for ten or fifteen years, or even longer. As 
we have already said, the fatal termination at last appears from some intercurrent 
disease, or as a result of the final appearance of dangerous bulbar symptoms, 
paralysis of deglutition and respiration. 

The results of treatment are accordingly very slight. An electrical treatment, 
continued for months and years with very great perseverance and persistence, can 
alone produce a little improvement or check the advance of the atrophy somewhat. 
Temporary improvement may also sometimes be attained by a methodical massage 
of the muscles and a rationally conducted gymnastic treatment. In other respects, 
the treatment must be purely symptomatic. 

APPENDIX. 

THE PRIMARY MYOPATHIC FORMS OF MUSCULAR ATROPHY. 

(Hereditary or Juvenile Forms of Muscular Atrophy. Pseudo-hypertrophy of the Muscles. Pseudo- 
hypertrophic Muscular Paralysis.) 

Beside the spinal form of progressive muscular atrophy, just described, there 
are also morbid conditions of the muscles, which develop exclusively in the mus- 
cles themselves, independently of any discoverable affection of the spinal or 
peripheral motor nerve-tracts, and which also lead to a very considerable atrophy 
and a corresponding disturbance of function in them. Beside this anatomical dis- 
tinction, which is still more sharply pronounced in the special form of the disease 
of the muscles {vide infra), an essential clinical distinction between the spinal 
and the myopathic forms of muscular atrophy is shown by the fact that, with few 
exceptions, the myopathic form appears in youth, and often even in childhood, and 
that it very often attacks several members of the same family. We may, therefore^ 
imagine that a congenital defective predisposition of the muscular system is the 
chief cause of myopathic muscular atrophy. 

The form of this class of muscular diseases longest known is the so-called 
pseudo-hypertrophy of the muscles, a disease in which the actual atrophy of the 
muscular fibers is in part so concealed by an increase of the interstitial fatty tissue 
that the atrophied muscles show even an increase of volume. Griesinger in 1864 
gave the first accurate description of this condition in Germany, while Duchenne 
first called attention to the disease in France, and in 1868 was able to give a very 



622 



THE DISEASES OF THE SPINAL CORD. 



complete description of the clinical aspect of the disease. M. Eulenburg and 
Cohnheim, by the first careful anatomical examination of the nervous system, 
had already before this (in 1866) made out that its condition was perfectly normal. 

Of late, however, we have reached the opinion that juvenile myopathic 
muscular atrophy need not always appear wholly in the form of lipomatous 
pseudo-hypertrophy, but that it may develop partly, if not exclusively, as simple 
muscular atrophy with a considerable loss of volume in the muscles. Erb in par- 
ticular has lately described a number of cases, which have led him to establish a 
second special form of juvenile muscular atrophy. In fact, we can not deny that 
we can establish different " types " of myopathic muscular atrophy on the ground 
of certain peculiarities ; but it is shown by increasing experience, as Erb himself 
has already stated, that the individual types do not differ in principle, but that 
they may run into one another in various ways. In what follows, the separate 
description of the chief types known at present is to be regarded as separate only 
in a clinical sense. We hold firmly, however, to the general distinction between 
these types and the spinal form of muscular atrophy. The constant confusion of 
these two forms of disease has been the main cause of the errors that obtained until 
a short time ago in regard to all the questions with reference to this subject. It is 
still advisable at present, however, especially from didactic reasons, to describe 
the myopathic forms directly after the spinal forms. 

1. Pseudo - hypertrophy of the Muscles (Lipomatosis luxurians mus- 
cularis progressiva of Heller ; Atrophia musculorum lipomatosa of Seidel). — 
Pseudo-hypertrophy develops almost invariably in childhood, somewhere between 
the ages of five and eight years. It very often depends upon a pronounced heredi- 
tary predisposition, since several children of the family are affected by the disease 
in the greater part of the cases. More rarely we can make out the same disease 




Fig. 88.— Positions of a child with hereditary (pseudo-hypertrophic) muscular atrophy, on rising to an 

erect attitude. (From Gowers.) 

in the patient's antecedents. The male sex is decidedly more disposed to the dis- 
ease than the female. Sometimes, but not always, we also find in the affected 
families some disposition to a nervous taint, such as hysteria, epilepsy, feeble- 
mindedness, anomalies of the skull, etc. 

The disease begins gradually and almost always without a special exciting 



PRIMARY MYOPATHIC FORMS OF MUSCULAR ATROPHY. 623 



cause. The parents notice that the child, who had been previously perfectly 
well and strong, becomes insecure on his legs, so that he can no longer jump or go 
up-stairs as well as he used to do. This points to the first characteristic peculiarity 
wherein pseudo-hypertrophy differs from progressive muscular atrophy. It begins, 
with rare exceptions, in the muscles of the trunk, especially in the muscles of the 
back and loins, and in the muscles of the lower extremities, especially in those of 
the thigh. While the arms and hands are still perfectly 
normal, walking constantly grows more and more diffi- 
cult, and the gait very soon assumes so characteristic a 
type that from this alone the diagnosis can often be made 
at the first glance. The gait becomes waddling, the belly 
appears very prominent, the vertebral column is arched 
forward in the lumbar region in marked lordosis, and the 
whole upper part of the body is balanced on the legs. The 
legs are raised slowly and with difficulty, and the toes 
usually droop from paresis of the dorsal flexors. The 
child's movements, when he tries to raise himself from the 
floor or pick up any object, are very characteristic, and 
are alike in almost all cases. Since it is impossible to raise 
the trunk, the child usually gets on all fours first, and then 
gradually straightens himself up by leaning his arms on 
his knees (see Fig. 88). Later on disturbances of motion 
appear in the upper extremities also, and in general they 
are very similar to those to be described more fully in the 
next type. 

If we examine the patient more closely we shall usually 
find at the first glance an extraordinary increase in the 
volume of single muscles (see Fig. 89). The calves are dis- 
proportionately thick, and sometimes the thighs also ; the 
arms are affected later, especially the deltoids, the triceps, 
etc. This increase of volume is caused by an abnormal 
interstitial development of fat, " pseudo - hypertrophy . " 
Hence the muscles do not feel firm, but soft and spongy. 
It is by no means rare, however, that, beside the pseudo- 
hypertrophy in some muscles, a genuine atrophy develops 
in others, with a pronounced loss of substance and without FlG - 89.— Pseudo-hypertro- 

. . , , phy of the muscles. 

any co-existing development of fat. This is seen especially (From Duchenne.) 
in the upper extremities. Finally, there seems to be in 

addition even a genuine muscular hypertrophy. In several cases we have seen a 
marked increase in volume in the muscles of the calves, which were capable of 
quite an extraordinary display of strength. In such cases, however, there is 
probably, in our opinion, a sort of compensatory hypertrophy, since the muscles 
that are still able to work are exerted immoderately. 

Fibrillary twitchings of the muscles can only very rarely be plainly noticed, 
which is probably connected with the form of atrophy (vide infra). Electrical 
examination shows a diminution of excitability corresponding to the atrophy and 
to the increased deposit of fat, but never reaction of degeneration. This is a fact 
of great importance because it agrees with the anatomical condition of the dis- 
eased muscles and is in remarkable contrast to the occurrence of reaction of 
degeneration in spinal muscular atrophy. The sensibility remains perfectly nor- 
mal, and also micturition and defecation ; the patellar reflex was absent in some 
of the cases examined by us. It is noticeable that the skin, especially in the legs, 
very often shows a peculiar bluish marbled coloring. Bulbar symptoms probably 





624: 



THE DISEASES OF THE SPINAL COED. 



never occur. The intelligence in most cases is perfectly normal, but it sometimes 
happens that children with hereditary muscular atrophy at the same time show 
manifest signs of mental or even of moral weakness. 

The disease advances very slowly but without remissions. Finally the patient 
can not walk at all ; he is confined to the bed, and becomes more and more help- 
less. Death usually ensues from some intercurrent disease, but sometimes from 
insufficiency of the respiratory muscles. 

The anatomical lesions in all cases of genuine pseudo-hypertrophy, whether 
hereditary or arising in childhood, which have been carefully examined up to the 
present time (Charcot, F. Schultze, Berger, and others), have been completely 
negative with regard to the nervous system. Except for accidental and insig- 
nificant complications, the spinal cord, and especially its anterior gray matter, have 
been perfectly normal. In the muscles microscopic examination shows a very con- 
siderable increase of the interstitial connective tissue, and especially of the fatty 
tissue between the single fibers of the muscle. This may sometimes be seen, even 
during the patient's life, by harpooning or excising little pieces of muscle. The 
fibers themselves have not undergone fatty degeneration, and they show but very 
little degenerative atrophy, but they show everywhere their transverse striation 
plainly. Some of them are perfectly normal in volume, others decidedly smaller, 
and some are even actually hypertrophied (compensatory hypertrophy ?). We see, 
then, that the anatomical lesions of the muscular disease are essentially different 
from the purely degenerative changes in the muscles in spinal muscular atrophy. 

2. Erb's Form of Juvenile or Hereditary Muscular Atrophy. — This form 
also begins almost always in youth, before the age of twenty, but, as a rule, some- 
what later than the form associated witb pseudo-hypertrophy. It is occasionally 
or even very often hereditary or family (that is, occurring in families), and the 
female members of the family are often attacked by this form, while pseudo- 
hypertrophy is seen especially in boys. The disease is also, like pseudo-hyper- 
trophy, sometimes seen to begin in the back and legs, but quite frequently the 
shoulders and upper extremities are first attacked. There is also a remarkable 
regularity in the choice of the muscles attacked. According to Erb, the following 
muscles are almost constantly diseased in the trunk and the upper extremities : 
the pectoralis major and minor, the trapezius, the latissimus dorsi, the serratus 
magnus, the rhomboidei, the sacro-lumbalis and longissimus dorsi, and later the 
triceps. The following, however, almost always remain normal : the sterno-mas- 
toid, the levator anguli scapulae, the coraco-brachialis, the teres major and minor, 
the deltoid, the supra-spinatus and infra-spinatus, and, in distinction from what 
was especially stated in regard to spinal muscular atrophy, the small muscles of 
the hand. The muscles of the forearm, too, except the supinator longus, remain 
intact for a long time, if not entirely. In the lower extremities the atrophy 
attacks chiefly the glutei, the quadriceps, the peronei, and the tibialis anticus, 
while the sartorius and the muscles of the calf are usually spared for a long time. 
Fibrillary twitchings in the affected muscles are generally absent, and there is 
never any reaction of degeneration. 

The disturbances of function due to this condition are self-evident, so that a 
full description of them may be omitted. The arms usually suffer first, as we 
have said. The marked projection of the scapulae, from the paralysis of the ser- 
ratus, is especially characteristic. The gait soon becomes waddling, as in pseudo- 
hypertrophy, and, finally, walking is utterly impossible. The whole course of the 
disease is always very chronic. Erb describes cases in which the disease has existed 
from twenty-three to thirty-eight years. Bulbar symptoms are as few as in mus- 
cular hypertrophy. It is of significance that the diaphragm may atrophy, and the 
consequent respiratory disturbance may be the cause of death. 



THE SO-CALLED SPASTIC SPINAL PARALYSIS. 



625 



Apparently very nearly allied to the cases just described is that form of juve- 
nile and family (that is, repeatedly seen in members of the same family) muscular 
atrophy which begins in the facial muscles. It was first described by Duchenne, 
and lately, with especial fullness, by Landouzy and Dejerine, and the purely myo- 
pathic nature of the affection, the absence of changes in the peripheral nerves and 
the spinal cord, could be made out in one of their cases that came to autopsy. In 
this form the atrophy begins in the muscles of the face, which thus takes on a 
peculiar flaccid, expressionless appearance, with puffy lips. Only later does the 
atrophy invade the muscles of the shoulders and arms, when it shows almost pre- 
cisely the same distribution as in the previous form. The muscles of mastication, 
the ocular muscles, the supra-spinatus and infra-spinatus, and the flexors of the 
hand and fingers, almost always remain normal. A peculiar retraction of the 
biceps is characteristic. Fibrillary twitchings and reaction of degeneration are 
completely absent in the muscles. 

That the form of juvenile atrophy just described and pseudo-hypertrophy are, 
at bottom, probably identical diseases follows, not only from all the other simi- 
larities mentioned, but also from the fact that sometimes one of the children 
affected in the family displays rather the type of pseudo- hypertrophy, another the 
type of simple juvenile atrophy. We also find various transitions between the 
different forms. Thus, for example, pseudo-hypertrophy in the legs may be asso- 
ciated with simple atrophy of the arms. The affection may also begin in the 
arms, while later the facial muscles are also affected. We do not know what 
causes produce the great increase of fat-tissue in a part of the cases. Even in the 
cases without the interstitial development of fat, the atrophy of the muscles is 
essentially simple, not degenerative, and the motor nerves and spinal cord remain 
normal, at least according to all present experience. Erb groups the two forms 
together, under the name of "dystrophia muscularis progressiva.'' 1 

The differential diagnosis between the myopathic and the spinal muscular 
atrophies is not difficult, if we pay attention to the juvenile or family character of 
the former, and also to its characteristic localization, affecting the extensors of the 
spine and leaving free the small muscles of the hand, etc., and to the absence of 
fibrillary twitchings and of reaction of degeneration in the muscles. 

The treatment can scarcely ever be expected to give permanent results, but 
sometimes, even in juvenile muscular atrophies, some considerable improvement 
has been obtained by a very persistent electrical treatment and massage of the 
muscles. 



CHAPTER IX. 

THE SO-CALLED SPASTIC SPINAL PARALYSIS. 

{Primary Lateral Sclerosis. Spasmodic Tabes Dorsalis.) 

In the year 1875 Erb, and soon after Charcot, called attention to a clinical form 
of spinal paralysis, by no means rare, which is characterized "by a gradually 
increasing paresis and paralysis, usually advancing slowly from below upward, 
with muscular tension, reflex contractions and contractures, with a marked increase 
of the tendon reflexes, with complete absence of sensory and trophic disturbances, 
of vesical and sexual weakness, and of any cerebral disturbance." Both observers 
agreed in assuming a " primary symmetrical sclerosis of the lateral columns " as 
the anatomical cause of this condition. 

The numerous observations published in the following years have shown that 
the type of disease just briefly described is, in fact, often to be met with, and may 
40 



626 



THE DISEASES OF THE SPINAL COED. 



easily be distinguished from the other forms of spinal paralysis. The hypothesis 
as to its anatomical basis has not yet been confirmed, however, since, in all the 
cases that have come to autopsy so far, other anatomical changes were found 
instead of the primary lateral sclerosis supposed to be the only lesion ; but it can 
not be denied that, beside other lesions, of course, a disease of the lateral columns 
has been repeatedly made out in such cases ; and that this was certainly not with- 
out significance for the occurrence of the group of symptoms in question. It is 
also not at all impossible that there may be an isolated systemic disease of the 
lateral columns, especially of the pyramidal tracts, without any disease of the gray 
matter or of other portions of the cord at the same time, which disease is closely 
connected with amyotrophic lateral sclerosis in particular, and is a further link 
in tbe chain of primary diseases of the motor conducting tract ; but, as we have 
said, a definite case of isolated disease of the spinal pyramidal tracts, without 
invasion of the anterior gray cornua, has not yet been known. 

In what follows we will first describe the clinical peculiarities of spastic spinal 
paralysis, and then add the enumeration of its anatomical causes, as far as they 
are known at present. Hence we mean by " spastic spinal paralysis " only a group 
of symptoms which is so often observed that, from practical reasons, it is advisable 
to give it a short and unprejudiced name. 

Type of Spastic Spinal Paralysis. — Two symptoms predominate in the picture 
of spastic spinal paralysis : motor paresis, and the increase of the tendon reflexes — 
the patellar reflex, and the ankle clonus. The former — we are speaking at present 
only of the spastic paralysis of the legs, which is by far the most frequent and the 
most clearly marked — is found in various degrees, from a simple weakness of 
movement to a complete and more or less extensive paralysis. It is the second 
symptom, however, which gives to the disturbance of motion its characteristic 
feature of spastic paralysis. If the increase of the tendon reflexes is very consid- 
erable, the reflex contractions come on even upon the stretching and pulling of the 
tendons, which is excited by the weight of the limbs or by any active or passive 
movements. The reflex muscular tension opposes any attempt at motion. The 
muscles feel rigid and firm, and the legs are often found in almost permanent 
contracture and extended, with the feet in plantar flexion. If we try to flex the 
leg passively at the knee, or if we try to flex the foot dorsally, we find it almost 
impossible to do so. The more rapidly and suddenly we try to produce the motion, 
the more marked is the muscular resistance, which can scarcely be overcome. If, 
however, we go to work very slowly and cautiously, and avoid any sudden ten- 
sion of the tendons, we can almost always flex the leg without special trouble. 
If we put the patient on the edge of the bed, the legs do not hang down laxly, but 
they usually fall at once into a vigorous extensor tetanus, since the weight of the 
leg puts the quadriceps into contraction by the tension on the ligamentum patellae. 
A convulsive, reflex tremor of the whole leg often comes on at once, similar to 
ankle clonus. If we examine the patient while in the bath we find the spasms 
decidedly less, because in the water the influence of the weight of the limb is 
absent. 

Active motion, as is easily explained, must also be impaired from the inhibi- 
tory action of the reflex spasms. The degree of disturbance of motion is thus 
increased, and the paresis often seems greater than is really the case. The influ- 
ence of the muscular tension is especially manifest in the gait of the patient. As 
long as walking is still possible, we notice very plainly that it is rendered difficult, 
not only by the muscular paresis, but also by the stiffness of the legs. The 
patient walks with short and difficult steps, the legs are scarcely flexed at all at 
the knee, and the feet are scarcely raised at all. The feet " stick to the floor " and 
are slowly slid forward, and there is a marked tendency to walk on the toes from 



THE SO-CALLED SPASTIC SPINAL PARALYSIS. 



627 



the contraction in the muscles of the calves. The weight of the hody alone 
presses the feet downward. We term this very characteristic form of gait the 
spastic-paretic gait. 

The increase in the tendon reflexes may also exist without the presence of any 
special motor paresis of the muscles at the same time. Since, however, in this 
case, the motion is not a little influenced by the constant spasms, a disturbance of 
motility may be counterfeited, which might be called " spastic pseudo-paralysis," 
or, more properly, pseudo-paresis. In these cases the muscular strength is almost 
normal, and the patient can walk for quite a long time. Nevertheless, all his 
movements are stiff and difficult, and the gait shows all the peculiarities of the 
pure spastic gait. The steps are not very short and they follow one another quite 
rapidly, but the legs remain perfectly stiff and are scarcely raised from the 
ground, and the patient walks almost entirely on his toes. In the house the 
patient walks with a noisy shuffle, and in soft sand we can see the furrows drawn 
by the feet as they slide along the ground. 

Although we are doubtless justified in referring the spastic condition mainly 
to the increase in the tendon reflexes, we must also add that sometimes symptoms 
of direct motor irritation may occur — single rapid or slow contractions, for 
which we can not make out a reflex origin. It is, however, characteristic of spas- 
tic spinal paralysis, in the original sense of the term, that other spinal symptoms, 
especially disturbances of sensibility, disturbances in micturition and defecation, 
ataxia, muscular atrophy, and other trophic symptoms, are entirely absent. Only 
when such was the case have Erb and Charcot claimed that a special anatomical 
cause must lie at the bottom of the peculiar group of symptoms. In fact, the 
cases in which we happen to see the type of genuine spastic spinal paralysis with- 
out any other symptoms are not very rare. It develops slowly and gradually, 
without known cause, and usually in patients in youth and middle life. One leg 
is first affected, and then the other. The muscles of the trunk and of the arms 
are sometimes added to the list later on, and in the arms we find a paresis 
with a decided increase of the tendon reflexes and without any disturbance of 
sensibility or any muscular atrophy. This type of disease, however, only very 
rarely remains in its purity — at least, according to present experience. Sooner 
or later other symptoms are mixed with it, and in those cases, which so far have 
come to autopsy, the anatomical lesions are by no means always of the same 
sort. 

Pathological Lesions. — As we have already said, Erb and Charcot originally 
advanced the hypothesis that the anatomical basis of spastic spinal paralysis is 
to be found in a sclerosis of the lateral columns. This opinion is well-founded, 
inasmuch as the picture of the symptoms of spastic spinal paralysis manifestly 
recalls amyotrophic lateral sclerosis in many of its relations. In both diseases we 
find symptoms limited exclusively to the motor sphere, and an increase of the 
tendon reflexes. The only distinction is in the muscular atrophy, whose anatomi- 
cal cause is undoubtedly to be found in the atrophy of the anterior gray cornua. 
If we imagine the pyramidal tract exclusively affected, without co-existing disease 
of the gray matter, the result must be the picture of "spastic spinal paralysis." 
This line of reasoning, the justification of which must to-day be acknowledged, 
has, however, not yet been entirely confirmed by facts ; but we have learned to 
recognize a chain of circumstances under which, at least at times, the symptoms of 
spastic spinal paralysis may arise. 

We must first mention that cerebral changes, especially chronic hydrocephalus, 
may sometimes simulate the type of spastic spinal paralysis. Except for some 
anomalies in the skull, special cerebral symptoms may be entirely absent, while 
the motility of the legs (and arms) is diminished, and the tendon reflexes are so 



628 



THE DISEASES OF THE SPINAL COED. 



decidedly increased that the symptoms of spastic paralysis may result. R. Schulz 
and we ourselves have made such observations. 
The following changes are also to be considered : 

1. Transverse myelitis in the upper dorsal or the cervical cord. This some- 
times shows a remarkable symmetry in its distribution for some time, and a 
predominant localization in the lateral columns, while the posterior columns 
remain comparatively free. Hence, as we can easily understand, the result is 
a paralysis of the legs with greatly increased tendon reflexes, but with normal 
sensibility. Tumors of the cervical cord may more rarely cause similar appear- 
ances. 

2. Compression of the Spinal Cord. — A gentle compression of the cord in the 
cervical or dorsal region is followed, as we have seen, by paresis and increase of 
the reflexes, but not by sensory disturbance. We can understand that, if no 
manifest cause of compression can be made out, a primary affection of the cord 
may simulate the symptoms of spastic spinal paralysis. 

3. Multiple sclerosis may also frequently show such a localization of its nodules 
as to be followed by paresis and spastic symptoms without sensory disturbances. 
The case diagnosticated by Charcot himself as " spasmodic tabes dorsalis " turned 
out on autopsy to be multiple sclerosis. 

4. In a case observed by us, with almost the entire and pure type of symptoms 
of spastic spinal paralysis, the autopsy showed a hydromyelus with co-existing 
degeneration of the lateral columns. 

5. Spastic paralysis has been sometimes observed to come on after acute dis- 
eases, but the reports of autopsies in such cases are at present wanting. 

6. Finally, we will here briefly mention the combined systemic disease of the 
pyramidal tract, the lateral cerebellar tract, and the columns of Goll, in adults, 
described by us. In these cases we find a gradually increasing paralysis of the 
legs, and later of the arms, with increased tendon reflexes, spastic symptoms, and 
sensibility almost perfectly normal. Later on^ however, vesical disturbances arise, 
which are probably to be referred to the disease of the columns of Goll. Further 
observations must give us more definite knowledge as to the frequency and the 
possibility of diagnosis of this apparently especially limited form of spinal disease. 
Minkowsky has also recently reported a case in which anatomical examination 
showed nothing but primary degeneration of the pyramidal and cerebellar tracts 
in the two lateral columns as the cause of a spastic spinal paralysis. In this and 
in some similar cases, which come very close to Erb's and Charcot's theoretical 
postulate, syphilis was perhaps to be regarded as the special cause of the disease. 

Diagnosis. — The symptomatic diagnosis of spastic spinal paralysis is easy to 
make, with attention to the description given above. We must always, however, 
be very cautious at present in our anatomical diagnosis. Only the further course 
of the disease can give us data whereby we can first consider the morbid condi- 
tions mentioned above. 

Prognosis. — The prognosis of most cases which show the symptoms of spastic 
spinal paralysis is just as unfavorable as most of the other diseases of the spinal 
cord, but we must always bear in mind that many of these cases run a very slow 
course. The disease seems to stand perfectly still for a long time, the symptoms 
are less severe than in other spinal diseases, there are no pain and no incontinence, 
and sometimes we have seen manifest improvement and even a few recoveries, 
but such cases at present lack definite anatomical proof. 

Treatment. — The treatment of spastic spinal paralysis in general agrees with 
that of chronic myelitis {vide supra). Galvanic treatment usually gives compara- 
tively the best results. We must also mention especially that prolonged warm 
baths often act well against the spastic symptoms. They may last for half an 



ACUTE AND CHRONIC POLIOMYELITIS. 



629 



hour to an hour and a half, and should be of a temperature of 90°, or at most 95° 
(26°-28° P.). The legs are more flexible and more movable after them. Among 
internal remedies we may try nitrate of silver and ergotine. If there is a suspicion 
of syphilis, for which we should always look carefully, it is an absolute necessity 
to employ inunction, and to prescribe iodide of potassium internally. 



CHAPTER X. 
ACUTE AND CHRONIC POLIOMYELITIS. 

1. Spinal Paralysis of Children. 

(Acute Poliomyelitis in Children.) 

iEtiology and Pathological Anatomy. — In children there is quite frequently a 
definite and well-characterized form of paralysis, for the first accurate knowledge 
of which we must thank Jac. von Heine in 1840. Although Heine later, in 1860, 
expressed the opinion that a disease of the spinal cord formed the basis of the 
paralysis, the first actual confirmation of this opinion was furnished later by Prevost 
and Vulpian, Charcot and Joffroy, and others, so that at present we are justified 
in exchanging the old term "essential paralysis of children" for the name of 
"spinal paralysis of children." 

As the name indicates, the affection occurs chiefly, if not exclusively {vide 
infra), in children, and is most frequent in the earlier years, somewhere between 
one and four. An exciting cause, like taking cold, has hardly ever been made 
out. The children are almost always perfectly healthy * previously, and come of 
healthy families without any neuropathic predisposition. The whole course of 
the disease makes the hypothesis very probable that we have to do with an acute 
infectious disease — with an infectious process, which first causes a general infec- 
tion of the body, and then is 



localized chiefly in a circum- 
scribed portion of the spinal 
cord. It also, perhaps, bears 
some relation to the nature 
of the disease as just signified 
that most of the cases occur 
in warm weather. 

With reference to its anat- 
omy, the disease may be de- 
fined as an acute inflamma- 
tion, which affects chiefly a 
definite extent of the ante- 
rior gray matter of the spinal 
cord, usually attacking only 




the anterior gray COrnu of FlG go._Section through the cervical enlargement in anterior 
One side • yet it does not al- poliomyelitis : the left anterior column is very much con- 

t . 1 . ; • . tp • , tracted and is without ganglion-cells. (From Charcot and 

ways limit itself strictly to Joffroy.) 
this, but it may involve the 

white matter in the vicinity somewhat, although, of course, to a lesser extent 
than the gray matter. Although fresh cases have so far been examined in very 



* The paralyses arising after acute diseases— like measles, scarlet fever, small-pox, etc. — are perhaps 
partly of spinal origin, but they can not be identified with the idiopathic spinal paralysis of children. 



630 



THE DISEASES OF THE SPINAL CORD. 



scanty numbers, still we can sometimes make out clearly the remains of inflam- 
mation in the older centers of disease. The ordinary lesion in old cases, which is 
most frequently found, consists of a considerable atrophy of one anterior cornu, 
which is changed to a dense sclerosed tissue, often pierced by dilated and thickened 
vessels, and which contains scarcely a single normal ganglion-cell. If the paral- 
ysis affects one arm, the corresponding anterior cornu in the cervical enlargement 
is atrophied (see Fig. 90) ; if the leg be paralyzed, the process is seated in the lum- 
bar enlargement. In bilateral paralysis we must think of an affection of both 
anterior cornua at the corresponding level of the cord. 

This inflammation of the anterior cornu, the poliomyelitis, is to be regarded as 
the primary center of disease. From this point, as in every severe lesion of the 
motor ganglion-cells there situated, there develops a secondary degeneration, 
which, extending to the periphery, affects the corresponding anterior roots, and 
later their appropriate motor nerves and the muscles supplied by them. In the 
paralyzed muscles and nerves we accordingly find a marked pure degenerative 
atrophy, such as we have learned to recognize in severe peripheral paralyses. 

Although at present the spinal origin of the atrophic paralysis of children is 
regarded as sufficiently certain, we would not deny that some authors, especially 
Leyden, have assumed a peripheral origin for some cases — that is, a primary neu- 
ritis, without a material implication of the spinal cord. In fact, it does not seem 
impossible that the same morbid setiological factor, which we have supposed to be 
infectious, may exceptionally be localized chiefly in a peripheral motor nerve. 
In the chapter on cerebral paralysis of children, which is by no means very rare, 
we shall see that a manifestly closely allied acute process in children — one, per- 
haps, even serologically identical — may also develop in the motor regions of the 
cortex cerebri. 

Clinical History. — The disease almost always begins suddenly. A child who 
was previously perfectly well and lively is all at once attacked with severe fever, 
often reaching 105° or 106° (40°-41° C), which is associated with quite severe gen- 
eral symptoms even from the beginning. The child complains of headache, and 
sometimes of pain in the loins and in the limbs, and is decidedly stupid and som- 
nolent. Very often still more marked cerebral symptoms develop : complete loss 
of consciousness, single twitchings in the face or the extremities, or general con- 
vulsions. The eclamptic attacks, turning of the eyes, and clonic contractions in 
the face and the extremities, often appear even at the beginning of the disease. 
The whole of the initial symptoms, whose intensity varies very much in the dif- 
ferent cases, sometimes last only a very short time, a day or two, although they 
often continue for a week or two. Indeed, we even know cases in which, as the 
mothers have assured us, the children are said to have "]ain in spasms," almost 
uninterruptedly, even for four or five weeks before the beginning of the paralysis 
— that is, before it became noticeable. On the other hand, however, it may happen 
that the initial symptoms, especially the severe cerebral symptoms, are entirely 
absent or only intimated. 

After the initial period of the disease just described has passed away, the 
parents usually notice that the child is attacked by a more or less extensive paraly- 
sis. If its development can be followed more closely, we always find that it spreads 
rapidly, often in single spurts which rapidly follow one another, so that it usually 
reaches quite a great extent in a short time. Either both legs, or the legs and one 
arm, or all the extremities, and even the muscles of the trunk, are affected; but the 
paralysis scarcely ever remains permanently as extensively distributed as at first ; 
it is reduced much more rapidly, and soon draws back to a definite muscular 
region, which remains permanently paralyzed. In some cases the paralysis may 
even entirely disappear, but as a rule a complete paralysis is left in one extremity, 



ACUTE AND CHRONIC POLIOMYELITIS. 



631 



or at least in a portion of it ; most frequently in one leg, especially in the peroneal 
muscles ; somewhat more rarely in the arm, chiefly in the deltoid ; sometimes in 
both legs ; or, very rarely in spinal paralysis, in one arm and leg on the same side 
or on opposite sides. Meantime the child's general health has been completely 
restored. He is well and vigorous, has an excellent appetite, never shows any 
permanent cerebral disturbance — only the painless, flaccid paralysis, the inability 
to use the affected extremity, is left behind. In the following weeks and months 
a further, slower advance in the improvement in the power of motion often 
becomes noticeable, but, in by far the greatest number of cases, a permanent and 
more or less complete paralysis of certain muscles remains. 

In regard to the more intimate peculiarities of this remaining paralysis, it may 
invariably be characterized as a flaccid atrophic paralysis. A marked atrophy of 
the paralyzed muscles shows itself a few weeks after the beginning of the paralysis. 
This atrophy gradually advances further and may finally attain the highest degree. 
The atrophy is often, but not always, partly concealed by a more abundant devel- 
opment of fat tissue. The changes in the electrical excitability of the paralyzed 
nerves and muscles come on still more rapidly than the visible atrophy. Since 
we have to do with a pure degenerative atrophy of nerve and muscle, as follows 
from the anatomical basis of the disease, a pronounced reaction of degeneration 
must necessarily develop in the affected parts. Duchenne found that usually the 
faradic excitability of the nerves and muscles is completely lost after a week or two. 
On galvanic examination, we can at first detect an increase of excitability in the 
muscles with a predominance of slow anodic closure contractions (AnSZ), while 
later, after two or three months, the galvanic excitability also sinks very consider- 
ably ; but the muscular contractions preserve their qualitative peculiarities charac- 
teristic of reaction of degeneration (see page 519). Very often the whole affected 
extremity remains backward in its growth, so that later the bones may show a 
shortening of several centimetres. The parallel between the muscular atrophy 
and the stunted growth is not, however, present in all cases, as Volkmann, in 
particular, has stated. 

Passive motion of the paralyzed extremity is at first, and even later, perfectly 
free, except for the contractures that set in later {vide infra). Many joints are 
so flaccid that we can actually make flapping movements and give the paralyzed 
limbs the most extraordinary positions. The tendon reflexes are invariably 
completely absent in the paralyzed extremities, and so almost always are the 
cutaneous reflexes, a condition which may sometimes be of diagnostic significance. 
The skin often shows certain trophic disturbances ; it feels cool and has a cyanotic 
appearance. Its sensibility, however, is completely retained in all cases. Micturi- 
tion is sometimes' a little disturbed at the beginning of the disease, but in most 
cases this disturbance completely disappears later. 

After the paralysis has existed for a long time, certain secondary contrac- 
tures almost always develop in the paralyzed parts, which are in part of a very 
characteristic type. In the legs especially the "paralytic club-foot" {talipes 
varo-equinus) is a symptom long known. It is due to the fact that, from the 
paralysis of the peronei muscles and of the tibialis anticus, the point of the foot 
constantly droops, and that a contracture is gradually developed in the antago- 
nistic muscles of the calf, whose points of insertion are permanently approxi- 
mated. In paralysis of the muscles of the calf there arises, on the other hand, a 
moderate degree of calcaneus from the contracture of the antagonists. In the arms 
and in the vertebral column, in paralyses of the spinal muscles, the most manifold 
and sometimes very considerable contractures and deformities may also arise, the 
chief cause of which is always to be referred to the contracture of unparalyzed 
antagonists and to external mechanical conditions, like weight and pressure. 



632 



THE DISEASES OF THE SPINAL COED. 



In conclusion, if we simply compare the type of disease sketched with its ana- 
tomical cause, the general agreement of the two may at once be seen. The affec- 
tion of the anterior gray cornu must have as a result a paralysis with a subsequent 
atrophy and reaction of degeneration, in which the reflexes must be lost by the 
destruction of the reflex arc, but the sensibility must remain perfectly normal from 
the persistence of the sensory conduction (the posterior columns and the posterior 
gray cornua), and the vesical functions must also remain normal. The subsequent 
paralysis is the result of the destruction which the morbid process, in itself com- 
pletely ended, has caused in the spinal cord. 

Diagnosis. — The diagnosis of the spinal paralysis of children is almost alway s 
easy to make and certain if we hold strictly to the definition and peculiarities of 
the disease, and do not reckon as spinal paralysis every paralysis appearing in a 
child. We should consider chiefly the acute beginning, the subsequent flaccid 
paralysis with atrophy and reaction of degeneration, with the loss of the reflexes, 
but with retained sensibility. If we observe these features, we are sufficiently 
protected against confusion with cerebral diseases and other diseases like spondy- 
litis, hereditary muscular atrophy, or spastic spinal paralysis. 

Prognosis. — It is not impossible, but it is not yet proved, that many of the cases 
where children die speedily with convulsions are to be regarded as the initial 
stage of acute poliomyelitis. If, however, the first stage of the disease is past, the 
prognosis as regards life is entirely favorable, since the rest of the child's physical 
development is no further affected in any way. The prognosis as regards the 
complete restoration of the disturbance of function is, however, much more 
unfavorable. What has not recovered in the first weeks or months usually 
remains paralyzed for the whole life. Nevertheless, this experience should not 
restrain us from persevering in treatment, at least in the first years, since some- 
times a very noticeable improvement in the functions of the paralyzed parts can 
thus be procured. 

Treatment. — If we have an opportunity, even during the initial stage of the 
disease (when, of course, the diagnosis can not usually be made with certainty), to 
attack the disease by our treatment, we may prescribe cold compresses or an ice- 
bag to the head, and eventually, where there is high fever or great stupor, a tepid 
bath with cool affusions. We are but rarely led to try local blood-letting by 
leeches behind the ears or on the temples, where there are signs of marked cerebral 
hyperaeinia. Internally we usually prescribe a mild " intestinal derivative," such 
as half a grain or a grain (grm. 0*03-0 '05) of powdered calomel every two or three 
hours, infusion of senna, etc. 

After paralysis appears, we can expect the most success from electrical treat- 
ment, kept up consecutively for months, and, with interruptions, for years. We 
put a large, broad electrode on the vertebral column at the spot which corresponds 
to the place of the lesion in the spinal cord — on the cervical vertebrae in paralysis 
of the arm, and the lower dorsal in paralysis of the leg — while the other electrode 
serves for peripheral application to the paralyzed nerves and muscles. In this 
way we apply a moderately strong constant current, reversing it occasionally, for 
two or three minutes, partly stabile and partly by passing the kathode, or eventu- 
ally the anode, slowly over the paralyzed muscles and nerves. We may also 
employ occasional interruptions and changes of the current. Duchenne has also 
found persistent treatment by the faradic current of advantage. The sittings 
should take place three or four times a week, and later even oftener, if possible. 

Beside electrical treatment, methodical gymnastic exercises of the muscles, that 
can still be moved somewhat actively, may be of distinct advantage. Regular and 
persistent massage of the muscles is also to be recommended in the later stages. In 
practice we can not avoid prescribing certain embrocations, like spirits of camphor, 



ACUTE AND CHRONIC POLIOMYELITIS. 



633 



spirits of mustard, or spirits of formic acid. Passive motion is very important to 
guard against contractures, and to improve the already existing deformities. In 
regard to the further details of orthopaedic treatment, which is of great importance, 
we must refer to the appropriate special works on surgery and orthopaedics. 

The use of baths, of brine or ferruginous waters, is to be recommended, 
although, of course, they must not be overvalued. They may be given at home. 
If circumstances permit sending the child to a bath during the summer months, 
we should chiefly consider the brine baths at Reichenhall, Kreuznach, Kosen, and 
Colberg; the acid salines at Rehme, Nauheim, and Soden; and eventually, with 
weak and anaemic children, the use of the iron baths at Driburg, Pyrmont, or 
Schwalbach. Good results are sometimes obtained at the indifferent thermal 
baths at Teplitz, Wildbad, Ragaz, or Gastein, but these must be used only with 
caution. We also obtain good results, especially with older children, at the cold- 
water cures. 

Very little is to be expected from the use of internal remedies. Iodide of potas- 
sium and strychnine are recommended, the latter in the form of subcutaneous 
injections, -fa to ¥ V grain (grm. 0 '001-0 '003) daily. 

In old cases, where there is no longer any hope of further improvement of the 
paralysis worth mentioning, the treatment may be limited to keeping up and 
strengthening the patient's general condition as much as possible by proper food 
and good air. 

2. x^cute Poliomyelitis of Adults. 

(Acute Atrophic Spinal Paralysis of Adults) 

Although it had been believed for a long time that the form of acute atrophic 
spinal paralysis, just described, occurred only in children, later observations by 
Moritz Meyer, Duchenne, Erb, F. Schultze, F. Miiller, and others, have established 
the fact that precisely analogous cases of disease may also develop, although 
decidedly less frequently, in adults, especially in young persons under thirty. 
There is no longer any doubt of this fact, especially if we consider an undoubted 
anatomical lesion found by F. Schultze. We have, however, already stated 
that for a long time we have regarded the diagnosis of acute and, as we 
shall soon see, of chronic poliomyelitis also as too readily made, and that cer- 
tainly very many of the cases diagnosticated and published as poliomyelitis are to 
be classed as primary neuritis (see page 548). Since we know that primary degen- 
erative processes may develop acutely and subacutely in the motor nerves, and 
that these also lead to an atrophic paralysis, a greater part of the teaching on 
poliomyelitis needs new and careful revision in order to exclude what does not 
belong to it. 

The type of acute poliomyelitis of adults, so far as it has been established by 
definite observations, which at present are not numerous, is, of course, not mate- 
rially different from the type of the spinal paralysis of children. 

We often can not make out any aetiological conditions ; sometimes exposure 
to cold, over-exertion, etc. , seem to favor the development of the disease. ' Cases 
are seen more frequently in the male sex than in the female. 

The disease likewise begins with quite severe initial symptoms, fever, headache, 
somnolence, delirium, and vomiting, which may last from a few days to a week or 
two. The violent spontaneous pains, which are very often reported as occurring 
in the loins, the back, and the extremities, usually belong probably to those 
cases in which a primary neuritis, but not a poliomyelitis, is the chief anatomi- 
cal lesion. After the end of this stage the paralysis appears. This develops 
with varying distribution, usually in single spurts, but always rather rapidly. 
The paralyzed muscles are perfectly flaccid, the cutaneous and tendon reflexes are 



634 



THE DISEASES OF THE SPINAL COED. 



wholly absent, and very soon a 'pronounced atrophy and reaction of degeneration 
appear, while the sensibility and the vesical and sexual functions remain normal. 

The distribution of the paralysis shows certain peculiarities, which must be 
briefly described here, since they can be studied much better in adults than in 
children. The paralysis may be very extensive, it may affect all four extremities, 
or it may occur in the form of paraplegia, or even of monoplegia. In the 
extremities we very often find certain groups of muscles paralyzed, to which E. 
Remak first called attention. Since the muscles that are paralyzed at the same 
time are not supplied by the same peripheral nerves, but usually are connected 
in their functions, we may suppose that the corresponding ganglion-cells in the 
anterior cornua of the spinal cord also lie together, without regard to the later 
distribution of their peripheral processes in the different motor nerves. Thus, for 
example, it is worthy of note that, in paralysis of the crural region, the sartorius 
often remains entirely free ; that in the leg the tibialis anticus, on the one hand, 
and the peronei and the extensor digitorum on the other, may be separately dis- 
eased; that in the forearm the supinator longus, supplied by the radial nerve, 
remains free, while all the other muscles on the extensor side of the forearm are 
paralyzed ("forearm type" of E. Eemak); and that, on the other hand, the supi- 
nator may be paralyzed alone or together with the biceps, brachialis anticus, and 
deltoid upper-arm type" of E. Remak). This latter form of paralysis is said to 
correspond to a lesion in the cord at the level of the fourth and fifth cervical roots, 
the forearm type to a lesion at the level of the eighth cervical and first dorsal 
roots. According to Kahler and Pick, the center for the muscles of the calf lies 
at the level of the fourth and fifth dorsal roots. Ferrier and Yeo, in their experi- 
ments on monkeys, by irritation of the anterior motor spinal roots have obtained 
results which, for the most part, agree very well with the observations on men. 

In regard to diagnosis in the future, especial attention must be paid to the dis- 
tinction between poliomyelitis and neuritis. The greatest stress is to be laid on 
the initial pains and any other slight disturbances of sensibility. In other respects, 
the course of the two diseases is so similar that we can indeed imagine that they 
are closely allied in their setiological relations, and exhibit merely different forms 
of localization of the same (probably infectious) morbid agency. Some observa- 
tions also seem to favor the theory that transitional forms may occur with a co- 
existing primary lesion of the cord and of the peripheral nerves. 

The prognosis is not wholly unfavorable, as in many cases a complete recovery 
has been observed, although only after months. Of course, it is not certain 
whether these cases were not multiple neuritis. On the other hand, however, the 
same permanent paralyses as hi spinal paralysis of children may be left, with 
atrophy and contractures. 

The treatment follows precisely the same rules that we have mentioned in the 
spinal paralysis of children. The internal or subcutaneous use of ergotine may 
be added on the recommendation of some physicians. F. Muller recommends a 
solution of two and a half drachms of ergotine (grm. 10) with a third of a grain 
of sulphate of atropine (grm. 0*02) in five drachms of water (grm. 20), of which 
he injects seven to fifteen minims twice a day. 

3. Subacute and Chronic Poliomyelitis. 

(Subacute and Chronic Atrophic Spinal Paralysis. Paralysie generale spindle anterieure 

subaigue [Duchenne]). 

While the anatomical basis of acute poliomyelitis in adults is still lacking in 
proof, our anatomical knowledge of the occurrence of a subacute and chronic 
poliomyelitis, in the sense of the term given it by various authors, is still com- 



ACUTE ASCENDING SPINAL PAEALYSIS. 



635 



pletely defective. Confusions with multiple neuritis are also undoubtedly very 
common here, and the diagnosis is not incontestable in all the cases published 
under the name of " subacute poliomyelitis." Therefore we will limit ourselves to 
reproducing here briefly the picture of the disease at present described under the 
above name, while we especially repeat that a certain and accurate confirmation 
of its anatomical basis must be left to the future. 

In the cases classed under this heading a paralysis, first of the two legs and 
somewhat later usually of the two arms, develops in a comparatively short time — 
in the course of some days, or weeks at most. It usually has no special cause 
or any severe initial symptoms. The patient complains at first of weakness 
in the legs ; he can no longer walk, and is confined to the bed. A short time 
later the same disturbances appear in the arms, and lead to a more or less complete 
paralysis. The patient often feels some slight paresthesia in the affected parts, 
but in general the sensibility remains perfectly normal. The paralyzed muscles 
are often quite sensitive to pressure (neuritic symptoms ?). Soon after the paraly- 
sis an equally extensive atrophy develops, and a distinct loss of electrical excita- 
bility, running parallel to it ; which passes over into a partial or, in all severe 
cases, a complete reaction of degeneration. The cutaneous and tendon reflexes 
are very much diminished and often entirely lost. The bladder and rectum, how- 
ever, remain intact, and bed-sores never develop. We sometimes notice a striking 
diminution of the sweat secretion. In rare cases the muscles of the neck, the 
hps, the tongue, and the pharynx are attacked by the disease. 

After the paralysis has reached its greatest extent there is usually a cessation. 
The condition remains stationary for months sometimes, and then a gradual 
improvement begins, which may sometimes go on to complete recovery, but 
often, of course, the recovery remains incomplete, so that the patient has a more 
or less marked disturbance of function for life. The " middle form of chronic 
poliomyelitis " described by Erb, in which there is only a partial reaction of degen- 
eration in the paralyzed muscles, almost always gives a good prognosis. Those 
rare cases, however, in which the muscles of deglutition and respiration are in- 
volved, may have an unfavorable termination, although even then the possibility 
of an improvement is not to be entirely excluded. 

Anatomical lesions, which confirm the hypothesis of a subacute (inflamma- 
tory ?) affection in the anterior cornua of the cord ascending from below upward, 
are to be found, as we have said, only in an extremely small number of cases, and 
in part of them they are even not entirely trustworthy. Clinically, of course, the 
disease is wel] characterized, and is easy to diagnosticate with proper attention and 
knowledge. Further investigations must be made as to its anatomical basis and 
its relations to acute poliomyelitis and the primary neuritides. 

As follows from the above description, the treatment is by no means fruitless, 
and electrical treatment especially may produce the most complete and rapid 
regeneration of the affected parts. 



CHAPTER XI. 

ACUTE ASCENDING SPINAL PARALYSIS. 

{Paralysis ascendem acuta. Landry's Paralysis.) 

In the year 1859 Landry described a disease under the name of " paralysie 
ascendante aigue," which is chiefly characterized clinically by the fact that first 
the lower, and soon after the upper extremities, and finally a number of the 



636 



THE DISEASES OF THE SPINAL COED. 



muscular regions supplied by the medulla, are attacked by a rapidly advancing 
paralysis, while the sensibility and the functions of the bladder and rectum 
remain normal. In many cases the disease terminates fatally. Examination of 
the nervous system has so far, however, shown no lesion which can be regarded 
with certainty as the anatomical cause of the disease. Considering the continued 
and quite numerous observations of the disease, it seems questionable, at any rate, 
whether we can establish a uniform anatomical basis for it. The diversity of 
many symptoms {vide infra, the condition of the reflexes, the condition of the 
electrical excitability) points rather to the fact that the seat of the disturbance is 
not always the same. Nevertheless, we can not doubt the clinical resemblance of 
most cases, and we must regard it as possible that the same cause of disease does 
not always need exactly the same localization to provoke the disease. "We may 
very well recognize the setiological unity of " acute ascending paralysis," without 
claiming that all cases also agree completely in the clinical and anatomical 
details. 

General Symptomatology. — Acute ascending paralysis attacks chiefly previously 
strong and healthy persons in youth or middle life, somewhere between twenty and 
thirty-five years of age. Some cases have also been seen in children and older peo- 
ple. The disease seems to be more frequent in men than in women. 

The affection almost always begins with certain prodromata. These consist of 
general malaise, moderate febrile symptoms, headache, loss of appetite, and quite 
frequently of dragging and tearing pains in the back and the extremities. After 
these symptoms have lasted some days, or more rarely some weeks, during which 
they are comparatively slight, or so severe that many patients are already con- 
fined to the bed, there usually comes on quite suddenly, or sometimes more 
gradually, a paresis, first of one, but very soon of the other leg, which rapidly 
increases, and usually in a few days leads to an almost complete motor para- 
plegia. 

The paralysis is flaccid in almost all cases. The legs may be moved passively 
without any muscular resistance, and the muscles show neither active nor reflex 
tension. Their electrical excitability remains perfectly normal in many cases, 
but there is sometimes a rapid loss of faradic muscular excitability. It is not yet 
proved whether complete reaction of degeneration occurs. The reflexes, both 
cutaneous and tendon reflexes, seem to be diminished or wholly lost in the 
majority of cases, but some exceptions to this rule have been known. 

Sensibility is sometimes perfectly intact, but slight alterations do occur, and 
quite rarely there may be even marked anaesthesia. Sometimes a noticeable delay 
of sensation is observed. We find no changes in the nerves of special sense. 
There is sometimes a slight oedema in the legs, which is perhaps to be regarded as 
a vaso-motor disturbance. The marked sweating, from which many patients 
suffer, is also worthy of mention. The bladder and rectum in most cases are not 
at all affected, or they present merely slight and temporary disturbances. 

A short time after the legs are attacked, the arms also begin to be paretic. 
A marked motor weakness appears first in one, then in the other arm, and this 
may also increase to almost complete paralysis. The sensibility, the reflexes, and 
the electrical excitability show conditions like those in the lower extremities. The 
muscles of the trunk are also affected at the same time as, or still earlier than, the 
arms. The patient can no longer sit up in bed, turn on his side, etc. In some 
cases a paralysis of the muscles of the neck has also been observed. 

The third and last stage of the disease is characterized by the appearance of 
respiratory disturbances and bulbar symptoms. Manifest signs of a beginning 
respiratory paralysis appear; the respiration is labored and difficult, the move- 
ments of the diaphragm grow less, and the paroxysms of coughing are weaker. 



ACUTE ASCENDING SPINAL PARALYSIS. 



637 



Disturbances in swallowing, disturbances in articulation, and paresis of the soft 
palate and the lips may set in. In a few cases a facial paralysis and disturbances 
of the ocular muscles have been observed. The condition grows worse acutely, 
and, as we have said, in many cases death ensues. 

Beside the symptoms thus far mentioned, referable to the nervous system, we 
find certain other symptoms in almost every case, which are less striking, but yet 
are of greater significance in judging of the disease. The first of these is fever. 
The temperature is usually elevated from the beginning ; it may temporarily 
show quite a considerable increase, up to 104° (40° C), and later it varies some- 
where between 100° and 102° (38°-39° C), but there are even more marked remis- 
sions down to normal. Of the internal organs the spleen shows the most frequent 
changes. It is usually swollen moderately, but still it is swollen to a clearly 
manifest extent. There is also sometimes a slight albuminuria. 

In the cases with a fatal termination the whole duration of the disease is some- 
times only a few days, and as a rule a week or two, or rarely more. Fortunately, 
however, all cases do not terminate fatally. The disease may come to a stand- 
still at any time, even if the most threatening symptoms are present. Then the 
paralysis shows no further advance, the disturbances present disappear, and 
recovery ensues after a course of several weeks. It is, of course, usually quite a 
long time before the patient again feels himself in possession of his full powers. 

Pathological Anatomy and Pathogenesis.— If we consider the whole picture of 
acute ascending paralysis, the idea is necessarily forced upon us that we have to 
do here with an acute infection of the body, with a predominating localization in 
the motor nervous system, an opinion which was first expressed by Westphal. 
The beginning of the disease with general malaise corresponds perfectly to the 
prodromal stage of many other acute infectious diseases. The fever, the acute 
splenic tumor, and the occasional albuminuria can also scarcely be explained in 
any other way, according to our present views, except by the above hypothesis. 

The anatomical examination has, of course, as yet brought no certain proof for 
this theory. A notable case, published by Baumgarten, in which many rods, like 
the bacilli of splenic fever, were found in the spinal cord, is at present wholly 
unique ; but the completely negative anatomical lesions in many cases seem to 
point to the fact that we must look for the cause of the severe nervous symptoms 
chiefly in the disturbance of function excited by a toxic (infectious) influence. 
We have already signified that the point of attack of the infectious agent need 
not always be precisely the same. The condition of the reflexes and the rapid 
loss of electrical excitability, in connection with the pains at the beginning, seem 
to justify the hypothesis that the disturbance sometimes has its chief seat in the 
peripheral motor nerves, that the disease then exhibits the most acute form of 
infectious "multiple neuritis 1 ' (vide supra). More accurate anatomical investi- 
gations directed to this point will perhaps procure some positive support for this 
theory. In other cases, however, the motor portions of the spinal cord, the lat- 
eral columns, and the anterior gray cornua, are perhaps chiefly affected. This 
idea is supported by the occasional discovery (R. Schulz and F. Schultze, von 
den Delden) of an acute myelitic affection in the parts named. 

Diagnosis and Prognosis.— In every paralysis of the lower extremities begin- 
ning acutely and accompanied by general symptoms and fever we must consider 
the possibility of an acute ascending paralysis, but only the further course of the 
disease can decide the question. Inasmuch as only a well-characterized clinical 
group of symptoms is meant by the above term, the diagnosis is always easy to 
make, with attention to the peculiarities given above. It is more difficult, how- 
ever, to decide accurately whether the case corresponds rather to the type of an 
acute multiple neuritis or to the type of an acute ascending spinal paralysis. We 



638 



THE DISEASES OF THE SPINAL COED. 



can judge as to this point only by careful attention to the single symptoms, espe- 
cially the condition of the sensibility (pains, anaesthesia), of the reflexes, and of 
the electrical excitability. 

The prognosis must at first be made with great reserve, and we must especially 
bear in mind the possibility of a rapidly fatal termination. If the first acute stage 
passes off fortunately and there is a decided cessation in the extension of the 
symptoms of paralysis, the prognosis is quite favorable, for we may then expect 
that the patient will be completely restored. 

Treatment. — We can not be certain whether an energetic " derivative treat- 
ment " is of advantage in the beginning of the disease. Dry cups along the verte- 
bral column are recommended, and even the use of the hot iron to the back. We 
would hardly advise the latter. It may be recommended, however, to prescribe 
an inunction with mercurial ointment, thirty to forty-five grains a day, as in anti- 
syphilitic treatment. Of internal medicines we may give iodide of potassium 
or ergotine. It also seems to be a good plan to begin galvanic treatment early, 
galvanism to the spine and peripherally. If threatening attacks of respiratory 
insufficiency come on, electrical excitement of the phrenic nerve and of the respir- 
atory muscles sometimes affords relief to the patient. 

If the symptoms are arrested, electrical treatment and the use of baths may do 
most to hasten convalescence. 



CHAPTER XII. 

NEW GROWTHS OF THE SPINAL CORD AND OF ITS MEMBRANES. 

Pathological Anatomy. — Tumors of the spinal cord are rare. The commonest 
primary new growth is the glioma, which probably arises from the neuroglia, and 
is a cellular and vascular tumor. We often find in gliomata secondary softening 
(the formation of cavities, see the following chapter) and haemorrhages. The 
tumor is situated most frequently in the cervical or upper dorsal cord, and may 
have a considerable longitudinal extent, and a transverse diameter of several 
centimetres. 

Of other new growths in the spinal cord we may mention solitary tubercles, 
syphilomata, and myxomata (myxo-sarcomata). 

In the spinal meninges have been found sarcomata, fibromata, lipomata, myxo- 
mata, and syphilomata. A carcinoma arising from the vertebrae may also reach 
the spinal meninges by direct invasion. Marked signs of compression, and the 
consequent secondary degenerations, often show themselves in the spinal cord at 
the point where a new growth is situated in the meninges. 

We know practically nothing of the aetiology of new growths in the spinal 
cord. It is merely worthy of note that, in the cases of glioma of the spinal cord 
observed, an injury, such as a fall on the back, etc., very often preceded the appear- 
ance of the first symptoms. 

Symptomatology. — A general description of the tumors of the spinal cord can 
not be given, since, of course, the individual symptoms must differ in almost every 
case, according to the seat and the extent of the new growth. 

In tumors of the meninges the symptoms of compression of the cord are often 
quite prominent. In the beginning we notice pronounced " root symptoms " — 
that is, shooting pains, stiffness, paraesthesia, anaesthesia, etc. Later on the results 
of the compression of the cord show themselves : motor weakness, which may 
increase to a complete motor and sensory paraplegia. We can not here go more 



CAVITIES AND FISSURES IN THE SPINAL CORD. 



639 



fully into the details. They follow of themselves from attention to the general 
laws to be considered for localization of lesions in the spinal cord. 

In tumors of the spinal cord marked symptoms of sensory irritation are usually 
absent at first. A complicated type of spinal disease gradually develops, in which 
all those symptoms may be present in a single case which we have learned to recog- 
nize more exactly in the description of diffuse chronic myelitis. In fact, the dif- 
ferential diagnosis between tumor and transverse myelitis is often impossible, but 
certain peculiarities in the type of disease are sometimes present, which at least 
turn our suspicions to the possibility of a tumor. Among them especially is the 
early asymmetry of the symptoms on the two sides. Since a tumor may at first 
be confined to one half of the spinal cord (which scarcely ever happens in mye- 
litis), the signs of a unilateral lesion of the spinal cord {vide infra, Chapter XV) 
are often observed in tumors in a more or less pronounced fashion. A certain 
change in the symptoms, improvements, and new and quite sudden changes for 
the worse, are sometimes noticed, a circumstance which is probably to be referred 
to a change in the fullness of the vessels, or to haemorrhages in the substance of 
the tumor. The diagnosis of a tumor of the spinal cord, however, can at most be 
made with a certain probability. The decision as to the seat and the extent of the 
tumor is based upon precisely the same rules as in the diagnosis of the different 
forms of myelitis. We can hardly ever predict anything definite as to the kind 
of tumor. 

The prognosis of tumors of the spinal cord is utterly unfavorable. The course 
of the disease is often protracted for several years, but the final termination is 
always fatal, from general weakness, cysto-pyelitis, and bed-sores. The treatment 
is purely symptomatic, and is the same as in chronic myelitis. If there is a sus- 
picion of a previous syphilis, we must try inunction and the internal exhibition of 
iodide of potassium. 



CHAPTER XIII. 

THE FORMATION OF CAVITIES AND FISSURES IN THE SPINAL 

CORD. 

Pathological Anatomy and Pathogenesis.— The abnormal formation of cavi- 
ties in the spinal cord either arises from a dilatation of the central canal (hydro- 
myelus), or it develops outside of the central canal, and near it (syringomyelia). 
The cases of pure hydromyelus are recognized by the fact that the cavity is 
found in the middle of the cord, corresponding to the position of the central 
canal, and that its walls are covered by cylindrical epithelium. Slight degrees of 
hydromyelus, in which the dilated central canal has a diameter of a millimetre, 
or a millimetre and a half, are quite frequently found. The dilatation usually 
extends over only a portion of the spinal cord. Higher degrees of hydromyelus, 
where the central canal is dilated to a diameter of half a centimetre, or a centi- 
metre, are much rarer. In such cases the substance of the cord suffers from the 
internal pressure on it. 

In regard to the origin of hydromyelus, following Leyden's example, we may 
consider anomalies of development in the formation of the central canal to be a 
cause in at least a part of the cases. Certainly only exceptionally do we have a 
process of stasis, as Langhans has found in some cases, which may have its origin 
in an increased pressure in the posterior fossa of the skull, from tumors, etc. 

As to most cases of syringomyelia, however, the discoveries of Westphal, Simon, 
and F. Schultze leave scarcely a doubt but that they arise from a destruction of 



640 



THE DISEASES OF THE SPINAL COED. 



proliferated masses of neuroglia. We have the formation of a central glioma, 
probably arising usually from the ependyma of the central canal itself, or from 
its vicinity, with a secondary disintegration and the formation of a cavity. In 
these cases we can make out the newly formed masses of neuroglia about the cavi- 
ties, either proliferating or disintegrating. The cavity is usually situated quite 
close to the center, and extends most frequently into the substance of the posterior 
columns. In its longitudinal extent it may involve a great part of the cord. 

Clinical Symptoms. — We can not give a uniform picture for the formation of 
cavities in the spinal cord, since the symptoms, of course, must vary very much, 
according to the seat and the extent of the change. Slight dilatations of the cen- 
tral canal may run their course entirely without symptoms. In the cases of exten- 
sive cavity formation, with much damage to the surrounding substance of the 
cord, there usually arises a severe and complex array of spinal symptoms, whose 
correct interpretation can hardly ever be made with certainty during the patient's 
life. If the posterior columns and posterior cornua are chiefly involved in the 
cavity formation, the results of the disturbance of function of those parts are espe- 
cially prominent. In the celebrated case of general anaesthesia which Spath and 
Schiippel have described, a very extensive syringomyelia was found in the spinal 
cord on autopsy. In other cases, where the gray matter of the anterior cornua is 
chiefly affected, extensive atrophic paralyses develop, so that the type of disease 
may very much resemble amyotrophic lateral sclerosis. In complicated forms of 
disease especially, with atrophic paralysis of the upper extremities, we must think 
of the possibility of a syringomyelia. The diagnosis, however, can never be made 
with certainty, but only hypothetically by the exclusion of other possibilities. 

The prognosis is, of course, always unfavorable, but the course is veiy slow, 
and there are long-continued apparent cessations of the disease. 

The treatment is purely symptomatic, and follows the same rules as in chronic 
myelitis. 

APPENDIX. 

SPINA BIFIDA. 

{Hydrorrhachis. Myelocele. Meningocele.) 

We give the name of spina bifida to a congenital fissure-formation on the pos- 
terior side of the vertebral arches, due to anomalies of development, and associated 
with a hernia-like protrusion of the sac of the dura. The most frequent seat of the 
malformation is in the sacral and lumbar regions. Only rarely is the tumor so great 
as to hinder the birth of the child. Children afflicted with spina bifida are usually 
born normally, and only after delivery do we find the tumor in the sacral region, 
whose size may be from that of a small nut to that of the fist and over. The skin 
above the tumor is sometimes entirely normal, but in other cases very tense and 
reddened. If we have an oi3portunity to examine the tumor carefully anatomic- 
ally, we usually find beneath the skin the protruded sac of the dura, and beneath 
it the arachnoid. Only rarely is the dura also fissured, so that the sac is formed 
exclusively of the arachnoid. It is filled with a clear fluid which is precisely 
identical with the cerebro-spinal fluid. In rare cases there is also a dilatation of 
the central canal, hydromyelus ; then the substance of the cord is atrophied to a 
greater or less extent, and the central canal communicates directly with the cavity 
of the spina bifida. In other cases the condition of the cord is normal ; sometimes 
its lower end is adherent to one spot of the sac. We must refer to the text-books 
of pathological anatomy in regard to the many further details of the anatomy 
and the history of development. 

In regard to the clinical symptoms of spina bifida, the condition of most chil- 



SECOND AEY DEGENERATIONS IN THE SPINAL CORD. 641 



dren at first is perfectly normal, apart from the malformation. The tumor itself 
usually feels tense. If we exert pressure on it with the hand, we can often force 
part of its contents hack into the vertebral canal. This causes an increase of the 
cerebral pressure, and we notice, beside the lessening of the spina bifida, a marked 
expansion of the f ontanelles, and also the appearance of somnolence, contractions, 
and changes in the pulse and respiration, which demand a speedy interruption 
of this rather dangerous experiment. If such symptoms do not appear at all, 
we can conclude that the sac is completely constricted and closed. 

Only rarely, however, does the child's condition remain normal later on. The 
tumor usually shows a slow growth, and the results of pressure on the spinal 
cord or on the can da equina gradually appear. Paralysis, anaesthesia, vesical dis- 
turbances, bed-sores, etc., develop, and these symptoms finally lead to death. Still 
more frequently the sac bursts, or its walls inflame, and this becomes fatal from 
the onset of a purulent meningitis. 

The prognosis of most cases of spina bifida is accordingly to be regarded as 
unfavorable unless we succeed in curing the disease by surgical treatment. 
Recovery has been brought about in many cases by methodical compression of 
the sac, and by puncture, with evacuation of the fluid and a subsequent injection 
of a solution of iodine to obtain an obliteration of the sac ; but, on the other hand, 
the operative treatment of spina bifida is attended with many dangers, such as 
meningitis, so that we can note frequent bad results as well as favorable ones. 
We can not here go into the details of the surgical methods for the cure of spina 
bifida ; they can be found in full in the text-books of surgery. 



CHAPTER XIV. 
SECONDARY DEGENERATIONS IN THE SPINAL CORD. 

Although the secondary degenerations in the spinal cord are chiefly interesting 
merely from an anatomical point of view, we must briefly describe them, because, 
in the first place, a clinical significance has been ascribed to them in certain quar- 
ters, and also because the study of secondary degenerations has been the starting- 
point of all our present knowledge as to the systemic diseases of the spinal cord. 

1. Secondary Degeneration in the Spinal Cord after Cerebral Lesions. — We 
already know (compare page 521) that every lesion of the great motor ganglion- 
cells in the anterior cornua of the spinal cord, and every permanent break in con- 
duction in the motor nerves themselves, is followed by a secondary degeneration 
of the peripheral portion of the motor fibers. We assume as the reason for this, 
as we have seen, a " trophic influence " of the said ganglion-cells on the motor 
fibers arising from them, so that the latter degenerate when the conduction of 
that trophic influence is interrupted, or when the trophic ganglion-cells them- 
selves are destroyed. Precisely analogous conditions exist for the first great por- 
tion of the motor conducting tract, the lateral pyramidal tract, from the cortex 
cerebri to the anterior cornua of the spinal cord. The great ganglion-cells of the 
motor portion of the cortex cerebri also exert a trophic influence on the motor 
fibers arising from them, which extends to the motor ganglion-cells of the spinal 
cord. If there is disease situated in the motor portion of the cortex cerebri itself, 
or in any part of the motor tract in the brain (the motor fibers of the corona radi- 
ata, the internal capsule, the crus, or the pons), by which disease the conduction is 
interrupted — if there is disease there, we repeat, a secondary descending degenera- 
tion of the motor fibers sets in in the whole portion below, down to, but exclusive of, 
41 



642 



THE DISEASES OF THE SPINAL COED. 







the anterior cornua of the gray matter. This secondary descending" degeneration 
of the pyramidal tract is found correspondingly in the pyramid of the same side 
on which the focus of disease in the brain is situated. From 
this point we can trace the main part of the degeneration 
farther down the lateral column of the spinal cord on the 
opposite side (secondary degeneration of the lateral crossed 
pyramidal tract (see Fig. 91), while in many cases beside we 
find a slighter secondary degeneration in the anterior column 
of the spinal cord on the same side (secondary degenera- 
tion of the anterior uncrossed pyramidal tract). As we 
know from Flechsig's investigations, the relative amounts 
of the crossed lateral fibers, and the anterior fibers that re- 
main uncrossed, vary in individual cases within certain 
limits. In the cases where no anterior pyramidal tract exists 
— that is, where all the motor fibers pass over to the lateral 
column of the opposite half of the spinal cord in the decus- 
sation of the pyramids — of course a descending degenera- 
tion in the anterior column is wholly wanting. We must 
add, however, that in some cases a small number of fibers 
seem to proceed uncrossed in the lateral column, so that 
accordingly we may also have a slight secondary descend- 
ing degeneration in the lateral pyramidal tract of the same 
(affected) side (Pitres). 

2. Secondary Degenerations in the Spinal Cord in 
Transverse Affections of the Spinal Cord itself. — If a 
lesion is situated in any part of the spinal cord, by which 
more or less of its transverse section is affected, the inter- 
ruption of conduction in these fibers is also followed by the 
appearance of secondary degenerations which may be made 
out both in a descending and in an ascending direction 
(see Fig. 92). It is most frequently transverse myelitis, 
compression of the spinal cord, and tumors of the cord, 
which give rise to secondary degenerations. The latter, 
however, of course, are never due to the sort of lesion, but 
only to its seat, and to the interruption of conduction 
caused by it. 

The secondary descending degeneration affects the py- 
ramidal tract in a fashion precisely analogous to that which 
we have also learned to recognize in secondary degenera- 
tions after cerebral lesions ; but, since the primary affec- 
tion usually affects the pyramidal tract on the two sides, the 
descending secondary degeneration of course develops in 
both lateral pyramidal tracts, and also in the anterior py- 
ramidal tracts, if they exist below the point of lesion. 

The secondary ascending degeneration, developing up- 
ward from the primary point of disease, affects two systems 
of fibers, the so-called columns of Goll (the internal por- 
tion of the posterior columns), and also at the same time 
the lateral cerebellar tracts * on the periphery of the lateral 







Fig. 91.— Secondary de- 
scending degeneration 
of the pyramidal tracts 
in a primary lesion of 
the left half of the cer- 
ebrum. The lateral 
pyramidal tract of the 
right half of the cord is 
degenerated down to 
the lowest part of the 
lumbar region (1-8) ; 
the anterior pyramidal 
tract of the left half of 
the cord is degener- 
ated to the beginning 
of the lumbar enlarge- 
ment (1-6). 



* The area of the ascending degeneration of the "lateral cerebellar 
tract," as may be seen in the picture, shows at its anterior end a marked 
expansion. Possibly this anterior portion of the degenerated fibers cor- 
responds to another system (Bechterew). 



UNILATERAL LESION OF THE SPINAL CORD. 



643 



columns and external to the lateral pyramidal tracts. Both systems of fibers 
mentioned, whose conduction is in a centripetal direction, must accordingly 
receive trophic influences from more peripheral ganglion- 
cells. The connection of the columns of Goll with the 
gray matter (spinal ganglia ? posterior cornua ?) is not yet 
accurately known. The fibers of the lateral cerebellar 
tracts, however, are certainly connected with the cells of 
the columns of Clarke. If these also are destroyed by any 
process in the lower dorsal and upper lumbar cord, an 
ascending degeneration of the lateral cerebellar tracts de- 
velops, which may be traced upward into the restiform 
body. The further course of the fibers to the cerebellum is 
not yet certainly known. 

Although no clinical significance at all can be attributed 
to secondary ascending degeneration, the theory first ad- 
vanced by the French observers (Charcot and others) pre- 
vails almost universally, that secondary descending degen- 
eration causes definite clinical symptoms. The secondary 
contractures and the increase of the tendon reflexes in the 
paralyzed limbs, occurring in hemiplegia, are especially 
referred to this. We shall see in a later section that this 
theory is by no means proved, and is even improbable, so 
that, in our opinion, the secondary descending degeneration 
also has no material clinical significance. 

3. Secondary Degeneration in the Spinal Cord after 
Injuries of the Cauda Equina. — After injuries of the 
cauda equina — for example, after fractures or caries of the 
lower lumbar vertebrae and of the sacrum, in new growths 
in this region, etc. — a secondary ascending degeneration 
occurs in the spinal cord, if an actual solution of conti- 
nuity of the fibers has existed for a long time, which de- 
pends exclusively upon the lesion of the affected posterior 
root-fibers. This is accordingly limited to the posterior columns of the spinal 
cord, and in its distribution it shows a great resemblance to the condition of the 
degeneration in locomotor ataxia. In the lumbar cord the greater portion of the 
posterior columns is degenerated, with the exception of a little median zone and 
the most anterior portion (compare Fig. 84). The degeneration grows smaller 
upward, and finally limits itself in the cervical cord to the region of the columns 
of Goll. Thus this condition again affords a proof of the correctness of the state- 
ments advanced by Singer, Kahler, and others, that the columns of Goll form, 
at least in part, the prolongation of the fibers from the root-zones of the lumbar 
cord (compare page 480). 



CHAPTER XV. 

UNILATERAL LESION OP THE SPINAL CORD. 

(Brown-Sequard's Spinal Paralysis.) 

Unilateral lesion is not a definite disease of the spinal cord, but a peculiar 
group of symptoms, which occurs whenever an interruption of conduction is 
produced by any affection in one lateral half of the spinal cord. Since the symp- 




Fig. 92. — Secondary as- 
cending and descend- 
ing degeneration in a 
transverse affection of 
the upper dorsal re- 
gion. The columns of 
Goll and the direct 
cerebellar tracts are 
degenerated upwards. 
The lateral pyramidal 
tracts are degenerated 
downwards. 



644 



THE DISEASES OF THE SPINAL COED. 



toms in these cases were first carefully studied clinically and experimentally by 
Brown-Sequard in particular, we often call the type of disease in question " Brown- 
Sequard's paralysis." We see this paralysis most frequently and in its purest 
form in injuries of the spinal cord. Almost perfectly exact sections of one lateral 
half of the spinal cord are repeatedly produced by stabs from a knife, a sword, etc. 
Inflammatory processes, compression, and especially tumors of the cord, may also, 
during a certain period of their course, cause the symptoms of a more or less 
sharply defined unilateral lesion. 

The peculiar condition of the symptoms in unilateral lesion is easily explained 
by a consideration of the course of the fibers in the spinal cord. In the accom- 
panying diagram (see Fig. 93) the motor 
fibers from the anterior roots are marked 
v, the sensory fibers from the posterior 
roots, h. As we have already said, the 
sensory fibers, h, pass at once into the op- 
posite half of the spinal cord, and accord- 
ingly decussate with the corresponding 
sensory fibers of the other side. The 
motor fibers, v, however, pass upward un- 
crossed on the side* they enter the spinal 
cord, especially in the lateral column. If 
now, for example, there is situated on 
the right side of the spinal cord at a a 
lesion, like a section of one half the cord, 
the conduction of those motor fibers 
which come from the right side is inter- 
rupted, as well as the conduction of those 
sensory fibers which come from the left 
side. From this it follows that there 
must be a motor paralysis on the same side 
of the body as the lesion in the spinal 
cord, and a sensory paralysis (anaesthesia) 
on the other side of the body. If the 
affection is situated in the dorsal or lum- 
bar cord, the leg on the corresponding 
side is paralyzed, and the leg on the other 
side is anaesthetic. If the lesion is situ- 
ated in the cervical cord, above the en- 
trance of the nerves for the upper ex- 
tremities, the arm and the leg on the side 
of the lesion are both paralyzed (spinal 
hemiplegia), while the arm and the leg on the other side are anaesthetic, but their 
motility is normal. 

On more careful examination, further conditions of physiological interest 
appear. The sensibility on the side of the motor paralysis is usually not only 
normal, but there is even a pronounced hyperesthesia for all, or at least for some, 
of the forms of irritation. Slight pricks are very painful, and tickling the soles of 
the feet is felt with abnormal strength. The muscular sense alone (the feeling 
for passive motion) is a noteworthy exception, since it is usually markedly dimin- 
ished on the paralyzed side. We can explain this fact only by Brown-Sequard's 
theory that the fibers for the muscular sensibility (see 2 and 2' in Fig. 93), in dis- 
tinction from all the other sensory fibers, run their course in the spinal cord 
uncrossed, just like the motor fibers. 




Fig. 93.— (From Erb.) Schematic representation 
of the course of the main tracts in the cord, 
represented for a single pair of roots, v. An- 
terior roots, h. Posterior roots. 1. Paths for 
motor and vaso-motor conduction. 2. Paths 
for muscular sense. 3. Paths for cutaneous 
sensibility on the right. 1', 2', 3'. The same 
paths on the left. The arrows indicate the 
direction of physiological conduction. 



UNILATERAL LESION OF THE SPINAL CORD. 



645 



Above the hyperaesthetic territory in the skin we usually find a small anaes- 
thetic zone (Pig. 94, b), and above this at times again a small hypersesthetic strip 
(see Fig. 94, c). The anaesthetic zone is easily 
explained. It corresponds precisely to the 
level of the lesion in the spinal cord — that is, 
to those sensory fibers coming from the same 
side, which are immediately involved as soon 
as they enter the cord ; but a satisfactory ex- 
planation is entirely lacking for the appear- 
ance of the hyperaesthesia on the paralyzed 
side, and for the origin of the uppermost small 
hyperaesthetic zone. 

The reflexes, especially the tendon reflexes, 
are usually increased on the paralyzed side. 
There is often a vigorous ankle clonus, a symp- 
tom which must be explained by the loss of 
the reflex inhibitory influences coming from 
above. Finally, we often find on the side of 
the lesion the signs of a vaso-motor paralysis, 
especially a marked rise in the cutaneous tem- 
perature of even 2° (1° C), or more. 

On the anaesthetic side, however, in pure 
cases, the motility, and also the muscular sense, 
are perfectly normal, in distinction from the 
other forms of sensation. Above the anaes- 
thetic region we also find frequently a small 
hyperaesthetic zone (see Fig. 94, c). The re- 
flexes are usually normal, or only a little in- 
creased. 

Of the other spinal symptoms we have still 
to mention the almost invariable disturbance 
of micturition and defecation, neuralgic pains, 
now more on one side and now more on the 
other, muscular atrophy, changes in the elec- 
trical excitability, etc. All these symptoms 
are not characteristic of the unilateral lesion 
as such, and are always easily explained in 
any given case from the localization of the 
disease. We must also mention that the symp- 
toms of unilateral lesion are often not per- 
fectly pure, but we can recognize only a few 
prominent features of them. 

We need add nothing as to the prognosis and treatment of unilateral lesion, 
because, of course, they are governed entirely by the form of the primary disease. 




Fig. 94.— Schematic representation of the 
chief symptoms in unilateral lesion of 
the left dorsal cord. (After Erb.) The 
oblique shading signifies motor and 
vaso-motor paralysis ; the vertical 
shading signifies cutaneous anaesthe- 
sia ; the dots signify cutaneous hyper- 
esthesia. 



THE DISEASES OF THE MEDULLA OBLONGATA. 



IV.— The Diseases of the Medulla Oblongata. 



CHAPTER I. 

PROGRESSIVE BULBAR PARALYSIS. 

( Glosso-labio-laryngeal Paralysis. ) 

Duchenke in 1860 described for the first time with completeness the symptoms 
of a disease to which Wachsmuth has since given the name of progressive bulbar 
paralysis. Duchenne did not, however, recognize the true seat of the disease, and 
it was not till 1870 that Charcot in France, and E. Leyden in Germany, were 
enabled to confirm the suggestion of Wachsmuth that the lesion is a progressive 
degeneration and atrophy of the nuclei in the medulla oblongata. Since then 
our knowledge of the disease has grown rapidly, both from the clinical and the 
anatomical standpoints ; and Kussmaul and others have thoroughly investigated 
its relations to two other closely allied forms of disease— amyotrophic lateral 
sclerosis, and progressive muscular atrophy. 

etiology. — We have scarcely any certain information about the cause of the 
disease. Heredity seems of slight importance. In some cases its origin is ascribed 
to catching cold, emotional excitement, traumatic influences, and excessive bodily 
exertion. Perhaps it is sometimes occasioned by excessive use of the muscles to 
which the disease is chiefly confined, as in playing on wind-instruments ; but in 
many instances no possible cause can be found. Men seem somewhat more liable 
to be attacked than women. The disease hardly ever appears till middle or old 
age — that is, after thirty-five. 

Clinical History. — The symptoms are almost always very slow in their develop- 
ment. There may be mild premonitory symptoms — such as painful sensations in 
the back of the neck. Then there is a very gradual appearance of difficulty in 
articulation. Many words are pronounced indistinctly. The first trouble is noticed 
especially with letters in the utterance of which the tongue plays an essential part : 
E, R, L, S, G (hard), K, D, T, and N.* It is easily seen that the derangement is not 
aphasic. There is no forgetting or confounding of the words or letters ; but the 
innervation of the tongue has become impaired. Long before the ordinary move- 
ments of this member are visibly embarrassed, the patient has lost the ability to 
make those more delicate manipulations of it which are essential to normal 
speech. This disturbance of articulation is termed alalia or anarthria. 

By the time this has become somewhat marked, it is usually possible to detect, 
on close examination, that the tongue is beginning to atrophy. It seems flabby, 
thin, and less rounded. Here and there its surface presents furrows and depres- 
sions; and often the individual fasciculi exhibit active fibrillary contractions. 
Just as in progressive muscular atrophy, the impairment of motion usually 
keeps equal pace f with the atrophy. The greater the atrophy, the less is the 

* [Except as otherwise specified, the letters and words used as examples here and later on are to 
be given the ordinary English pronunciations. — Trans.] 

t At the commencement of the disease the paralysis may possibly seem greater than the atrophy, 
so far as the latter can be detected. Nor would it be impossible for a primary lesion of the nuclei of 
nerves to result in a paralysis before the secondary descending degeneration had become completely 
developed. On the other hand, it must be borne in mind that numerous individual fibers in the lip or 
tongue might be already atrophied before the eye or the touch could appreciate any change in bulk. 



PROGRESSIVE BULBAR PARALYSIS. 



mobility. Finally it becomes quite impossible to project the tongue from the 
mouth or move it from side to side. The tongue lies flat and limp on the floor of 
the mouth. Its surface is often diversified with furrows and depressions, contain- 
ing much desquamated epithelium or the like. Evidently any great impairment 
of motility in the tongue hinders not only speaking, but also chewing and swal- 
lowing. The organ can no longer bring out such portions of the food as get 
between the cheeks and the teeth, nor can it push the bolus backward within the 
grasp of the pharyngeal constrictors. 

Even before the atrophy of the tongue becomes extreme, analogous disturb- 
ances usually appear in neighboring groups of muscles. As a rule, the muscles of 
the lips are next affected after the tongue. The first thing the patient notices is 
a peculiar feeling of stiffness or tension in the lips. Movement becomes gradually 
more and more difficult ; and the patient becomes unable to pucker up his lips so as 
to whistle. Speech is also noticeably interfered with, for now all those letters the 
pronunciation of which demands labial movements are very imperfectly articu- 
lated, and at last can not be uttered at all. These are 0, A (long), P, F, B, M, 
and V ; and also the sound of double O, as in tool. It also becomes gradually 
evident that the lips atrophy. They grow thin, with sharp edges and wrinkled 
skin. Fibrillary contractions are not infrequently visible. 

This atrophy of the orbicularis oris is followed by atrophy and paresis of some 
of the other muscles of expression supplied by the lower division of the facial 
nerve. The general facial expression of a patient with bulbar paralysis thus 
comes to bear a very characteristic stamp : the mouth remains half open, and 
seems to be broadened out, the lower lip hangs down, the naso-labial folds are 
deepened, and indeed the whole aspect is persistently lachrymose. Even in 
laughing, the lower half of the face relaxes comparatively little; while the region 
supplied by the upper division of the facial nerve, and the movements of the eye- 
ball, remain as a rule perfectly normal. 

The third group of muscles affected are those of the pharynx and larynx. 
The soft palate becomes paretic, and produces further trouble in swallowing. 
Quite often the liquid ingesta are regurgitated through the nose. The voice 
becomes nasal. The production of many sounds, and in particular of B and P, 
is now impossible, since, in addition to the labial paresis, a portion of the essential 
current of air escapes through the nostrils. This explains why the letters men- 
tioned can sometimes be pronounced better if the nose be compressed. The 
paralysis of the constrictors of the pharynx impedes deglutition more and more, 
till the impairment of nutrition becomes extreme. 

The enfeebled action of the laryngeal muscles is betrayed, in the earlier 
stages of the disease, by a certain weakness and monotony in speaking. Modula- 
tions of the voice, and the production of the higher notes, as in singing, are no 
longer possible. If the innervation of the larynx becomes still more impaired, it 
becomes a very serious matter. If the arytaenoid cartilages do not press together 
firmly on swallowing, the entrance to the larynx is inadequately closed, and food 
is often swallowed the wrong way. Liquid and even solid ingesta get into the 
larynx, and excite a violent cough ; or, being inhaled into the air-passages, they 
cause bronchitis or lobular pneumonia. The paralysis may reach such a degree 
that the voice is at best a hoarse whisper. With the laryngoscope we can see that 
the vocal cords are paralyzed. The inability to close the glottis tightly is 
extremely unfavorable, for it renders the patient unable to cough vigorously. 
Mucous accumulations may therefore come to be the source of extreme dyspnoea. 

The catalogue of symptoms is not yet ended. As we have seen, the muscular 
atrophy of the tongue and lips can invariably be detected. That of the pharyn- 
geal and laryngeal muscles can not be demonstrated during life, although it is to 



648 THE DISEASES OF THE MEDULLA OBLONGATA. 



be found post mortem. Inasmuch as the process is one of genuine degeneration 
with consequent atrophy, the affected fibers ought to give the reaction of degenera- 
tion to electricity ; but this is difficult of actual proof, just as it is in progressive 
muscular atrophy, because numerous healthy fibers lie side by side with the 
degenerated ones. Still, in an advanced case, careful examination will usually 
bring out an evident degenerative reaction here and there in the tongue and 
lips. 

The disturbance of reflex action is often striking. Usually the reflexes are 
greatly diminished or even absent, so that one can tickle the root of the tongue and 
the epiglottis without causing the patient to gag. In a few instances the facial 
muscles exhibit an increase of tendon reflex, as can be shown by tapping upon 
the tendons, the periosteum of the jaws, or the bridge of the nose. This behavior 
reminds one of the condition of the muscles in amyotrophic lateral sclerosis (q. v.). 

Exceptionally, still other muscular groups are involved. Of such disturbances, 
the most frequent is in the region supplied by the motor branch of the trigeminus, 
impairing mastication. The impairment of these muscles now combines with the 
labial and lingual atrophy to render chewing almost impossible. In very rare 
cases the ocular muscles are also involved, with resulting ptosis and strabismus. 

All the symptoms thus far enumerated are exclusively motor. Sensation is 
perfect to the end. The sensibility of the skin of the face and of the mucous 
membrane of the tongue and mouth, as well as the sense of taste, are unimpaired. 
Disturbances of sensation in the distribution of the trigeminus, and more or less 
deafness, have been reported in one or two cases ; but there is some doubt about 
the observations. It does, however, seem certain that secretory and vaso-motor 
derangements are frequent. Salivation deserves especial mention. In many 
cases of bulbar paralysis it is a constant symptom, so that the patient is obliged 
to keep a pocket-handkerchief to his mouth, to catch the fluid as it dribbles away. 
This is due, to a certain extent, to the fact that the secreted saliva can not be 
swallowed, and, as the lips do not shut tightly, it naturally escapes from the 
mouth ; but volumetric examinations have rendered it pretty certain that the 
amount of saliva is abnormally large. The explanation of this has not been 
determined. Nor as yet do we know much about the vaso-motor disturbances. 
Many patients complain of a feeling of heat and " boiling " in the head. We 
may also mention in this connection that occasionally, toward the close of the 
disease, the pulse becomes very rapid (140-160). This is probably due to paralysis 
of the vagus. 

The course of the disease is invariably protracted. The order in which the 
symptoms appear is, as a rule, that in which they have just been described. The 
atrophy and paresis appear first in the tongue, then in the lips and the neighbor- 
ing muscles of the face, and lastly in the muscles of the soft palate, pharynx, and 
larynx. Still, there may be some deviation from this. Usually the progress of 
the disease is very gradual. There may be an apparent arrest of the trouble ; or 
less often there are quite sudden exacerbations. When all the different symj)toms 
are well developed, the clinical picture is unusually characteristic. The peculiar 
immobility of expression; the broad, slightly gaping mouth, with the atrophied 
lips; the almost unintelligible speech, low, monotonous, and labored; and the 
inability to swallow — these often betray the disease at once. The last stage of 
the illness is the more distressing, in that the intelligence remains to the end 
entirely unclouded. 

The entire duration of the disease is usually several years — say two to five. If 
death is not caused by some intercurrent trouble, it is brought about in one of 
three ways : either through inanition, due to the increasing difficulty of degluti- 
tion ; or through pulmonary complications — namely, bronchitis, lobular pneumo- 



PROGRESSIVE BULBAR PARALYSIS. 



649 



nia, or gangrene, as a result of food passing down the trachea ; or through sudden 
asphyxia or cardiac failure. 

Pathology. Nature of the Disease, and its Appearance as a Symptom of Pro- 
gressive Muscular Atrophy or of Amyotrophic Lateral Sclerosis.— If we seek the 
anatomical lesion corresponding to the group of symptoms above depicted, we 
shall find, on microscopic examination of the nervous system, in all cases of this 
description, a typical disease of the medulla oblongata. The ganglionic nuclei 
and the nerves, corresponding to those muscles which we have found to undergo 
atrophy in bulbar paralysis, present distinct evidences of degeneration. This is 
most readily demonstrated in the nucleus of the hypoglossus. The ganglionic 
cells have some of them entirely disappeared, while others are greatly atrophied. 
The connective tissue is increased in amount, and the walls of the blood-vessels 
traversing the nucleus are thickened. In the earlier stages there are often many 
cells which contain granules of fat. The same changes, though perhaps less pro- 
nounced, are exhibited by the common nucleus of the vagus and accessorius, that 
of the facial, and sometimes also that of the glosso-pharyngeal nerve. The other 
nuclei are perfectly normal. We never find a diffuse "inflammation," but in 
every case a primary degeneration of the nuclei, which spreads no farther. 

Starting from these nuclei, the degeneration and atrophy may be seen to 
extend into the nerve-fibers which issue from them. The roots of the hypo- 
glossus, vagus, accessory, and facial nerves can often be seen by the naked eye to 
be diminished in size and of a gray color. The microscope always shows a partial 
atrophy of their fibers. Finally, there is a corresponding atrophy of muscles of 
the tongue, lips, and other parts. We need not enter into detail, for the histolo- 
gical conditions are precisely those seen in the muscles of the trunk and extremi- 
ties in progressive muscular atrophy. 

Thus we find progressive bulbar paralysis perfectly analogous with progressive 
muscular atrophy. The nuclei in the medulla oblongata are the motor and trophic 
centers of the bulbar nerves and of the muscles which these nerves supply. The 
relation is precisely that which exists between the anterior cornua of the spinal 
cord on the one hand, and the spinal nerves and the muscles which they inner- 
vate on the other. In both diseases there is a degeneration and atrophy of the 
trophic and motor center and the corresponding nerves and muscles. In both 
diseases the atrophy and the functional disability of the muscles keep pace with 
each other, and in both the affection is strictly limited to the motor tract, sensibility 
suffering no impairment whatever. Certain questions about bulbar paralysis are 
as unsettled as similar ones about progressive muscular atrophy. It is uncertain 
whether the primary degenerative process is limited to the bulbar nuclei, and the 
degeneration of the nerves and muscles is to be regarded as secondary ; or whether 
the entire motor apparatus, from the ganglionic eel] to the muscular fiber, is simul- 
taneously attacked ; or, finally, whether, as Friedreich maintains, the atrophy 
begins in the muscles, and thence ascends along the nerve-fibers to the medulla. 
We think it improbable that these points will be cleared up very speedily. Their 
solution would seem to be only of theoretical interest. 

We certainly must recognize, however, the essential identity of progressive 
bulbar paralysis and progressive muscular atrophy. The resemblance becomes 
even more striking if we consider that very frequently both diseases are present 
simultaneously. Often, after a case of progressive muscular atrophy has lasted 
for some time, the symptoms of bulbar paralysis also appear. And, on the other 
hand, an illness may begin with bulbar symptoms, and later on be complicated by 
atrophy of the muscles of the extremities — almost always first seen in the arms. 
If cases of this sort come to autopsy, we find a combination of the anatomical 
lesions of both diseases; in addition to the degeneration of the nuclei in the 



650 THE DISEASES OF THE MEDULLA OBLONGATA. 



medulla oblongata, there is marked atrophy of the ganglionic cells in correspond- 
ing places in the anterior gray cornua of the spinal cord. 

We must here refer again to the occurrence of the symptoms of bulbar paraly- 
sis in amyotrophic lateral sclerosis (see Chapter VII). In this disease, too, there 
is the same combination of a degeneration of the nuclei in the medulla oblongata 
and of the anterior cornua of the gray matter of the cord ; but in addition there is a 
derangement of the motor tract in the lateral columns. This addition modifies the 
picture, but otherwise the symptoms are almost precisely the same as in progressive 
muscular atrophy. Even the derangement of the crossed pyramidal tract is in per- 
fect harmony with the other lesions, for it represents merely a further invasion of 
the tract by which motor impulses are conducted. It seems justifiable, therefore, to 
say that these three diseases — progressive bulbar paralysis, progressive muscular 
atrophy, and amyotrophic lateral sclerosis — differing as they do in the localization 
of their lesions, are yet closely allied. They are essentially — that is, pathogenetic- 
ally, and perhaps also serologically — different results of one disease ; or, at least, 
the pathological process in each case must be nearly the same. In each there is 
a primary chronic degeneration of portions of the chief motor tract, varying only 
in region or in extent. If we accustom ourselves to regard these three groups 
of symptoms as really identical, we shall be less puzzled by the slight variations 
which different cases may present than if we attempt to differentiate the disor- 
ders too nicely on account of unessential variations. 

Diagnosis. — The diagnosis of a typical case of progressive bulbar paralysis has 
no difficulties, if we only hold firmly to the definition of the disease and its symp- 
toms as above depicted. Upon careful examination of the other muscles, and con- 
sideration of the course of the disease as a whole, we shall be able in each case to 
determine whether the bulbar trouble is the sole disease, or merely a part of a 
more extended degeneration of the motor tract. If there are no symptoms but 
those referable to the medulla oblongata, we must bear in mind that the phe- 
nomena of genuine progressive bulbar paralysis may be closely simulated by other 
bulbar diseases. The acute troubles, like thrombosis or haemorrhage, although 
they produce similar symptoms, can easily be differentiated by the manner of their 
appearance, contrasting with the invariably slow development of genuine bulbar 
paralysis. It is, however, much more difficult to eliminate gradually forming 
tumors situated in the medulla oblongata or its vicinity. Here prolonged observa- 
tion is frequently needed, until finally such phenomena appear as are foreign to typ- 
ical bulbar paralysis. Such symptoms are disturbances of sensation and invasion of 
the upper division of the facial, the nerves of special sense, and the ocular muscles. 
The same is true of that rare trouble, diffuse sclerosis of the medulla oblongata. 

It should also be mentioned that bilateral cerebral trouble may occasion so 
complete a paralysis of the tongue and lips, according to Lepine and others, as to 
simulate bulbar paralysis. Such cases have been termed " glosso-labio-pharyngeal 
paralysis of cerebral origin," or pseudo-bulbar paralysis. Indeed, in rare instances, a 
similar group of symptoms seems to be referable to unilateral cerebral disturbances. 
This is explained by assuming that the muscles involved upon both sides receive 
at least a portion of their motor nervous fibers from the same hemisphere. And 
yet in most of these cases of pseudo-bulbar paralysis the exclusion of the genuine 
disease is possible, because certain variations from the typical course of the disease 
are pronounced enough to set us right. Thus there is an abrupt onset, the paralysis 
is not perfectly symmetrical, or the lips and tongue react normally to electricity. 

Prognosis and Treatment— Despite the unfavorable prognosis of progressive 
bulbar paralysis, we must at least try to check the progress of the disease. Elec- 
tricity might be regarded as the most promising means to employ. To influence 
the seat of the trouble, galvanization is chiefly used. The poles are applied to 



BARER FORMS OF CHRONIC BULBAR PARALYSIS. 651 



the two mastoid processes, if possible, every day for two or three minutes, and 
the current is repeatedly reversed. We may also galvanize the sympathetic 
nerve and the affected muscles of the lips and tongue. Upon the muscles the 
faradic current might also be tried. When deglutition begins to be impaired, it is 
an excellent thing to excite the action of swallowing, by galvanism. For this the 
anode is placed upon the nape of the neck, and the kathode upon one side of the 
larynx. At every kathodic closure (KaS), or every time that the kathode is passed 
across the side of the larynx, there is a reflex act of deglutition. The current 
should be of medium strength. 

It might be well to prescribe further a resort to treatment by baths, as at 
Rehme, or the u cold-water cure " might be cautiously tried. The same internal 
remedies are recommended as in the chronic diseases of the cord, especially argen- 
tic nitrate, ergotine, and potassic iodide.- For salivation, atropine may prove bene- 
ficial, in pills of T fo of a grain (grm. 0'0005), three or four to be taken daily. 

The way of giving nourishment is important if deglutition is impaired. We 
should try carefully to avoid having the food go down the wrong way, lest pul- 
monary complications ensue. It is therefore wise not to defer the use of the stom- 
ach-tube too long, through which we may introduce milk, eggs, wine, and the 
various infant foods. 

In the distressing close of the disease, narcotics must be exhibited to lessen the 
patient's suffering, at least as far as we can. 

APPENDIX. 

THE RARER FORMS OF CHRONIC BULBAR PARALYSIS, AND PROGRESSIVE OPHTHAL- 
MOPLEGIA. 

As we have seen, the typical form of chronic bulbar paralysis is practically 
limited in its effects to the distribution of the hypoglossus, the labial division of 
the facial, and the pharyngeal muscles. Possibly the reason it extends no farther 
is merely that death is so speedy. But there are a few rare cases where the chronic 
degenerative process comes to involve other motor nuclei, together with the corre- 
sponding nerve-fibers and muscles. Of course the clinical phenomena of these 
cases vary from the ordinary ; and yet there is no real reason to distinguish these 
from common bulbar paralysis, particularly as all sorts of transitional forms are 
to be observed. Thus, we have ourselves noticed that there is sometimes a sym- 
metrical and slowly progressive paresis of the upper division of the facial, and in 
particular of that portion which supplies the cheek, complicating the glossopha- 
ryngeal paralysis. In other cases we have seen the degeneration attack from the 
start the entire distribution of the facial, gradually producing a complete " diple- 
gia facialis.' 1 '' Sometimes, also, the ordinary symptoms of bulbar paralysis are 
accompanied by disturbances in the area of distribution of the ocular nerves, 
the result of degeneration of the corresponding nerve-nuclei. Erb relates a few 
cases where there were not only ptosis and impairment in the movements of the 
tongue and in deglutition, but also paresis of the muscles supplied by the accesso- 
rius and the motor branch of the trigeminus. 

What seems very remarkable is that the process may be confined entirely to 
the ocular muscles. A. von Graefe named this condition progressive ophthalmo- 
plegia. Another name is "anterior bulbar paralysis." The disease progresses 
with extreme slowness and is perfectly symmetrical. The movements of the eye 
are unpaired in all directions. Diplopia is never present. The pupil reacts to 
light, and usually the power of accommodation is preserved. Finally both eye- 
balls become absolutely motionless, and there is a well-marked though incomplete 
ptosis. There is, beyond a doubt, a progressive degeneration of the nuclei and 



652 



THE DISEASES OF THE MEDULLA OBLONGATA. 



fibers of the corresponding nerves — i. e., the abducens and motor oculi ; but with 
these the process may stop, spreading no farther. We have ourselves lately met 
with a patient who presented total bilateral ophthalmoplegia, and in whom this 
condition had existed without the slightest change for fifteen years.* 

We must add, in conclusion, that our anatomical knowledge concerning these 
rarer forms of chronic bulbar paralysis is very incomplete. The results of a few- 
autopsies, however, join with the clinical phenomena in strongly confirming the 
surmise above expressed as to the pathological lesions. 



CHAPTER II. 

ACUTE AND APOPLECTIFORM BULBAR PARALYSIS. 

1. HEMORRHAGE INTO THE MEDULLA OBLONGATA AND THE PONS. 

Hemorrhage into the medulla oblongata and the pons is much more frequent 
than into the spinal cord, but it is much rarer than cerebral haemorrhage. As to 
its production, the same views are held as will be considered in detail under cere- 
bral haemorrhage, in the next section. In the first place, there is probably always 
some disease of the blood-vessels — that is, atheroma or miliary aneurism — and 
then some factor productive of increased arterial tension. There may be cardiac 
hypertrophy, nephritis, excessive bodily exertion, or alcoholism. Now and then 
injuries of the occiput are followed by an effusion into the medulla. It is not rare 
to have secondary and usually small ecchymoses in acute inflammation of the 
spinal cord (vide infra), and in purulent meningitis or in connection with new 
growths which are richly vascular. 

The anatomical conditions produced by bulbar haemorrhage are so completely 
analogous with those of cerebral haemorrhage that the reader may safely be 
referred to the succeeding section about these also. The size of the lesion varies 
greatly. Bleeding extensive enough to affect the greater part of a transverse sec- 
tion is more frequent in the pons than in the medulla oblongata. If the blood 
is poured out close under the floor of the fourth ventricle, as has been repeatedly 
observed, it may break into the ventricle. If death be not speedy, the blood is 
mostly absorbed, and in its place develops either an " apoplectic scar " or an apo- 
plectic cyst. 

There may be slight prodromata, but the real symptoms of bulbar haemorrhage 
are very sudden. There is almost always a pronounced apoplectic seizure. The 
patient has a shock, falls down, and becomes dizzy or even unconscious. In other 
cases there may be headache, vomiting, tinnitus aurium, and clonic spasms, or 
even a typical epileptiform attack. 

In most cases death is speedy, if not immediate. This is probably due in every 
instance to grave lesions of the respiratory and circulatory centers, rendering 
continued existence impossible. Sometimes the initial symptoms abate, where- 
upon the local results of the lesion become appreciable. 

One of the characteristics of bulbar paralysis now seen is, that disturbances are 
particularly great in the distribution of the bulbar nerves. In cerebral apoplexy 
they never appear in the same way. Another point is, that these paralytic symp- 
toms are combined with paralysis of the extremities in a peculiar way, as a result 



* It seems that total ophthalmoplegia may also appear as one of the symptoms of locomotor ataxia 
or of general paralysis. It has been observed by Mendel as a sequel to diphtheria. In these cases, 
however, the symptom is probably in part due to a degeneration of the fibers of the peripheral nerves. 



ACUTE AND APOPLECTIFOEM BULBAR PARALYSIS. 653 



of the anatomical relations. For the same reason, the order of the paralysis in 
the extremities may also be peculiar. Of the bulbar paralyses we may mention 
more or less complete paralysis of the tongue, and a consequent difficulty in articu- 
lation (anarthria) ; frequent inability to swallow ; and paralysis in the distribu- 
tion of the accessorius, facial, and trigeminus. If there is a lesion of the pyram- 
idal tracts in the pons or medulla, we have paralysis of the extremities in addition 
to the specific bulbar symptoms. If the haemorrhage be extensive, all four 
extremities may be more or less completely paralyzed ; but in most instances the 
paralysis is unilateral. In the larger number of haemorrhages into the pons there 
is crossed paralysis. The paralysis of the extremities is 
upon one side, and that of the facial is on the other side. 
This is a great aid to diagnosis. It is easy to see how this 
happens if we bear in mind that the cerebral fibers of the 
facial cross at a point certainly much higher than the 
decussation of the pyramids, in which latter place the 
motor fibers of the extremities cross. Now a haemorrhage 
may be situated in one side of the pons, above the decussa- 
tion of the pyramids but below that of the facial. This 
would occasion (vide Fig. 95, 2/) a paralysis of the facial on 
the same side with the lesion, and of the extremities upon 
the opposite side ; but if the lesion be higher, above the place 
where the facial crosses over, all the paralytic symptoms 
would be on the opposite side of the body (vide Fig. 95, %}. 

In other, rarer instances we observe similar combina- 
tions; only some other bulbar nerve replaces the facial, 
such as the hypoglossus or abducens. In a few cases the 
lesion is at the very decussation of the pyramids. This 
is extremely rare in haemorrhage, though somewhat more 
frequent in troubles of a different nature. The result 
may be that the motor fibers for one extremity are cut 
off before they cross, and those of the other extremity 
after they have crossed. Thus is produced the rare phenomenon of a crossed 
hemiplegia — i. e., paralysis of the arm on one side and of the leg on the other. 

Disturbances of sensation in the skin of the paralyzed extremities sometimes 
result from trouble in the pons, but they are very seldom extreme, and can not 
be made available for making out the exact locality of the haemorrhage, since the 
course of the sensory fibers through the upper extremity of the spinal cord is still 
almost unknown. The anaesthesia sometimes observed in the distribution of the 
trigeminus is of more value, as this may be due to a lesion of the nucleus or root 
of the nerve. 

There are other symptoms, which are indeed rare, but which bear an impor- 
tant relation to certain nervous centers of the medulla. Thus, there may be 
marked respiratory disturbance ; the pulse may become rapid or irregular ; there 
may be vaso-motor derangement, as shown by a rise of the cutaneous temperature 
and by a subjective sensation of warmth ; and occasionally there are temporary 
albuminuria and glycosuria. The temperature of the body is generally normal at 
first, or nearly so ; but in case of a fatal termination it often rises greatly, even 
to 107*5° (42° C.) and higher. 

As to the prognosis of bulbar haemorrhage, speedy death has been repeatedly 
observed, as we have said. If the immediate effects be successfully withstood, the 
prospect becomes more favorable. The effusion is gradually absorbed, the symp- 
toms of compression abate, and there is a steady progress toward comparatively 
good or even perfect health. More often, however, some of the paralytic symp- 




Fio. 95.— Diagram of focal 
diseases in the pons. 
L. Left. R. Right. P. 
Pons. Mo. Medulla ob- 
longata. DP. Decussa- 
tion of the pyramids. 
E. Fibers to the ex- 
tremities. F. Facial 
fibers, x. Lesion in the 
upper half of the pons. 
y. Lesion in the lower 
half of the pons. 



654 



THE DISEASES OF THE MEDULLA OBLONGATA. 



toms remain stationary, either in the distribution of the bulbar nerves (like the 
lingual or pharyngeal), or in the extremities, as shown by persistent hemiplegia. 
If this latter be the case, the subsequent contractions and other symptoms are the 
same as in ordinary cerebral hemiplegia. 

The diagnosis of bulbar haemorrhage is based upon the apoplectic onset, and 
upon the presence of specific bulbar symptoms, such as disturbance of speech and 
of deglutition, and, most characteristic of all, if it occur, a crossed hemiplegia. 
The differential diagnosis between embolism and haemorrhage can hardly ever be 
made with certainty {vide infra). 

The treatment, not only of the seizure but of the persistent paralysis, should 
conform to the principles which will hereafter be set forth in describing the 
treatment of cerebral haemorrhage. If the bulbar nerves present obstinate symp- 
toms, we must employ the same means as in chronic bulbar paralysis, the most 
effective being electricity. 

2. Embolism and Thrombosis of the Basilar Artery. 

The medulla and pons receive their blood chiefly from branches of the anterior 
spinal, vertebral, and basilar arteries. These branches penetrate the anterior 
median fissure and then proceed to the nerve-nuclei. A far smaller portion of 
the circulation flows through the " arteries of the roots." These are minute off- 
shoots of the lateral branches of the basilar and vertebral arteries, which enter 
the cord at the roots of the nerves and penetrate to the corresponding nuclei. 
According to Duret, the nuclei of the hypoglossal and accessory nerves are sup- 
plied from the anterior spinal and vertebral arteries ; those of the vagus, glosso- 
pharyngeal, and auditory nerves by branches of the upper end of the vertebral 
arteries ; and the nuclei of the facial, trigeminus, and the three nerves to the ocular 
muscles by branches of the basilar. There may be individual exceptions to these 
rules. Occlusion by embolism or thrombosis of the arteries just named must 
occasion a secondary softening in corresponding portions of the medulla, and is, 
therefore, a not very infrequent cause of apoplectic, or at least very rapidly 
developed, bulbar paralysis. 

The causes of thrombosis or embolism in the arteries just mentioned are the 
same as we shall consider minutely when treating of cerebral softening. Emboli 
are most frequent in cardiac disease. They occur only in the vertebral arteries, 
oftenest in the left one, and are never primary in the basilar artery ; but an 
embolus may be enlarged by thrombosis after lodging in one of the vertebral arte- 
ries, and then block up the basilar. Thrombosis is of more frequent occurrence, 
and results from chronic changes in the arteries, mainly atheroma or syphilitic 
endarteritis. The latter disease, one favorite locality for which is the basilar 
artery, is the commonest cause of acute softening of the pons. 

The anatomical condition is likewise similar to that in cerebral softening 
(q. v.). In the region which is deprived of arterial blood by the occlusion of the 
affluent vessel, the acute anaemia entails necrosis and disintegration of tissue. A 
spot of "softening" results, made up mainly of vestiges of nervous tissue and 
numerous cells filled with granules of fat. 

When the basilar artery is blocked up, the symptoms appear very suddenly. 
There is either an apoplectic seizure, or at least a very rapid development of paralysis 
(occupying only a few days). The symptoms of the first onset are, in all essential 
points, those of bulbar or even of cerebral apoplexy. Although there is usually 
no marked loss of consciousness in apoplectic bulbar paralysis, yet no great diag- 
nostic significance can be assigned to its absence. The sudden obstruction of the 
basilar artery produces such a disturbance of the circulation even in anterior por- 
tions of the brain as may suspend consciousness. In some few instances this cir- 



ACUTE AND APOPLECTIFORM BULBAR PARALYSIS. 655 



dilatory derangement may even give rise to choked disk, as seen by the ophthal- 
moscope. Often there are noticeable respiratory and cardiac symptoms, such as 
Cheyne-Stokes' respiration, and rapid pulse. 

If death be not immediate, and we are therefore enabled to make out the symp- 
toms due to the local disturbance, we usually observe the same phenomena as have 
just been described under bulbar haemorrhage. There is sometimes paralysis of 
all the extremities, but usually there is trouble only upon one side. Then we 
have the characteristic crossed hemiplegia. The facial nerve or the nerves of the 
ocular muscles may be paralyzed. It has repeatedly happened that the paralysis 
seemed at first much greater upon one side, but after a few days changed over to 
the opposite one. This must be due to changes in the circulation ; the thrombus 
grows larger, or a collateral circulation is developed. The specific bulbar symp- 
toms are the familiar ones of all bulbar derangements — namely, lingual paralysis 
with resulting difficulty in articulation, pharyngeal paralysis, and rarely deafness, 
as a result of lesion of the acoustic center. Of course, the severity and extent 
of all these symptoms must vary according to the location and size of the spot of 
softening. 

The prognosis of cases of this sort is almost always unfavorable. Death 
results at latest after a few days. It is often ushered in by a high temperature. 
Exceptionally, there is a transition into a chronic form. 

We need say nothing about treatment, except that the same remedies are 
employed as in other acute bulbar diseases. 

3. Acute, or Inflammatory, Bulbar Paralysis. 

(Acute Bulbar Myelitis) 

" Acute bulbar paralysis," in the stricter sense of the term, means a form of 
disease where marked symptoms of bulbar derangement appear acutely — that is, 
within a few days or weeks. The anatomical lesion is probably an acute inflam- 
mation of the medulla oblongata. It is a rare disorder, and its aetiology is doubt- 
ful. There are usually mild prodromata : vertigo, headache, and, in one case of 
our own, painful sensations in the back of the neck. Evident bulbar symptoms 
very quickly follow. Usually the first of these is dysphagia. Not only is deglu- 
tition impaired, but the paresis of the soft palate and of the laryngeal muscles 
allows liquids to enter the nostrils or the larynx. The tongue also becomes grad- 
ually paralyzed, speech becomes indistinct, and, if the soft palate be involved, nasal. 

Sometimes the extremities also become paretic, as a result of the extension of 
the disease to the region of the pyramids ; but in many instances the extremities 
remain unimpaired to the end. Paralyses of the facial nerve and of the ocular 
muscles are somewhat more frequent. The temperature is sometimes a little ele- 
vated (100°-102°, 38°-39° C), but not always. The pulse is almost invariably 
rapid ; in our patient it was 148. 

The prognosis is apparently always bad. Often death takes place in four to 
eight days, or it may be not till the end of two or three weeks. It is invariably 
preceded by all the tokens of paralysis of respiration. In our case there was 
well-marked paralysis of the diaphragm at the end. 

As yet, few autopsies have been reported. Generally the medulla presents no 
macroscopic changes. Exceptionally, it can be seen to be softened and mottled 
with minute haemorrhages. The microscope detects abundant evidence of inflam- 
mation : granule-cells, infiltration with nuclei around the blood-vessels, thicken- 
ing of the walls of some of the blood-vessels, small extravasations, swollen axis- 
cylinders, etc. It should also be borne in mind that precisely similar clinical 
phenomena seem often to be referable to peripheral changes, such as multiple 
neuritis affecting the bulbar nerves. 



656 



THE DISEASES OF THE MEDULLA OBLONGATA. 



The treatment of acute bulbar paralysis is, of course, almost hopeless. In 
early stages we should apply counter-irritation to the nape of the neck; and we 
might prescribe mercurial inunction. It might also be well to employ the con- 
stant current, applied at the back of the neck, and also used to excite the move- 
ments of deglutition. We found injections of strychnine useless. Toward the 
end, narcotics are indispensable. 



CHAPTER HI. 
COMPRESSION OF THE MEDULLA. 

Acute compression and other injuries of the medulla are most frequently due 
to fracture or dislocation of the atlas and axis. As is well known, dislocation of 
the axis, or backward dislocation of the atlas, usually causes instant death. 

Gradual compression is seen in chronic disease of the bones around the medulla, 
in caries and tumors of the occiput and of the first two vertebrae. Enchon- 
droma of the base of the skull ; new growths of the sphenoid, at its junction 
with the occipital ; tumors of the dura ; and sometimes even tumors of the cere- 
bellum — may all excite by their pressure the gravest bulbar symptoms. We 
should also mention aneurism of the vertebral artery at its upper end, and of the 
basilar, as capable of doing similar harm. In all these cases the main cause of 
disturbance is undoubtedly the mechanical pressure, either directly destroying 
the nervous tracts or interrupting the transmission of nervous influences ; but 
the circumstances may be further complicated by haemorrhages, and sometimes 
perhaps by inflammation of the medulla itself. 

The clinical phenomena of gradual bulbar compression resemble those of spinal 
compression, in that they usually begin with symptoms of irritation in the distri- 
bution of those nerves the roots of which are first affected. There are neuralgia 
of the trigeminus, twitching of the facial muscles, tinnitus aurium, etc. If the 
compression becomes greater, there are more serious bulbar symptoms : disturb- 
ances of speech and deglutition, paralysis of the tongue, soft palate, face, and very 
likely motor and sensory symptoms in the extremities. Usually we also see gen- 
eral cerebral symptoms, such as vertigo, headache, vomiting, and sometimes epi- 
leptiform convulsions. 

We can not, of course, draw up a definite and rigid list of symptoms, since 
both the individual symptoms and the general course of the disease exhibit great 
variations according to the way in which the compression is brought about. The 
diagnosis can be made in those cases only where some aetiological factor like 
trauma or caries of the vertebrae is known to exist. Anemism of the vertebral 
artery is said by Moser sometimes to give rise to a loud systolic murmur heard 
between the mastoid process and the spine. In all other cases we can seldom do 
more than surmise the truth. Slow compression is distinguished from genuine 
progressive bulbar paralysis chiefly by the course it pursues — that is, there are 
initial symptoms of irritation — by the greater complexity of the clinical phenom- 
ena, like sensory lesions and hemiplegia, and sometimes by the asymmetry of cer- 
tain symptoms. If the anterior part of the medulla is compressed, in the region 
of the pyramids, there may for a time be no bulbar symptoms, but merely motor 
symptoms in the extremities. These are chiefly paretic or spastic. 

The prognosis is almost always bad, as can be inferred from the nature of the 
causative disease. Death is brought on either by inhalation-pneumonia, or by 
paralysis of respiration. Treatment must be purely symptomatic, and should fol- 
low the same rules as in progressive bulbar paralysis. 



HEMATOMA OF THE DURA MATER. 



657 



V.— The Diseases of the Brain. 



SECTION I. 
Diseases of the Cerebral Meninges. 

CHAPTER I. 

HEMATOMA OF THE DURA MATER. 

{Internal Hemorrhagic Pachymeningitis.) 

JEtiology and Pathology. — Haematoma of the dura mater is the name given to 
effusions of blood found on the inner surface of the dura mater. They are of con- 
siderable area, but of moderate thickness, and are usually encapsulated. There 
has been much discussion as to their mode of origin, and views still differ. One 
is that the haemorrhage is the primary lesion, and that the connective-tissue mem- 
branes are developed only by the organization of the clot. This conception was 
originally the prevailing one, but was opposed by Virchow, who was led by the 
results of his own investigations to maintain that the haemorrhage was always 
secondary. The primary process he believed to be a peculiar sort of inflammation 
— " haemorrhagic pachymeningitis." This gave rise to a new growth of richly 
vascular connective tissue, into which the haemorrhage took place. Of late, how- 
ever, the tendency is again to regard the haemorrhage as the initial change, at least 
in certain cases, and to refer it to an affection of the walls of the blood-vessels 
which diminishes their power of resistance. 

The mildest forms of internal pachymeningitis present a delicate membrane 
upon the inner surface of the dura mater, quite easily separable, of a reddish 
color, and dotted with numerous red and brownish spots. These spots are due to 
minute haemorrhages and collections of haematoidin. The membrane itself is a 
delicate interstitial tissue, traversed by numerous wide capillaries. 

In more advanced cases the thickening is much greater. There are usually sev- 
eral layers, the newest and most superficial being nearest the brain. The oldest, 
which is in apposition with the dura mater, is composed of connective tissue that 
has already become rather firm and fibrous. It is evident from this lamellar 
structure that the whole process goes on by fits and starts. The clinical course of 
the disease will be seen below to agree well with such a view. The effusions are 
sometimes very extensive, even larger than a hen's egg, and exercise no slight 
pressure upon the underlying cerebral parenchyma. The haemorrhage always 
takes place inside the mass, or between its layers. The effusion may, however, 
break through the innermost layer, so that the blood flows into the arachnoid 
spaces ; this is known as " intermeningeal apoplexy." 

The favorite location of the haematoma is the parietal region. It is sometimes 
found at the base of the brain, in the posterior or middle fossa. Occasionally the 
haematoma is bilateral. 

Haemorrhagic pachymeningitis is not a rare disease. It is sometimes found to 
exist in a moderate degree in chronic cardiac, renal, or pulmonary cases, which 
come to autopsy. Usually there have been no special symptoms, the lesion being 
discovered incidentally. It has been found in like manner in connection with 
42 



658 



THE DISEASES OF THE BRAIN. 



a great many acute infectious diseases, like typhoid fever and small-pox. It is a 
more important and more frequent complication in other chronic cerebral diseases, 
in particular such as induce marked atrophy of the brain as a whole. It is espe- 
cially common in general paralysis of the insane and in other forms of demen- 
tia. Chronic alcoholism is also regarded as a potent aetiological factor. In topers 
it is not very unusual for the haematoma to be so extensive, if it occurs at all, 
as to cause grave cerebral derangement. Very likely changes in the vascular 
walls, like atheroma and fatty degeneration, contribute an important j>art to the 
result in such patients. Haematoma may also occur in all diseases where there is 
a general haemorrhagic diathesis. Thus it is seen in pernicious anaemia, leukae- 
mia, and scurvy. Here certainly the haemorrhage is the primary event, as it also 
is in . the traumatic cases, of which a number have been observed. 

As might be inferred from the aetiological factors enumerated, the disease is 
found chiefly in advanced life, and much oftener in men than in women. 

Symptoms. — Not infrequently a haematoma of the dura is found post mortem, 
which had during life been entirely unsuspected. Either the haemorrhage was 
not extensive enough to cause any symptoms, or the brain exercised that remark- 
able tolerance which it sometimes shows even when there are wide-reaching 
lesions ; or such symptoms as there may have been escaped particular notice, in the 
severity of the more general symptoms (of typhoid fever or some similar disease). 
But in other cases haemorrhagic pachymeningitis excites grave symptoms, although 
they are seldom so characteristic as to reveal the diagnosis ; for individual cases 
vary greatly, according to the size of the haemorrhages, their location, and the fre- 
quency of their recurrence. 

Almost always the beginning of the disease is rather sudden. It may even be 
like an apoplectic seizure. The symptoms are referable partly to the general 
effect of the haemorrhage upon the brain, and partly to the exact locality of the 
haemorrhage. The more general symptoms comprise headache; impairment of 
intelligence (that is, stupor or even complete coma) ; slow or irregular pulse ; vom- 
iting ; and contracted pupils — all being symptoms of cerebral compression. Now 
and then we even find choked disk. Other phenomena are added to the above 
when the haematoma occupies its usual position, upon one side and in the neigh- 
borhood of the motor cortical region, or central convolutions. The hemiplegic 
symptoms are not infrequent, such as hemiparesis, and, from the irritation which 
the effusion produces in the motor centers, twitchings and convulsions in one half 
of the body. Sometimes these symptoms are limited to a single extremity or to 
the distribution of the facial nerve. Aphasia has been repeatedly observed when 
the haemorrhage was near the island of Eeil. If the effusion increases, the motor 
disturbance becomes correspondingly aggravated, and may become bilateral. Sen- 
sation is usually little impaired. 

The further course of the disease varies greatly in different cases. In the 
worst cases there is speedy death, usually ushered in by deep coma. In others, the 
first symptoms are followed by improvement, although mild indications of cerebral 
pressure persist, such as headache or vertigo, or else local symptoms, like hemi- 
paresis. It is possible for the effused blood to be absorbed, and complete recovery 
to ensue ; but usually new haemorrhages and corresponding symptoms arise. It 
is precisely this appearance of the symptoms in separate attacks, this frequent 
recurrence of severe cerebral disturbances, that is characteristic of haematoma of 
the dura mater. As already intimated, the way in which the anatomical lesions 
develop explains this perfectly. Thus the disease may drag on for months and 
years, sometimes improving and sometimes aggravated. Then some attack at last 
proves fatal. Arrest and actual improvement are still possible even in the later 
stages, although often the features of the case have meanwhile undergone essen- 



PURULENT MENINGITIS. 



659 



tial alteration because of the progress of some causative disease. In general, the 
clinical phenomena of haematoma of the dura are often complicated and obscured 
by the co-existence of the primary disease. 

The diagnosis is therefore difficult. The main points may be recapitulated as 
follows : First, the existence of serological factors, like alcoholism, or chronic 
cerebral disease ; second, the sudden onset, and also the abrupt appearance of 
further symptoms, the alternation of rapid aggravation and improvement; and 
third, the existence of symptoms which experience has taught us to refer mainly 
to the cortex of the brain, namely, unilateral convulsions, monoplegic paresis 
and contractures; and contracted pupils. Nevertheless, frequent errors in diagnosis 
can not be avoided. 

Treatment. — The possibility of therapeutic interference being successful is very 
small. In apoplectic shocks, ice to the head is useful ; and if the patient be robust, 
it may also be advisable to use local depletion, by leeches on the temples or behind 
the ears. It is also customary to prescribe some such thing as senna or calomel 
for "intestinal depletion." 

If the first onset is successfully withstood, the main things as to further treat- 
ment are general hygienic and dietetic directions, so as to guard as far as possible 
against fresh haemorrhages. Alcohol and excessive bodily or mental exertion 
should be forbidden. Of course, paralysis or other persistent disturbances may 
call for special treatment. 



CHAPTER n. 

PURULENT MENINGITIS. 

(Purulent Cerebral Leptomeningitis. Meningitis of the Convexity.) 

JEtiology. — Purulent inflammation of the dura mater has no clinical impor- 
tance, for it is very rare, and occurs only as the result of the extension of disease 
from neighboring parts. We shall accordingly consider below purulent inflam- 
mation of the pia mater only. One important variety of this disease has already 
been discussed (see page 93 et seq.) as one of the infectious diseases, under the name 
of epidemic cerebro-spinal meningitis. There we saw also that the occasional 
sporadic cases of primary or " idiopathic " meningitis are probably identical setiolo- 
gically with those of epidemic meningitis. In all other instances, purulent menin- 
gitis is a secondary disease — that is, the specific agent, which excites the purulent 
inflammation, originates in some other organ primarily, and affects the meninges 
only secondarily. We should, therefore, seek most carefully in every case of puru- 
lent meningitis, at the bedside and more particularly at the autopsy, to discover 
the way by which the pathogenetic virus reached the meninges. We have no 
right to say that the case is one of primary meningitis, strictly so called, until we 
have made a most careful examination with a negative result. From a clinical 
standpoint, it is true that many cases of secondary meningitis do seem as if they 
were primary, because not infrequently the really primary disease excites insig- 
nificant symptoms, or perhaps no symptoms at all. 

Secondary purulent meningitis is most often due to disease of the cranial bones, 
and in particular to disease of the petrous portion of the temporal bone, with the 
auditory apparatus therein contained. If we consider the anatomical relations of 
the middle and internal parts of the ear, we can easily understand why inflamma- 
tion in them is not infrequently followed by meningitis. Usually it is a caries of 
the petrous portion, itself due to an otitis media, which leads to an irruption into 
the cranial cavity. This is especially apt to take place through the thin vault of 



660 



THE DISEASES OF THE BEAIN. 



the tympanic cavity. It may also extend from the mastoid cells, or by direct 
propagation along the sheaths of the acoustic or facial nerves, or along the vessels 
which lie in the petroso-squamous suture. The dura is first attacked, and then 
the pia. In many instances, the neighboring venous sinuses (transverse, caver- 
nous, and superior petrosal) transmit the inflammation, being first attacked by a 
suppurative thrombo-phlebitis. Again, exceptionally, a purulent inflammation in 
the upper part of the nasal cavity may lead to meningitis. 

Another and frequent source of meningitis is found in the various traumatic 
injuries of the cranium. In the great majority of these cases there is an open 
wound, admitting infectious agents which are suspended in the air. The suppura- 
tion often commences in the spongy texture of the diploe, thence extending to the 
dura and pia, either directly or by way of a purulent thrombosis of some sinus 
into which the veins of the diploe enter. It is, indeed, generally affirmed that we 
may have a traumatic purulent meningitis without any open wound ; but this is 
not easily explained, according to our present views as to the origin of purulent 
inflammations. It is equally difficult to understand, what many authors affirm, 
that the heat of the sun's rays, striking upon an uncovered head, may excite 
purulent meningitis. In most cases of sunstroke we find marked hyperemia of 
the meninges, but no inflammation. 

Meningitis may have an intra-cranial origin ; it is sometimes the sequel of 
cerebral abscess. No matter what starts the abscess, if it extends to the surface of 
the brain, it causes a more or less extensive purulent meningitis at that point. 
An abscess may burst into one of the lateral ventricles, and the infection be 
carried from that point to the pia at the base of the brain. 

All the cases thus far contemplated allow of the explanation that the inflam- 
mation reaches the meninges by direct extension ; but there is another group of 
cases where the agent that infects the pia mater originates at some distant part of 
the body, and is probably conveyed by the blood or lymph currents. These cases 
are often termed metastatic meningitis. 

Of this sort is the secondary meningitis seen in connection with genuine lobar 
pneumonia, a combination already discussed (see page 183). The meningitis is 
also sometimes a complication of empyema, rarely of pyaemia and septicaemia, 
ulcerative endocarditis, and very rarely of typhoid and the acute exanthemata 
(small-pox, scarlet fever), and of acute articular rheumatism. In each case we 
must, of course, determine whether the meningitis may not have a connecting 
link between itself and the primary disease, such as otitis in scarlatina, or second- 
ary empyema in typhoid fever. 

Pathology. — For the pathological anatomy of purulent meningitis, we may refer 
mainly to the statements made on page 94, under epidemic meningitis, for the 
lesions are similar. The only way to determine whether a meningitis is secondary 
or primary is by finding or failing to find disease in neighboring or remote parts, 
for example pneumonia. The seat of the meningitis will vary according to that of 
the primary inflammation, if there be any. If the meningitis is due to caries of the 
petrous bone or to an injury of the skull, the purulent exudation is usually most 
abundant in the immediate neighborhood of the primary lesion, between the pia and 
arachnoid. Thence it gradually extends along the surface of the brain, sometimes 
chiefly on the convexity and sometimes at the base. But in general it may be said 
that both the secondary and the metastatic varieties of meningitis as a rule affect 
the convexity, although this is by no means invariably the case. This rule explains 
why these cases are sometimes termed meningitis of the convexity, in contrast to 
tubercular meningitis, which latter, as we shall find, has a preference for the base 
of the brain, and hence is called basilar meningitis. The spinal pia mater is 
sometimes simultaneously attacked, but not so constantly as in primary, or epi- 



PURULENT MENINGITIS. 



661 



demic meningitis. The brain is almost always involved — the inflammation extends 
along the vessels which dip from the pia mater into the cerebral parenchyma. It 
is not a rare thing to find minute abscesses or ecchymoses in the interior of the 
brain. The whole parenchyma is usually moist, cedematous, and of a doughy 
consistence. The meningeal exudation exerts upon the brain a pressure which 
gives rise to important symptoms ; by it the superficial cerebral convolutions are 
often considerably flattened. The lateral ventricles almost always contain more 
or less sero-pus. 

Clinical History. — So varied are the primary diseases which may entail a men- 
ingitis, that it is hardly possible to make a sketch of the disease which would suit 
all cases. If the meningitis comes on during the course of pyaemia, pneumonia, 
or some other severe illness, its proper symptoms are often inextricably confused 
with those of the primary trouble; and when the skull or the brain has been 
mechanically injured, it is very hard to determine whether a meningitis has been 
excited, because the trauma may of itself produce such serious effects. The fol- 
lowing description, therefore, applies chiefly to cases of apparently primary men- 
ingitis, or to cases where the meningitis, although secondary, is well marked. 

The beginning in such cases may be sudden, or it may be somewhat insidious. 
Sometimes the grave symptoms appear almost at once, accompanied by a chill and 
high fever. Sometimes there are for a while indefinite and more or less ambigu- 
ous prodromata, but almost always it is the headache which first attracts attention. 
This grows worse with more or less rapidity, and almost always becomes very 
violent. Exceptionally it may be insignificant. Not infrequently it varies con- 
siderably, being much worse at some hours or on some days than on others. The 
location of the pain is sometimes frontal, sometimes occipital, and sometimes over 
the whole head. Next in prominence to the headache, particularly in the later 
stages of the disease, is the mental disturbance. The patient complains of vertigo, 
becomes dull and stupid, or begins to wander. The delirium may be extremely 
violent, but usually there is depression rather than exaltation, and the stupor 
merges into coma. That the headache still continues may be inferred from the 
frequent raising of the hand to the head and the grimace of pain whenever the 
head is moved, till finally the coma becomes so profound that even these reflex 
actions cease. 

Usually these general cerebral symptoms are attended by others referable to 
the particular locality affected. The neck is rigid. This is most marked when 
the posterior fossa and the medulla are affected. Then there are all sorts of 
paralytic or irritative symptoms in the distribution of the cranial nerves, mainly 
due to lesions of the nerves where they emerge from the base of the brain ; there 
is derangement of the motores oculi, as shown by paralysis or nystagmus ; the 
pupils are unequal, or are contracted or dilated, and do not react to light ; there 
is paresis of the facial, or trismus, or grinding of the teeth; All these symptoms 
may appear equally plainly in other forms of meningitis. Sometimes we can 
detect optic neuritis with the ophthalmoscope. Other symptoms are due to cere- 
bral disturbance, often apparently located chiefly in the cortex. Thus there may be 
twitchings of individual muscles, or even pronounced convulsions in one or more 
limbs, or paralysis of one extremity or of half the body. Sometimes the autopsy 
explains these phenomena, but often we fail to find any marked anatomical lesion 
to correspond to them, and are obliged to ascribe them to circulatory or functional 
derangement. 

Of the remaining symptoms, the fever is most important. Almost always the 
temperature is decidedly elevated, not infrequently reaching 104° or 105° (40 o -40'5° 
C). The fever is, however, very irregular. There may be repeated chills with 
great elevations of temperature. The pulse is generally rapid, and often some- 



662 



THE DISEASES OF THE BEAIN. 



what irregular. Exceptionally it is less frequent than normal, because of cerebral 
compression. Vomiting is not a rare symptom, particularly at first. There is 
almost invariably constipation, and the abdomen is often tense and concave. The 
urine is scanty, and often contains a trace of albumen. Secondary diseases are 
sometimes found post mortem, such as lobular pneumonia, due to inhalation of 
food during the comatose state. 

The entire course of the disease occupies only a few days in very acute cases, 
and scarcely ever exceeds a week or ten days. The termination is almost sure 
to be fatal. In the few cases of recovery which have been reported the diagnosis 
is doubtful. In most instances deep coma precedes death, though sometimes it is 
ushered in by convulsions. There is often a great rise of temperature (107 '5°, 42° 
C, or higher) before the close of life. 

Diagnosis. — The diagnosis of purulent meningitis is sometimes pretty evident; 
but it may be very obscure, so that we can not always avoid confounding it with 
other severe acute diseases, such as typhoid, pyaemia, and general tuberculosis. In 
general the most characteristic symptoms of any variety of meningitis are intense 
headache, rapid onset of grave cerebral disturbances, delirium and insensibility, 
stiffness of the neck, and disturbances in the distribution of the cranial nerves 
(especially impaired motion of the eyeball and optic neuritis). These last, although 
often slight, are generally present ; and in connection with these separate symp- 
toms we must also always consider the whole course of the disease and any aetio- 
logical factors which may exist. Typhoid fever is excluded by its usually slower 
onset, the greater delay in the appearance of grave cerebral symptoms, the rose- 
spots, the greater size of the spleen, the characteristic stools, and the peculiar fever- 
curve. Severe septic and pyaeinic diseases, including ulcerative endocarditis, like- 
wise excite cerebral disturbances which might be misleading, but these diseases 
are to be recognized by their aetiology (external wounds, abortion, etc.), cutaneous 
ecchymoses, septic retinitis, swelling of the joints, and repeated rigors. Uraemia 
may also simulate meningitis. Sometimes the character of the urine, and the 
predominance of convulsions, will set us right, but not always. We may state 
in conclusion that every one who sees many cases (including ourselves), must 
repeatedly have met with patients presenting the symptoms of a severe and acute 
cerebral affection apparently primary, without demonstrable cause, and seeming to 
justify a diagnosis of meningitis, but yet yielding post mortem no signs of disease 
beyond " hyperaemia," " cedematous swelling," and similar changes of only second- 
ary importance. We are as yet wholly unable to explain such cases. 

Granting that meningitis exists, what variety is present ? The aetiology is a 
great help in answering this question. We should endeavor to learn whether 
there has been traumatism or some old ear trouble. It is well to employ the aural 
speculum. We can not say that a patient has epidemic meningitis unless several 
cases occur simultaneously, although herpes is very characteristic, as it appears 
only exceptionally in other varieties. Usually tubercular meningitis also can 
be diagnosticated only by means of the aetiology. Its symptoms, of course, are in 
almost all particulars identical with those of purulent meningitis. Sometimes, 
however, tubercles can be detected in the choroid by means of the ophthalmoscope. 
For further particulars see the next chapter. 

Treatment. — The treatment of the different forms of meningitis varies but little. 
Locally, the favorite remedies are ice applied to the head, which should be shaved 
if practicable, and local depletion by means of leeches behind the ears or on the 
temples. Many physicians recommend cutting off the hair and rubbing in anti- 
monial ointment, or applying ethereal tincture of iodine. We have never tried 
this. Cool baths with douching can not be employed unless the patient can be 
moved without too much pain. For violent pain or great restlessness we must 



TUBERCULAR MENINGITIS. 



663 



use narcotics. The best is morphine subcutaneously. We can not hope for much 
benefit from other internal remedies, such as iodide of potassium or calomel. 

Prophylaxis demands, above all, prompt recourse to the otologist for aural 
trouble of any kind, and strictly antiseptic treatment of all injuries of the skull. 



CHAPTER III. 

TUBERCULAR MENINGITIS. 

(Basilar Meningitis.) 

JEtiology.— Tuberculosis of the leptomeninges is always a secondary affection — 
a sequel to previously existing tubercular disease of some other organ. Why the 
pia mater should be so often singled out for secondary infection with the tuber- 
cular virus, or what path that virus traverses to reach the pia — about these ques- 
tions we know very little. We can merely state what the other tubercular diseases 
are, which, as experience shows, entail tubercular meningitis most frequently. 
These primary affections may be of themselves productive of grave clinical phe- 
nomena, the meningitis merely adding to the complexity of the picture. Again, 
the primary trouble may not have betrayed itself at all, or its symptoms may have 
been long ago arrested, so that the meningitis seems to be a primary disease. In 
some cases even the most careful examination will fail to detect the origin of the 
trouble. 

Tubercular meningitis is oftenest a sequel to pulmonary tuberculosis. It may 
appear as a terminal complication in cases of advanced phthisis, or it may come on 
while the signs of pulmonary disease are as yet very slight. Next in order as a 
causative affection comes tubercular pleurisy. This origin is not infrequent. As 
we have already seen, most cases of apparently primary pleurisy are due to tuber- 
cle. This statement is supported by the fact that it is not very exceptional for the 
symptoms of tubercular meningitis to supervene suddenly upon what had seemed 
to be genuine convalescence from pleurisy. In children, and sometimes in adults, 
the virus may be carried to the meninges from cheesy, tubercular, bronchial or 
mesenteric glands, or from tubercular or " fungous " disease of the bones or joints. 
Another danger to adults is tubercular disease of the genito-urinary apparatus. 
It should also be noticed that a single large tubercle in the brain may lead to mili- 
ary tuberculosis of the meninges. In short, we see that it is not impossible for any 
tubercular infiltration, wherever situated, to communicate infection either to the 
meninges alone (in some remarkable way), or simultaneously to them and many 
other organs. In this last case, where in all probability the blood carries the 
virus through the system, the meningitis is merely a part of a general miliary 
tuberculosis (see page 218). When the meninges are alone or predominantly 
affected, there must be some peculiar manner of infection, about which, how- 
ever, as we have already confessed, we have no information. 

We sometimes hear the attack ascribed to such causes as over-exertion, mental 
excitement, or traumatism ; but we need hardly say that these can not be properly 
regarded as setiological factors, and that usually they are merely coincidences. 
Age, however, does have an influence ; children are much of tener attacked than 
adults, although the latter also are liable to it. 

Pathology. — As in tuberculosis of serous membranes, so in tuberculosis of the 
pia, there are two effects of infection to be distinguished from each other : (1) the 
development of the specific new growth — that is, of miliary tubercles ; and (2) 
the inflammation. The relative degree of these two varies. Sometimes the 



THE DISEASES OF THE BRAIN. 



tubercles are very abundant and the inflammatory exudation comparatively 
scanty ; and in other cases the inflammation is considerable, although relatively 
few tubercles are discoverable. The tubercles are usually found in greatest 
number along the course of the larger blood-vessels, and therefore chiefly in the 
furrows and clefts of the surface of the brain, in the fissure of Sylvius, at the 
chiasma, the pons, the medulla, and the cerebellum. And, in general, the base of 
the brain is usually more affected than the convexity — hence, as we have said, the 
name of "basilar meningitis." There are, however, exceptions to this rule. We 
very often find that the region supplied by one or more arteries suffers above 
other parts; this must be due to the manner of infection. The inflammatory 
lesions consist of hypersemia, usually well marked, and a sero-gelatinous exuda- 
tion of variable amount. That this exudation is partly cellular can always be 
proved by the microscope, and often even macroscopically from the great cloudi- 
ness of the pia ; but still we seldom find enough to justify us in calling the pro- 
cess one of genuine purulent inflammation. Small haemorrhages into the pia are 
quite often found. The brain itself is usually flattened from the pressure of the 
meningeal exudation. Often the inflammation involves the brain-substance itself, 
as shown microscopically by tubercles, inflammatory changes, and capillary 
haemorrhages. The ventricles usually contain, although not invariably, a hydro- 
cephalic effusion. This led earlier observers to term the disease " acute hydro- 
cephalus." The effusion is serous, but generally turbid from cellular constituents, 
and not infrequently tinged with blood. The choroid plexus is engorged, and may 
present tubercles. The spinal cord, in the majority of cases, shares in the tuber- 
cular disease. Here, too, we find inflammation of the pia and miliary tubercles. 
This fact has a clinical bearing, being explanatory of many of the symptoms. 

Clinical History. — Tubercular meningitis almost always begins with a pro- 
dromal stage, which is often brief, but may last one or two weeks, or even longer. 
The patient may be apparently well (vide supra) until this comes on, or he may 
have already shown signs of some other tubercular affection. He now feels badly, 
at any rate, and begins to complain of headache, worse at some times than at 
others. There is anorexia and very often constipation. Another frequent pro- 
drome is an attack of vomiting, which may or may not recur. Sleep is disturbed, 
either by the headache or by a certain general restlessness. We have occasionally 
met with cases where the illness began with pronounced mental disturbance. The 
patient became irrational and said and did queer things, and then a few days later 
there appeared distinctive meningeal symptoms. In two patients, who were 
topers, the disease began just like delirium tremens. 

After an initial period of variable duration, the general health becomes more 
and more impaired. The headache increases. The patient takes to his bed, begins 
to be delirious, and soon presents well-marked symptoms of grave brain trouble. 
Intelligence becomes more and more impaired. The patient is sleepy, and can be 
roused imperfectly by the voice, if at all. At the same time he is usually quite 
restless at first, grasping at invisible objects in the air, picking the bed-clothes, 
and continually moving his legs. The delirium may be- low or noisy ; the patient 
may keep up a constant singing or screaming, or whistling. The persistence of 
the headache even in this stage is shown by the facial contortions and complaints 
of the sufferer, whenever there is a temporary approach to consciousness. There 
is also, as a rule, decided tenderness in the nape of the neck on pressure, frequently 
accompanied by great stiffness of the neck. Sometimes there is stiffness of the 
entire spinal column, and pain in the same. This is certainly due to the coinci- 
dent spinal meningitis. 

Another group of symptoms in the distribution of the cranial nerves are iden- 
tical with those seen in the other forms of meningitis. Ptosis is not infrequent, 



TUBERCULAR MENINGITIS. 



665 



on one or both sides, due to paresis of the motor oculi. There is strabismus, either 
internal or external. Symptoms of irritation of the nerves governing- the move- 
ments of the eye are very frequent, especially in the early stages of the disease. 
Thus we see slow involuntary lateral movements of the eyeballs, and sometimes 
nystagmus. The pupils are often unequal ; they may be enlarged or contracted, 
and often they undergo marked and repeated variations in size. The reaction of 
the pupils to light is usually sluggish, and may be absent. With the ophthal- 
moscope we find not infrequently neuritis, or choked disk. In some instances, 
but not in all, we find also tubercles in the choroid, which, of course, greatly 
assists diagnosis. Sometimes there is occasional twitching in the distribution of 
the facial nerve, or a slight tonic contraction, or again paresis on one side. The 
natural explanation of all these phenomena is that the nerve-trunks are inter- 
fered with at the base of the brain, whether by the pressure of the exudation or by 
participation in the inflammatory process, or by the minute haemorrhages which 
sometimes take place into the sheath of the nerves. 

Disturbances in the extremities may be caused by various lesions. Motor 
symptoms of irritation are apparently referable for the most part to changes in 
the cortex of the brain. We see occasional twitching of larger or smaller groups 
of muscles, or rarely convulsions. These latter may be unilateral, or in a single 
extremity. Sometimes there is well-marked paresis of one half the body or 
paralysis of one limb, or there may be aphasia, although it is only in a part of the 
cases that we find post mortem any lesion which explains these symptoms. In 
most cases there is a particularly large collection of tubercles in certain places 
upon the cortex cerebri, occasioning a local compression or an inflammatory oede- 
ma, which in its turn excites the phenomena mentioned. Sometimes the brain- 
substance itself is found in a state of red softening underneath these spots. An- 
other and not very rare symptom is a peculiar stiffness of the limbs, due either to 
direct irritation or to reflex action. The reflexes in the lower extremities are gen- 
erally exaggerated at first, but later on become diminished, and finally abolished. 
The reflexes upon one side may be more vigorous than upon the other. As to 
sensation, it is hard to reach definite conclusions, because of the patient's stupor. 
Sometimes there is well-marked cutaneous hypersesthesia, probably referable to an 
implication of the spinal cord in the process. 

The behavior of the pulse and temperature is interesting. The temperature 
is usually elevated, but often only to a slight extent — that is, varying between 
100-5° and 102° (38° and 39° C). Often the temperature falls quite low, only to 
rise again, the alternations being at irregular intervals. Exceptionally the tem- 
perature may remain high (104° F., 40° C.) most of the time. Toward the end 
there is usually a decided change in temperature, either upward or downward. 
In many instances there is a very low temperature before death ; in two cases we 
have seen a temperature of 87*8° (31° C). Or the temperature may rise to 106° 
(41° C.) or higher just before death. The pulse is often abnormally slow in the 
early stages of the disease, even numbering only 40 to 50 beats per minute. This 
is referable without doubt to the increased intra-cranial pressure. Later on the 
pulse becomes small and rapid. The transition may be very sudden. The vagus 
is at first irritated, and then paralyzed. The pulse is often irregular. 

Respiration is generally moderately accelerated. If the breathing is very deep 
and rapid, we should always think of simultaneous miliary tuberculosis of the 
lungs. Toward the close of the disease the respiration often assumes the Cheyne- 
Stokes type : there is a long pause, followed by very superficial and gentle respi- 
ration, which gradually grows deeper and deeper, then diminishes again, and is 
succeeded by another complete pause. This symptom is always most ominous, for 
it indicates that the excitability of the respiratory center is already greatly impaired. 



666 



THE DISEASES OF THE BRAIN. 



Symptoms referable to still other organs are few. Vomiting is rare in the 
later stages of the disease. The abdomen often presents a " boat-shaped " concav- 
ity, as the result of tonic muscular contraction, and is hard and tense. There is 
almost always constipation. The spleen may be somewhat enlarged. The urine 
sometimes contains a trace of albumen. On account of the drowsiness, it is usu- 
ally voided in the bed or retained in the bladder. Almost invariably there is rapid 
marasmus. 

The entire duration of tubercular meningitis varies somewhat, chiefly because 
of the varied length of the first stage. When the disease is once fully developed, 
the illness seldom lasts more than three to ten days longer. Frequently the 
illness is divided into three stages : 1. The stage of cerebral irritation, with head- 
ache, stiff neck, vomiting, and delirium ; 2. The stage of cerebral compression, 
chiefly due to the hydrocephalus, and causing drowsiness, slowness of the pulse, 
paralysis of the motores oculi, hemiplegia, etc. ; and 3. The paralytic stage, pre- 
senting deep coma, relaxation of the previously contracted muscles, accelerated 
pulse, and marked variations of temperature. Such a division is too diagrammatic 
to correspond accurately to the real phenomena, but will, nevertheless, often aid 
us in getting a general idea of the course of the disease. 

The termination of tubercular meningitis seems to be inevitably fatal. Sooner 
or later the patient loses consciousness completely, his pulse grows very small and 
rapid, his respirations irregular and intermittent (Cheyne-Stokes), his temperature, 
as we have said, either rises high or falls far below normal, and, finally, death is 
ushered in by a paralysis of all the vital functions. A few physicians have 
reported cases of recovery ; but was the diagnosis correct ? While we would by 
no means absolutely deny that recovery from tubercular meningitis might occur, 
it would certainly be very difficult to prove, in any particular instance, that such 
a thing had happened. 

Tubercular Meningitis in Children.— The disease is so prone to attack children 
that it seems desirable to subjoin a few remarks about the peculiarities of the affec- 
tion as observed in them. 

Often the little patient is pale and weakly, with tubercular antecedents ; but 
sometimes apparently healthy and vigorous children are attacked. Tubercular 
meningitis may be the sequel of measles, whooping-cough, or some other disease, 
which has occasioned the development of the tubercular process. Usually the 
severer symptoms are preceded by a rather long prodromal stage, during which 
the child is fretful, eats little, and grows thin and pale. In children as well as 
adults, the second stage is generally ushered in by headache and vomiting. The 
headache is not very often violent ; but children complain with remarkable 
frequency of pain in the abdomen and chest. The cause of this symptom is 
unknown. The pulse is almost invariably slow, often somewhat irregular, and 
it frequently undergoes surprisingly rapid changes in rate — for example, varying 
twenty or more beats inside of a few hours. Very early the child becomes dull 
and drowsy. Frequently it emits a peculiar deep sigh, or that sudden loud scream 
or " cephalic cry " which physicians long ago learned to recognize and fear. The 
symptoms referable to the cranial nerves and the nervous disturbances in the 
limbs are similar to those seen in adults. Strabismus is almost constant. Very 
often there is trismus, and a distinctly audible grinding of the teeth, most dis- 
tressing to the by-standers. Trousseau laid weight upon the appearance of red 
spots (taches cerebrales) upon the skin after it has been mechanically irritated ; 
but these have no diagnostic value. They are due to increased reflex action, and 
are seen in all sorts of acute diseases. The fever is generally, as in adults, not 
very high, 100° to 102° (38°-39° C). Respiration is usually rapid, and often is 
irregular. 



TUBERCULAK MENINGITIS. 



667 



The change from bad to worse is almost always announced by a rapid increase 
in the pulse-rate, to 160 or 200. The child becomes completely comatose. Very 
often there are repeated epileptiform convulsions, either universal or affecting 
single extremities. Death is usually preceded by a decided rise in temperature. 

Diagnosis. — When the symptoms are pronounced, the diagnosis of meningitis 
is easy, and we have merely to determine just what variety is before us. That 
the disease is due to tuberculosis is never to be ascertained by means of the 
meningeal symptoms themselves, but is rendered possible only by the aetiology, if 
that be discoverable. Here, as in all tubercular diseases, we have chiefly to con- 
sider (1) heredity and (2) the evidence of previous or existing tubercular affections 
in other parts of the body. Under this second head are to be considered scrofula, 
diseases of the bones and joints, pulmonary tuberculosis, pleurisy, and tuberculosis 
of the genitals or of the choroid. If our search be unsuccessful, we may some- 
times get a hint of the truth from the general appearance of the patient : for 
example, he may be pale, or narrow-chested. And, again, the absence of trauma, 
aural disease, or epidemic meningitis will make tuberculosis more probable. 

In its early stages, or when it varies from the usual course, tubercular menin- 
gitis may be very difficult to diagnosticate. This is particularly true when the 
patient is a child. The early malaise and vomiting are treated as "ordinary 
gastric catarrh " until the grave cerebral symptoms disclose the mistake in diag- 
nosis. In such cases we should be careful not to disregard the initial slowness 
and irregularity of the pulse. This alone should make our prognosis guarded. 
The fever may be prominent at the commencement, and tempt us to call the case 
one of incipient typhoid fever ; and, indeed, the correct diagnosis is often impos- 
sible until the disease develops further. In regard to this, see the preceding 
chapter on purulent meningitis, where the exclusion of severe septic diseases and 
of uraemia is also considered. 

Before the autopsy we must remain in great uncertainty as to the number and 
distribution of the tubercles, the existence of a large effusion into the lateral 
ventricles, etc. We are often amazed at the post-mortem examination by the 
apparent insignificance of the lesions. Paralysis of the cranial nerves (eyes, face) 
implies that the base of the brain is gravely affected. If such symptoms are 
absent, and there are mental disturbances, and motor symptoms of irritation dis- 
played in the extremities, we are led to infer meningitis of the convexity. If the 
nervous disorder be mainly unilateral, we may assume that one hemisphere is 
more affected than the other. 

Treatment. — However hopeless the prospect, we are nevertheless bound to 
employ all the remedies at our command, as in other forms of meningitis. 
Above all, we should be thorough in applying ice to the head, and may also try 
local depletion and lukewarm baths, with douching. The inunction of mercurial 
ointment has a] so been recommended. The most common internal remedies are 
calomel — half a grain to a grain (grm. 0 "03-0 '05) for a child every two hours — and 
infusion of senna. Iodide of potassium may also be freely given, fifteen grains 
daily to a child, and two or three times as much to an adult. Whether it does 
any good is extremely doubtful. If the patient is very restless, narcotics are 
indispensable. Stimulants are often given in the last stage of the disease, but 
generally without effect.* 

About prophylaxis, we need merely refer to the general statements on page 
214, in regard to prophylaxis from the various tubercular diseases. 



* [One or two cures (?) have lately been reported from the application of a thick layer of iodoform 
ointment to the shaven scalp for thirty hours or more. — Trans.] 



668 



THE DISEASES OF THE BRAIN. 



CHAPTEE IV. 
THROMBOSIS OF THE CEREBRAL SINUSES. 

JEtiology and Pathology. — The sinuses of the dura mater sometimes present a 
thrombosis, under circumstances similar to those which induce the same process 
in other veins. The most frequent occasion for such thrombosis is marasmus, 
however brought about, with the accompanying feebleness of circulation. This 
is the explanation of those not very rare cases found among wretched and ill- 
nourished children in the first year of life, and also among adults in a similar 
physical condition, as in phthisis. In many of these instances passive congestion 
also seems to contribute to the formation of the thrombus. 

Half way between marantic thrombosis and the inflammatory variety imme- 
diately to be described, come those cases which are seen in typhoid fever and 
other severe acute infectious diseases. Here the specific virus apparently plays 
an important part (just as in thrombosis of the femoral vein), although very 
likely the cardiac weakness also promotes the thrombosis. 

Genuine inflammatory thrombosis — that is, thrombosis in connection with real 
phlebitis of the sinus — is almost always due to the extension of inflammation from 
some neighboring part. The most fruitful cause is suppuration in the petrous 
bone, the result of otitis or caries. This spreads to the walls of the transverse or 
petrosal sinuses, which are close by. Also wounds, necrosis, or other affections of 
other cranial bones may excite thrombosis ; likewise, although seldom, deep- 
seated inflammation of the soft parts of the head and face, like large furuncles or 
erysipelatous abscesses, may produce the same result. 

Thrombosis due to marasmus is most frequently found in the superior longi- 
tudinal sinus, while the inflammatory variety usually occupies either the trans- 
verse, petrosal, or cavernous sinuses. Of course the thrombus may grow out from 
its original sinus into neighboring ones. Important clinical symptoms are caused 
by secondary venous stasis in the veins which empty into the occluded sinus. 
These symptoms are most pronounced when the longitudinal sinus is affected ; 
objectively, we find the meningeal veins which lie on the surface of the brain dis- 
tended and tortuous ; and often there are extensive meningeal ecchymoses. Even 
the cerebral parenchyma beneath shows distinct evidence of passive congestion, 
and minute capillary haemorrhages have been repeatedly found in it. 

Symptoms. — In some instances moderate thrombosis of the cerebral sinuses 
has been found post mortem, although there had been no symptom suggesting it 
before death. In other cases the thrombosis does excite undeniable cerebral dis- 
order, but the symptoms are so general and ambiguous that the most we can do 
is to suspect the existence of the clot without being at all certain about it. 

Sinus thrombosis in marantic children usually causes coma, stiffness of the 
neck and back, strabismus, nystagmus, and sometimes clonic spasms in the face 
and limbs. The symptoms in adults are similar, comprising headache, drowsi- 
ness, occasionally delirium, sometimes coma, and varying symptoms of irritation 
or of paralysis in the distribution of the cranial nerves (nystagmus, strabismus, 
trismus) and in the extremities. But even all these symptoms are insufficient to 
make the diagnosis certain. They must be re-enforced by certain other phenom- 
ena more distinctly referable to the peculiar circulatory disturbances occasioned 
by the thrombosis. Occlusion of the cavernous sinus sometimes excites well- 
marked symptoms of stasis in the ophthalmic veins. Thus the retina may be 
seen through the ophthalmoscope to be passively congested, there is oedema of 
eyelids and the conjunctiva, the eyeball is unusually prominent, and the frontal 



DISTURBANCES OF CIRCULATION IN THE BRAIN. 669 



vein is distended. In case of an inflammatory thrombosis, the periphlebitic swell- 
ing may cause symptoms in the distribution of the neighboring nerves, especially 
paresis of the oculo-motor or abducens, or trigeminal neuralgia. In thrombosis of 
the transverse sinus an oedematous swelling is occasionally seen behind the ear, 
near the mastoid process. If the clot projects into the petrosal sinus or even actu- 
ally into the internal jugular, the lower part of this vein collapses. And inas- 
much as the external jugular can empty itself with unusual ease into the unfilled 
internal jugular vein, the external jugular is also affected and becomes less promi- 
nent upon the affected than upon the normal side. Sometimes it is even possible 
to feel the thrombus in the internal jugular. Such thrombosis causes pain and 
swelling in the neck on the abnormal side. When the superior longitudinal 
sinus is blocked up, there are symptoms of nasal engorgement (epistaxis), and 
distention of the veins about the temples, which veins are connected with the lon- 
gitudinal sinus by emissary veins. We must confess, however, that all these 
special symptoms are comparatively rare, and often difficult of demonstration 
even when present. 

The symptoms become more complex where there is a suppurative phlebitis, 
because there are usually pyaemic symptoms as the disease progresses. Thus, 
there may be rigors and high fever, pulmonary abscess, suppurative arthritis, etc. 
We have already mentioned the combination of thrombosis of a sinus with puru- 
lent meningitis. 

The prognosis is almost always bad, both because of the nature of the causa- 
tive disease and because of the grave cerebral derangement or the secondary 
pyaemia. Treatment can be only symptomatic. 



SECTION II, 
Diseases of the Brain-Substance. 

CHAPTER I. 

DISTURBANCES OF CIRCULATION IN THE BRAIN. 

{Cerebral Hypercemia. Cerebral Anamiia.) 

It is presumable that so sensitive an organ as the brain is much influenced even 
by slight disturbances of circulation ; but as yet we have comparatively little 
knowledge of the production and character of such disturbances, their very exist- 
ence being very difficult to demonstrate. There are many instances where marked 
cerebral symptoms justify the assumption that the brain is in some abnormal con- 
dition, and yet where there are many arguments against any marked anatomical 
lesion. Here we surmise that there is some circulatory derangement, although 
we have no actual and direct arguments to rely upon. For example, we refer to 
this cause certain cases of headache, sensations of pressure in the head, vertigo, 
general hyperesthesia, and of that protean and nevertheless easily distinguishable 
disease known as cerebral neurasthenia (q. v.). At present, however, we can not 
determine how far circulatory disturbances are actually concerned in these cases, 
or of what kind they are, or whether there may not be purely functional dis- 
ease of the brain entirely independent of changes in the blood-vessels. 

Certain groups of cerebral symptoms, which come on in paroxysms, seem the 
most clearly referable of all to circulatory disturbance. There can hardly be a 



670 



THE DISEASES OF THE BRAIN. 



doubt that the phenomenon known as fainting or syncope is due to sudden cerebral 
anaemia. As is well known, fainting is usually the result of a clearly demon- 
strable cause. Frequent and familiar causes are emotional excitement, terror, 
unusual psychical impressions (like the sight of blood), the influence of great heat, 
or great physical strain, as by long standing. The condition of the stomach has 
certainly a great influence in many cases. There are many persons who, if they 
go long beyond the usual time without eating (particularly without breakfast), are 
very liable to syncope. Some individuals are especially subject to fainting fits. 
Such persons are often slight and anaemic (for example, convalescents), but some 
are in appearance robust and vigorous. Many children are subject to fainting. 

Just what causes the cerebral anaemia in all these cases is doubtful. Mental 
excitement is usually supposed to lead, in fainting, to a contraction of the minute 
cerebral arteries. It is not, however, impossible that in these cases also, as in 
others, sudden cardiac weakness is one factor, although, if so, it is strange that we 
never see a trace of cyanosis. Where the attack is apparently connected with 
unusual conditions of the abdominal organs we are reminded of the relations of 
the splanchnic nerve to the heart (Goltz's experiment of beating the belly of a 
frog), and of the possibility that the brain might be left anaemic if the abdominal 
vessels suddenly dilated and absorbed a large proportion of the whole blood- 
supply. 

The symptoms of an ordinary fainting fit are known to every one. There are 
usually certain prodromata. The person begins to " feel badly." Dizziness comes 
on, the senses are confused, the ears ring, there are spots before the eyes or total 
darkness, the floor seems to move, and surrounding objects begin to spin around. 
All this is almost always accompanied by nausea, and sometimes there is actual 
vomiting. If the person can lie down promptly the attack is sometimes averted 
without complete loss of consciousness. Otherwise there is unconsciousness for a 
time varying from some minutes to even a half -hour or longer. What the by- 
stander notices most, even at the first, is the pallor which overspreads the face and 
often becomes extreme, and which is the visible expression of the coincident cere- 
bral anaemia. Very often the face and body are bathed in cold perspiration. The 
pulse is usually small and rapid. 

There is no real danger in an ordinary attack. The most important therapeu- 
tic measure is to lay the patient horizontally as soon as possible, to favor the 
return of blood to the brain. Mild stimulants should also be employed ; the face 
should be sprinkled with cold water, the temples rubbed with vinegar or cologne- 
water ; brandy or wine should be administered. We can overcome a tendency to 
fainting fits only by strengthening the constitution. 

The results of chronic cerebral anaemia are observable when the cerebral con- 
dition is part of excessive general anaemia. Almost all cases of chlorosis, per- 
nicious anaemia, and acute anaemia from loss of blood (as in ulcer of the stomach) 
display most plainly the symptoms of cerebral anaemia. The phenomena are 
essentially the same as in syncope, only less in degree. Consciousness is main- 
tained, except in the worst cases. A sort of persistent drowsiness, however, often 
attended by frequent gaping, is one of the most constant symptoms. The patient 
is most distressed, as a rule, by loud tinnitus aurium, persistent nausea, and some- 
times by obstinate headache. All these symptoms are aggravated if the patient 
sits up in bed, and are least marked when he lies as quietly as possible in a hori- 
zontal position. The treatment of this condition is of course identical with that 
of the causative disease and the general anaemia. 

Cerebral hyperaemia, like cerebral anaemia, may be either chronic or paroxys- 
mal. Of the chronic variety we know almost nothing. It seems doubtful, to say 
the least, whether there is really a " general plethora," or whether the headaches 



THE LOCALIZATION OF CEREBRAL DISEASES. 671 



and vertigo that " full-blooded " persons complain of are due to hyperemia of the 
brain. Nor have we any direct proof that the cerebral symptoms resulting from 
chronic poisoning (alcohol, tobacco), or from persistent mental over-exertion, are 
brought about by hypersemia, as some assume, and not rather by functional dis- 
order of the nervous elements themselves. 

We have the best reason to claim cerebral hypersemia as the cause of cerebral 
symptoms in instances of "cerebral congestion" or "rush of blood to the head." 
There is a more or less sudden appearance of general excitement, with a sensation 
of warmth in the head and neck, strong pulsation of the carotids, a red face, gen- 
eral hypersesthesia and irritability, headache, vertigo, tinnitus, spots before the 
eyes, and nausea. An attack lasts half an hour to an hour. Apparently there is 
vaso-motor disturbance, causing a sudden enlargement of the cerebral blood-ves- 
sels, and due either to a paralysis of the vaso-constrictors or to a stimulation of the 
dilators. In severe cases there may be maniacal excitement, or there may be 
stupor and drowsiness and other symptoms of lowered intellectual activity, resem- 
bling a slight apoplectic attack (see a later chapter). In such a case we can not 
determine whether there is hypersemia alone, or whether there is not some further 
lesion, like a small hsemorrhage. 

In treating congestion we should keep the patient as quiet as possible, with 
head and shoulders raised ; and, secondly, we should endeavor to draw the blood 
away from the brain. This purpose will be served by hot foot-baths, sinapisms 
applied to the chest and the calves, and purgatives, like senna or colocynth. It is 
also beneficial to apply cold to the head. In a severe case it is proper to put 
leeches to the temples or the mastoid processes. 

To prevent, as far as possible, the recurrence of the attacks, we must have 
regard to the general constitution of the patient. We may mention, as of chief 
importance, diet (no alcohol) and a course at some watering-place, or " cold-water 
treatment." 



CHAPTER II. 

GENERAL PRELIMINARY REMARKS UPON THE LOCALIZATION OF 

CEREBRAL DISEASES. 

{Topical Diagnosis of Cerebral Lesions) 

The physiological relations of the brain are such that the symptoms of cere- 
bral disease are determined to a greater extent by the locality than by the nature 
of the lesion. If, for example, there arises at any place a break in the con- 
tinuity of the cerebral motor tract, the result, as we already know (see page 505), 
is hemiplegia upon the opposite side of the body. The result is precisely the 
same, whether the interruption is due to a hsemorrhage, an abscess, a new growth, 
or an embolic softening. If in any way the function of the motor fibers is sus- 
pended, then the necessary sequence in every case is a paralysis of definite extent 
• and definite characteristics. Much the same may be said of many other symptoms 
which appear when there is a lesion of one or more definite places, but which are 
never referable to a special abnormal process, regardless of the portion of brain 
thereby affected. 

However self-evident these simple statements may appear, it required a long 
time for them to gain universal acceptance among physicians. The chief cause of 
this was the conception entertained by the older physiologists in regard to the 
functions of the brain. Flourens, in 1842, taught that functionally all parts of the 
cerebrum were alike, and therefore any one part could act vicariously for any 



672 



THE DISEASES OF THE BRAIN. 



other ; and this view had numerous adherents among physicians, as well as physi- 
ologists. It was nevertheless experience at the bedside and the autopsy-table 
which first led to observations and discoveries irreconcilable with this view. 
Above all, it was the lesions found in aphasia which forced men to localize one 
cerebral symptom as due to an affection of one particular spot in the brain. In 1861 
Broca announced that the appearance of aphasia is always due to a lesion of the 
third left frontal convolution ; and this was the starting-point of the doctrine of 
localizations in general. Nine years later (1870) appeared the famous treatise of 
Fritsch and Hitzig detailing successful attempts at irritation of the surface of the 
brain in animals, and thus overthrowing the old idea that the gray cortical sub- 
stance could not be irritated. It was shown that irritation of certain places in the 
cortex is followed by muscular contractions in well-defined portions of the oppo- 
site side of the body, so that we are justified in assuming the existence of a num- 
ber of cortical centers, the boundaries of which are comparatively narrow. These 
results were soon confirmed by numerous observations in cerebral pathology in 
man ; and to-day our information about the motor functions of the cerebral cortex 
forms the best-known portion of the doctrine of cerebral localization. Of late 
years successful work has been done in this exceedingly difficult field by Mey- 
nert and Flechsig among anatomists ; Ferrier, Munk, Goltz, and other physiolo- 
gists ; and such pathologists as Charcot and his pupils, Nothnagel and Hughlings 
Jackson. It is true that we are only just beginning to know something about 
the subject. There are numerous contradictory views asserted, and numerous 
questions unanswered. The following summary, therefore, is to be regarded 
merely as expressing the prevailing opinions now existing. Much in it will surely 
be altered in the course of time ; but still this doctrine of special localization of the 
various cerebral functions marks out in general outlines the only foundation 
upon which we can hope to erect a system of cerebral pathology and diagnosis. 
In the following sketch we shall, for practical reasons, put the results of clinical 
observations in the foreground, and merely speak incidentally of the correspond- 
ing experimental achievements. This will be the quickest way to gain acquaint- 
ance with the practical points in the diagnosis of what Griesinger called the "focal 
diseases " ; and then, when we take up the separate varieties of cerebral disease, 
we shall have these general remarks to refer to. 

1. The Motor Region of the Cortex Cerebri. 

Clinical observation and the results of experiment both teach that a part of 
the cerebral cortex is distinct from the rest, inasmuch as it is the exclusive seat 
of motor functions. This "motor region" {vide Figs. 97 and 98, page 674) is 
made up of the two central convolutions (gyri centrales anterior et posterior, in 
Fig. 96), and the paracentral lobule (vide Fig. 98), which lies on the median sur- 
face of the cerebrum. It is also anatomically different from the other regions of 
the cortex, as Betz was the first to point out, for it alone possesses certain large 
pyramidal ganglion-cells, which are in all likelihood motor. However extensive 
the destructive processes which attack other parts of the surface of the brain, pro- 
vided they do not involve these particular convolutions, they cause no paralytic 
symptoms ;. while all diseases which destroy any considerable portion of the 
" motor " region inevitably result in a paralysis on the opposite side of the body. 

We can differentiate still further. There are separate regions which act as 
special centers for the various groups of muscles. The center for the movements 
of the facial muscles (lower division of the facial nerve) lies, as it would seem, at 
the lower end of the central convolutions, and particularly of the anterior central 
convolution. Near by, apparently still lower, is found the center for the move- 
ments of the tongue. The center for the movements of the arm lies somewhat 



THE LOCALIZATION OF CEREBRAL DISEASES. 



673 



higher than the center for the facial, occupying roughly the middle portion of the 
anterior central convolution. The center for the lower extremity is found partly 
in the uppermost portions of the central convolutions, but apparently lies for the 
most part in the paracentral lobule. Any minuter division is not yet possible. 

There are already quite a large number of cases of hemiplegia known which 
were caused by some disease in the motor region, like a tumor or spot of soften- 
ing. We should add, in regard to the pathological anatomy of these cases, that 
they all, without exception, presented a secondary descending degeneration of the 
pyramidal tract (compare page 641), extending through the internal capsule, crus 
cerebri, and medulla into the corresponding lateral and anterior columns [that is, 
on the same side in the anterior columns and on the opposite side in the lateral]. 
The hemiplegia due to cortical lesion does not differ from that due to focal disease 
lower down in the motor tract (compare page 503) in its clinical aspects. We shall 
consider the symptoms more particularly in the chapter on cerebral haemorrhage. 




Fig. 96.— Lateral aspect of the brain (from Ecker). The gyri and lobules are in Roman type, the sulci 

and fissures in italics. 

It is nevertheless possible in many instances to decide that the disease involves 
the motor portion of the cortex of the brain. This is due to the following pecu- 
liarities : 

In the first place, we have already remarked (page 505) that the relative posi- 
tions of the motor centers for the face, arm, and leg are such as to allow readily 
of isolated paralysis of any one of these portions of the body — that is, " mono- 
plegia." In fact, we already possess a long series of observations where circum- 
scribed lesions in the motor area of the cortex produced paralysis of one side of the 
face, or of one arm or leg, and of no other part. Such paralysis is termed mono- 
plegia of the face, or the arm, or the lower extremity. And it follows, from what 
has been said, that even during life we can state, with considerable accuracy, the 
spot on the surface of the brain where the disease must be situated. Still more 
frequently, a combined paralysis of two portions of the body is to be observed as a 
result of cortical lesion ; the commonest is a simultaneous paralysis of the arm 
43 



674 



THE DISEASES OF THE BRAIN. 



and face ; more rarely we see the arm and leg paralyzed together. On the other 
hand, we may feel certain, from the position of the motor centers, that no single 
center of disease could paralyze simultaneously the leg and the face, while the 
arm escaped injury. As a matter of fact, no such combination has ever been 
observed. 




Fig. 97.— Lateral aspect of the brain (after Ecker). The motor region of the cortex, consisting of the 
anterior and posterior centra^ convolutions, as well as of the paracentral lobule shown in Fig. 98, is 
shaded. 




Fig. 98.— Aspect of the median surface of the cerebrum, which is shown when the two hemispheres are 
separated from each other by a sagittal section. B. Corpus callosum. The differences in the type 
have the same meaning as in Fig. 96. The paracentral lobule, as a part of the motor region of the 
cortex, is shaded. (Copied from Ecker, only the paracentral lobule is made more sharply prominent 
than in the original). 



Beside this limitation of the paralysis just discussed, localized disease of the 
cortex has another characteristic. In it the symptoms of irritation of the motor 



THE LOCALIZATION OF CEREBRAL DISEASES. 



675 



centers are noticeably frequent. There are tonic and clonic spasms, which, like 
the paralysis, not infrequently affect a single arm, or an arm combined with 
half the face. Sometimes, however, they involve the entire half of the body. 
These paroxysmal spasms are termed " cortical epilepsy," or partial epilepsy, or 
Jacksonian epilepsy ; for the movements are just the same as in genuine epilepsy. 
Numerous cases of disease have taught us that these circumscribed epileptiform 
attacks occur almost exclusively in affections of the motor cortex. They furnish 
information as to the precise locality of the lesion ; for spasms in the distribution 
of the facial nerve imply that mainly the lower third of the central convolutions 
is affected ; of the arm, the middle third ; and of the lower extremity, the upper 
portions of the same. At the same time, the spasms and the paralysis vary 
greatly in their relations to each other. Often, for example, when there is 
haemorrhage into the central convolutions, violent unilateral convulsions come 



Fig. 99.— (Drawn according to Ecker). Explanation of the topographical relations between the surface of 
the brain and the skull, c. Fissure of Rolando. HC. and VC. Posterior and anterior central convolu- 
tions. S. Si. and Sn. Fissure of Sylvius. P l . P 2 . Upper and lower parietal lobes. O. Occipital lobe. 
Cb. Cerebellum. T. Temporal lobe. F. Frontal lobe. 

on simultaneously with the paralysis. In the case of tumors and other lesions 
which develop slowly, partial epileptiform spasms will often appear quite a long 
while before there are symptoms of paralysis. Finally, it is not rare for epilepti- 
form attacks to occur repeatedly in regions that are already paralytic. Either 
of the occurrences described in the two preceding sentences are particularly strong 
evidence that the cortex cerebri is diseased. Beside the pronounced epileptic 
attacks, disease of the motor region of the cortex may give rise to less violent 
symptoms of motor irritation, like occasional twitching, rhythmical twitching, 
and tonic contraction. 

About the condition of sensation when there is cortical paralysis we know as 
yet too little. The late experimental researches of Munk have led to the conclu- 
sion that, in animals, the so-called " sphere of sensation " lies in the same region 
as the motor centers of the cortex. We might, therefore, be somewhat inclined 
to presuppose that a disturbance of sensation would invariably accompany cortical 
paralysis in man also, but about this point clinical observations do not yet give 
perfectly harmonious results. In many cases sensation is undoubtedly normal, 




676 



THE DISEASES OF THE BEAIN. 



while in others simultaneous disturbances of sensation have been clearly demon- 
strated. Of especial interest is the well-attested fact that the muscular sense may 
be diminished in the extremities involved — that is, the patient can not tell, with 
eyes closed, the position of the affected limbs. 

2. The other Parts of the Cortex Cerebri, except the Center for 

Speech. 

1. Frontal Convolutions. — Unilateral disease of the anterior portion of the 
brain may be quite extensive without causing notable disturbance of any kind. 
Certainly the upper two frontal convolutions have no motor functions. It is, 
however, maintained that the portion contiguous to the anterior central convolu- 
tion, called the foot of the frontal convolutions, does contain motor centers ; but 
even about this doubt has lately arisen. The third (lowest) frontal convolution 
on the left side has, as we shall soon see, an undoubted connection with the motor 
processes of speech. 

There is a quite generally accepted view that the cortex of the frontal portion 
of the brain is to be regarded as the "seat of the higher psychical functions." 
Some few cases are on record where extensive bilateral lesions of these parts had 
for their only symptoms mental disturbances. In general paralysis also, and in 
other forms of dementia, it is very probable that the atrophy is greatest in the 
anterior part of the cerebrum. Nevertheless, we can not emphasize too much the 
fact that, at present, we have no certain knowledge about the minute relations of 
the psychical functions to the different sections of the brain. 

2. Parietal Convolutions. — We know practically nothing about the functions 
of the cortex of the parietal lobe, and the symptoms which might imply disease of 
that portion of the cerebrum. The results of clinical observations, thus far made 
with these points in view, are quite contradictory. Motor functions are not, appar- 
ently, bestowed upon this region. According to Flechsig, most of the sensory 
fibers of the tegmentum seem to have their central termination here, so that dis- 
ease in the parietal portion would be likely to impair cutaneous and muscular 
sensibility. 

3. Occipital Convolutions. — The clinical and experimental investigations of 
the last few years have all shown that the occipital portion of the cerebrum con- 
tains the cortical center for visual sensa- 
tions. It is here, in all probability, that 
the fibers of the optic nerve terminate in 
the cortex cerebri. A glance at the fol- 
lowing diagram (Fig. 100) will make it 
easy to understand the disturbances of vis- 
ion which result from lesions of the occi- 
pital lobe. L represents the left eye, and 
R the right, Ch the optic chiasma, where 
as is now certain some of the fibers of 
the optic nerves cross to the opposite side. 
The fibers (distinguished by a broken line) 
from the outer or temporal half of each 
retina extend, without crossing, into the 
corresponding optic tract (Tract, opt.), 
while those from the inner or nasal half 
of the retina cross over in the chiasma. 
The right occipital lobe, for example, 

comes in this way to receive the fibers from the outer half of the right retina, and 
from the inner half of the left. If the right occipital lobe becomes disorganized, 




Fig. 100. 



-Diagram of the course of the optic 
fibers in the chiasma. 



THE LOCALIZATION OF CEREBRAL DISEASES. 



677 



then the images formed upon the parts of the retinae just named, belonging* to the 
left half of the field of vision, are unperceived. With each eye, the patient sees 
only such objects as lie in the right half of his field of vision, and is blind to all 
that lies upon his left. This sort of visual disturbance, where each eye becomes 
blind to the same " homonymous " portions of the field of vision, is termed hemia- 
nopsia, or hemiopia. A lesion of the right occipital lobe causes, therefore, left- 
sided hemiopia, and, vice versa, destruction of the left occipital lobe entails right- 
sided hemiopia. 

It may also be well to mention briefly another peculiar disturbance of vision, 
which is perhaps due to a lesion of the occipital cortex. Furstner noticed certain 
phenomena in the insane, which implied that the patient, although he could see, 
and could not therefore properly be called blind, yet did not recognize the objects 
— that is, was no longer able to interpret the meaning of the visual image. Munk 
has given to this condition the name of " soul blindness," conceiving it to be a 
"loss of visual memory." 

4. Temporal Convolutions. — The relation of the temporal lobe to hearing is 
apparently analogous with that of the occipital to vision. Whether extensive 
disorganization of the temporal lobe, or of the fibers that enter it, can produce 
actual deafness of the opposite ear, has not yet been proved, inasmuch as very 
few cases have yet been studied. It may, however, be regarded as extremely 
probable that a lesion of the first, or uppermost, temporal convolution occasions 
that peculiar phenomenon known as " word deafness " or " soul deafness," with 
which we are at once to become more intimately acquainted. 

3. The Centers op Speech and the Disturbances of Speech. 

{Aphasia and allied Conditions.) 

The various Forms of Aphasia, and their Anatomical Localization.— As we 

remarked at the very beginning of this chapter, the peculiar derangements of 
speech observed in many cerebral diseases were the first symptoms which were 
found to be caused by a distinctly localized cerebral lesion. For the better under- 
standing of this extremely interesting subject, it is necessary that we should enter 
somewhat minutely into the processes connected with normal speech. 

Incitement to speech — that is, to the oral expression of our thoughts to others 
— comes either from an internal impulse or from external causes which excite this 
impulse. Speech always requires internal mental activities, the presence of ideas 
and their transformation into that which we wish to communicate by speech. 
Where there are no conceptions there can be no words. The idiot is silent, 
because, like the new-born infant or the brute, he has nothing to say; but, on 
the other hand, the impulse to speak must also be present. In melancholic 
insanity we sometimes observe persistent loss of speech, not from any lack of 
something to say, but because there is no incitement to the act, or because inhibi- 
tory influences immediately repress any tendency to utter words. If we take for 
granted that the mental material for speech exists, then the transformation of this 
material into actual speech is a result of the following complicated processes, the 
disturbance of which, individually, produces the various forms of aphasia. 

In the first place, the speaker must be acquainted with the word which expresses 
the mental conception. If, for instance, he wishes to tell another the name of 
some animal, he must know the appropriate word, "dog," "sparrow," "frog." 
This knowledge, which, as far as our mother tongue is concerned, we all acquired 
in childhood, may, as experience shows, be lost again in case of cerebral disease. 
Just as we may ourselves forget a word momentarily, or as any healthy person 
may, at the sight of an animal that is perhaps rather rare, be " unable at the 
minute to think of its name," so in disease one may forget all or a greater or less 



678 



THE DISEASES OF THE BKAIN. 



number of words. Such a patient sees a dog, and knows we]l enough that it is an 
animal possessed of such and such qualities, but he has forgotten its name. The 
association between the conception '* dog," and likewise between the perception of 
a dog by the eye, and the appropriate vocal representation " dog," is lost. This 
condition is termed amnesic aphasia, because it is due to complete or partial loss of 
the memory for words. The patient knows perfectly well what he wishes to say, 
but the words escape him. At the same time, in cases of pure amnesic aphasia, 
the power of repetition is unimpaired. As soon as we say " dog " to the patient, 
he repeats the word perfectly well. And sometimes he also perceives that this is 
really the correct word ; but in other instances, although the word is correctly 
repeated, the patient does not become conscious of its meaning (vide infra " word 
deafness "). 

Of great interest are certain cases where there was only partial amnesia. These 
have been repeatedly observed. Thus a patient forgot nothing but his own name, 
remembering all other words perfectly ; or the loss of words may be confined to 
but one language, the patient being still able to express himself tolerably well in 
another tongue. In a case observed by Graves, the patient still knew the initial 
letter of all words ; if, for example, he saw a cow, he would know that the corre- 
sponding word begins with C, and would look under C in a dictionary till he 
found the word. 

If the memory for words be retained, the next requisite for speaking is the 
transfer of the word image into such action of the muscles of our organs of speech 
as is calculated to produce the word in question as an actual sound. This motor 
process is so complicated that an extremely accurate co-ordination of movements 
is demanded for the correct pronunciation of the word. Man therefore possesses 
a separate center, in which this transfer of the word image into the motor pro- 
cesses of speech takes place. If this center be diseased, there again results a loss, 
or at least a greater or less impairment of speech. The patient is in this case well 
aware of the word he wishes to say, but he can not pronounce it. He has, if we 
may use the expression, forgotten the movements that are essential to speaking. 
His tongue and Hps are not really paralyzed, but the patient no longer knows how 
to make use of them for talking. He has reverted to the condition of childhood, 
before he had learned to talk. The patient often makes the greatest effort to 
speak. The word he wishes to utter u keeps hovering before him " ; he moves his 
mouth in the most striking manner, but brings out only an occasional sound, and 
that incorrect. This form is known as ataxic aphasia. Of course it is equally 
impossible for the patient to repeat a word after some one else. He keeps his eyes 
fixed on the mouth of the speaker, and endeavors to imitate the motions of his 
mouth, but is either partially or totally unable to reproduce the sound. 

Ataxic aphasia exhibits many degrees of intensity. On the one hand there are 
cases of complete aphasia, where the patient can utter only such separate sounds 
as " a," " e," etc. And, on the other hand, there are also very mild cases, where 
there are merely slight errors in pronunciation. The patient pronounces many 
words correctly, but with others there are such mistakes as the transposition of 
individual letters, the misplacement or omission of letters, or, finally, the adding 
on of letters. For example, he will say thens instead of then, widow instead of 
window, dipter instead of dipper, hefd instead of held, wrelster instead of wrest- 
ler, and belnow instead of below. This mildest form of ataxic disturbance is 
termed u stumbling over syllables " (Silbernstolpern), or "literal ataxia." In most 
instances the patient can pronounce some words tolerably well, others only imper- 
fectly and with difficulty, and still others not at all. Usually the patient gradu- 
ally learns a few common words and expressions (e. g., "good morning") by 
means of persistence in repeating them as they are uttered by another, so that he 



THE LOCALIZATION OF CEREBRAL DISEASES. 



679 



pronounces them better and better. What is very remarkable, and not so very 
rare, is that a patient will be able when in a passion to pronounce a word, such as 
an oath or an exclamation, perfectly well, because it is done to a certain extent 
involuntarily, while he can not utter the same words if he wishes to say them. 
Association also often exerts an appreciable influence ; for example, a patient who 
finds it absolutely impossible to pronounce " six," utters it with perfect distinct- 
ness if he begins to count from one, in the ordinary way, up to six. There are 
many facts connected with this subject which can not here be discussed. Each 
case demands separate and earnest study, and will usually be found to present an 
abundance of interesting peculiarities. 

Allied to ataxic aphasia are two other disturbances of speech, known as mono- 
phasia and paraphasia. Monophasia is very rare ; in it the patient has command 
of but one single syllable, or a single short phrase, and this is pronounced when- 
ever he attempts to talk. A patient of our own could for a long while utter noth- 
ing but the meaningless words, " selber sag ich namlich selber " (self say I namely 
self). The entire verbal thesaurus of another (female) patient whom we saw con- 
sisted of the meaningless sounds "bibi" and "eibibi." Still a third could say 
only "thine, tinne." The patient is quite well aware that what he says is wrong, 
but, despite all his efforts, every attempt to speak excites these same sounds. It 
produces a comical impression to see the patient use the same invariable word, 
with all sorts of facial expression. Thus the woman mentioned above begged for 
things, with "bibi," in a coaxing tone; while sometimes she would give vent to 
violent anger with a loud "bibibibi." 

Paraphasia is a confounding together of words. The association between the 
idea and the corresponding word is broken up, and instead other words come to 
the tongue. Some of these are proper words enough, but others are quite mean- 
ingless. Such a patient may talk a long while without conveying any idea to the 
listener, inasmuch as he says "brush" instead of "bed," or "gove" instead of 
" give," etc. 

As has been already shown, in amnesic aphasia the connection between the 
word and the conception it represents is so imperfect that the rising up to con- 
sciousness of the idea fails to call up the corresponding word. Now, on the other 
hand, the opposite may occur ; the word, when it is heard, may fail to call up the 
appropriate mental image. Kussmaul has given this condition the name of word 
deafness (Wernicke's sensory aphasia). The patient is not really deaf, for he 
hears everything, but he no longer understands what he hears, and has forgotten 
what the words signify. The vernacular sounds to him as a foreign tongue would 
to a healthy but unlearned man. A moderate amount of word deafness is very 
frequent in aphasia, particularly in the amnesic variety ; but this last and word 
dumbness are not identical. A person may forget the word corresponding to some 
idea, and yet understand the meaning of that word perfectly when he hears it. It 
is an easy matter to prove whether word dumbness exists or not by asking the 
patient to do something — for example, to touch certain parts of his body, or to 
perform certain motions (without, however, making any explanatory gestures our- 
selves), and seeing whether he understands and complies. Of course, the demon- 
stration of word deafness can usually be made with regard to the names of con- 
crete things only, and certain verbs and adjectives, but is hardly practicable in 
other cases (for example, with abstract words and adverbs), particularly if there is 
aphasia at the same time. 

These various forms of aphasia, just described, seldom occur single and 
unmixed. They are usually found in combinations, which vary greatly, so that a 
complete idea of the derangement existing in any case can be obtained only by 
careful examination and continued observation of the patient. Granting, how- 



680 



THE DISEASES OF THE BEAIN. 



ever, that the variety of aphasia has been determined, what light will this throw 
upon the localization of the cerebral disease ? 

As early as 1825 Bouillaud affirmed that disease of the anterior lobes of the 
brain is alone capable of producing disturbances of speech. In 1836 another 
French physician, Marc Dax, pointed out for the first time that only lesions of the 
left half of the brain cause aphasia ; and in 1861 Broca was able, as already stated, 
at last to declare that the " center for speech " lies in the third left frontal convo- 
lution. This statement has since been confirmed innumerable times, although it 
must be added that disease here is a cause of ataxic or motor aphasia alone. Still 
more accurately, it is the posterior portion of the third left frontal convolution, the 
pars opercularis, so called, which gives rise to this symptom. It is in this region, 
therefore, that those complicated processes of motor co-ordination, which are essen- 
tial to the utterance of a word, take place. Word deafness, on the other hand, 
according to all the newer observations of Wernicke, Kahler, and Pick, seems 
invariably to be referable to disease of the first or uppermost left temporal convo- 
lution. Probably the same is true of amnesic aphasia. It is apparently, then, this 
region which is essential to the normal association between the auditory image of the 
words we hear and the appropriate mental conceptions. Any minuter localization 
of these and the remaining forms of disturbance of speech is at present impossible. 
It is probable, though not certain, that the left island of Reil also has some con- 
nection with aphasic disorders. However this may be, the corresponding portions 
of the right hemisphere are not usually connected with this sort of disturbance — a 
fact perhaps analogous with the predominant use of the right hand ; that is, of the 
left cerebral hemisphere. It is only in a few exceptional cases — for example, of 
left-handed persons, or of such as present congenital defects in the left half of the 
brain — that observers have noticed aphasia in connection with disease of the cor- 
responding frontal and temporal convolutions of the right side. 

The diagnosis of aphasia in general is an easy matter if we stick closely to the 
true conception of aphasia. The examination would have to be a superficial one 
to lead to confounding it with bulbar symptoms like dysarthria (vide supra, page 
646), or with the disturbances of speech which result from other lesions which 
entail paresis or paralysis of the hypoglossus or certain fibers of the facial. 

No general rules can be laid down as to the prognosis and treatment of aphasia, 
inasmuch as everything must of course depend upon the nature of the disease 
which excites this symptom. We will merely emphasize here the therapeutic fact 
that methodical exercises in speaking and in language may be decidedly beneficial. 
In ataxic aphasia such instruction may be imparted in about the same way as to 
the deaf and dumb, sight and touch being invoked to aid in a fresh training of the 
appropriate muscles. In amnesic aphasia the memory must be trained, that the 
forgotten words may once more be " stamped " upon it. Of course, all such efforts 
demand great tact and patience, and accomplish little unless they are methodical 
and persistent. 

Disturbances allied to Aphasia: Agraphia, Alexia, Amimia, and Apraxia.— 

Aphasia is very often accompanied by a group of other symptoms, which are like- 
wise due to disturbance of the processes of association. Beside the language of 
words, we possess two other means of expression — writing and gesticulation. Our 
mental concepts are associated not only with certain sounds, but also with certain 
visible forms, so that, on the one hand, we use them to impart our thoughts to 
others, and, on the other, by their aid we learn the thoughts of other people. In 
aphasia this capability also is often more or less lost. If it is impossible for the 
patient to make himself understood by means of words, and we give him a pen, 
that he may write down his wishes, it is often found that this, too, is out of the 
question. The patient tries to write, and may indeed set down one or two words. 



THE LOCALIZATION OF CEREBRAL DISEASES. 681 



or one or two letters, but is no longer capable of writing a single sentence, or per- 
haps even a single word, correctly. This is termed "agraphia." Probably, in 
most instances, the agraphia is amnesic. The patient has forgotten the written 
characters. Usually, although not in every case, he can copy correctly what 
another has written. As a rule, alexia is also present ; the patient can not read 
any better than he can write — that is, the characters which he sees fail now to 
call up the associated mental conception. Alexia is not inseparably connected 
with word deafness. It is possible for a patient not to understand a spoken word, 
and yet to recognize it at once if written. 

The aphasic are also quite often unable to express themselves by pantomime or 
" dumb show." Frequently the patient makes no effort whatever of this kind, or 
what signs he does make are evidently wrong and misleading. We have repeat- 
edly seen an aphasic patient nod his head, when it was plain that he meant to say 
No, and vice versa. 

Finally, there is apraxia, a disturbance which, to be sure, is often associated 
with aphasia, but implies more extensive lesions. The essential point in apraxia 
is that the patient has more or less completely forgotten what the different objects 
about him really are. The condition must be closely allied to that in so-called 
"soul blindness." The patient sees the objects, but fails to recognize them for 
what they are. He takes a knife for a spoon, the wash-bowl for the chamber-pot, 
the soap for a piece of bread, and acts accordingly ! 

A definite anatomical localization of all these disorders, which have just been 
briefly alluded to, can not at present be given. Alexia, and still more apraxia, 
suggest lesion of those tracts which are connected with, or situated in, the posterior 
part of the cerebrum, the region of memory for visible objects. 

4. The Centrum Ovale, Internal Capsule, Central Ganglia, and Region 
of the Corpora Quadrigemina. 

Centrum Ovale. — The white substance of the hemispheres is made up, so far 
as we know at present, both of commissural fibers, which connect the various 
cortical centers together, and of fibers which proceed downward from the centers 
of the cortex and connect these centers with peripheral parts of the body (corona 
radiata). As to the symptoms caused by diseases which destroy the commissural 
fibers, there is hardly anything known. We can only surmise that in case of 
disturbances of association, such as we have studied under aphasia and kindred 
disorders, there may sometimes be a lesion of commissural fibers, as of those con- 
necting together the temporal and frontal lobes. A break in the continuity of 
the fibers of the corona radiata must of course result in the same symptoms as if 
the corresponding center were itself destroyed. This explains why circumscribed 
lesions of the centrum ovale, if they involve the motor fibers of the corona radi- 
ata, which proceed from the central convolutions (and only if they do this), cause 
hemiplegia, or, if very limited, monoplegia. In an analogous manner, disease of 
the white substance of the occipital lobe may entail hemiopia ; of the temporal 
lobe, auditory disturbances, such as word deafness. More than once, quite exten- 
sive disease of the white substance of the frontal lobe on one side has been discov- 
ered post mortem, although no symptoms whatever had been caused by it. Only 
when the coronal fibers which proceed from the third left frontal convolution are 
involved in disease, is motor or ataxic aphasia inevitable. 

Internal Capsule. — The most important facts relating to the functions of the 
internal capsule, as far as at present known, have been already stated. In par- 
ticular, it was pointed out that through the posterior limb of the internal capsule, 
in a comparatively narrow space, passes the pyramidal tract on its way from the 
central convolutions to the crura cerebri (see Fig. 63, page 503). Here, then, even a 



682 



THE DISEASES OF THE BEAIN. 



very limited focal disease must lead to complete hemiplegia on the opposite side 
of the body. Clinical experience also shows that the largest number of cases of 
persistent hemiplegia are occasioned by disease in this spot. In these cases the 
facial nerve is usually also involved, although its fibers apparently lie somewhat 
further forward than the tracts which are destined for the extremities. 

The sensory tract (compare page 481, and Fig. 63, page 503) lies at the posterior 
extremity of the internal capsule, and apparently includes not only the fibers for 
cutaneous sensation, but also for the organs of special sense. Complete disorgan- 
ization of this spot ought therefore to cause, in the opposite half of the body, not 
only anaesthesia of the skin, but also simultaneously a corresponding impairment 
of smell, taste, and hearing, and hemiopia — in short, a so-called complete cerebral 
hemianaesthesia. Still, in regard to this very point we are very much in need of 
further and definite observations. Charcot's statement that in these cases the 
disturbance of vision is not hemiopia, but total amblyopia of the eye opposite to 
the focal lesion, has caused great confusion, for such a fact would of course be 
hard to reconcile with the appearance of hemiopia in diseases of the occipital lobe, 
although this latter occurrence is well established. However, this statement of 
Charcot's is by no means absolutely proved, so that meanwhile we are at liberty 
to maintain the view that cerebral hemianaesthesia does cause hemiopia.* 

Certain practical conclusions in regard to diagnosis can be deduced from the 
preceding facts. A purely motor hemiplegia, unattended by impairment of sensa- 
tion, implies a lesion that does not involve the posterior portion of the internal 
capsule ; but probably this portion is also affected, when there is not only paraly- 
sis, but considerable sensory disturbance. The sensory disturbance does not 
invariably extend to all the senses ; quite often there is nothing but cutaneous 
anaesthesia. 

About the importance of the other parts of the internal capsule, not mentioned 
here, nothing is known. A statement made by Charcot should be added in con- 
clusion — namely, that when there are also post-hemiplegic symptoms of irrita- 
tion, such as post-hemiplegic chorea, there is very probably a lesion of the pos- 
terior extremity of the internal capsule. 

Central Ganglia: Caudate Nucleus (Corpus Striatum proper), Lenticular 
Nucleus, and Optic Thalamus— Before the course of the pyramidal tract had 
been accurately determined, ordinary cases of cerebral hemiplegia were almost 
universally ascribed to lesions of the central ganglia, and in particular of the 
caudate and lenticular nuclei. At present, however, observations seem to force 
one to the conclusion that a complete hemiplegia can be produced only by a 
cutting off of the pyramidal tract. There are, indeed, numerous cases of hemi- 
plegia presenting circumscribed disease of the central ganglia ; but they can 
probably all be explained by supposing either that the pyramidal tract, as it lies 
in the contiguous internal capsule, is directly involved in the disease, or that its 
functions are suspended by the indirect effects of the neighboring lesion — for 
instance, by the pressure it exercises. Accordingly, we find that circumscribed 
lesions of the central ganglia in the neighborhood of the internal capsule gener- 
ally produce a temporary hemiplegia — that is, the paralysis gradually improves 
as the indirect influence of the focal disease upon the internal capsule ceases. 
Chronic and incurable hemiplegia, however, if due to a lesion anywhere in this 
region, always implies an actual lesion of the pyramidal tract in the internal cap- 
sule. In regard to hemianaesthesia, also, the facts seem to be quite analogous. It 
was formerly held that this phenomenon was especially connected with a lesion 



* [Recent investigations (Seguin) have failed to find a single case that corroborates the theory that 
a focal lesion in the brain may cause amblyopia on the opposite side. — Tra^s.J 



THE LOCALIZATION OF CEREBRAL DISEASES. 



683 



of the optic thalamus, the reason being that the sensitive fibers lie so close to the 
thalamus, in the posterior extremity of the internal capsule, that they become 
themselves involved. 

About the symptoms which lesions of the central ganglia directly produce, little 
is definitely known. The results of both clinical observation and experiment are 
quite contradictory, and in repeated instances quite extensive disorganization of 
these parts has existed without producing any symptoms to speak of during life. 
In particular, it should be borne in mind that softening may occur in the lenticu- 
lar and caudate nuclei, and yet not a trace of hemiplegia be observable. It seems 
probable also that the optic thalamus has nothing to do with voluntary motion. 
As to perceptive functions, there is only one which the optic thalamus is certainly 
known to possess : the central termination of some fibers of the optic nerve is 
in its posterior portion known as the posterior tubercle or pulvinar, while other 
fibers go to the corpus geniculatum externum. Destruction of the hinder part of 
the thalamus accordingly produces complete hemiopia {vide page 676) of the 
opposite side. It has been affirmed that the optic thalamus has connections with 
other sensory tracts ; but definite proof is lacking. Focal disease of the thalamus 
has repeatedly occasioned u post-hemiplegic chorea" and other post-hemiplegic 
symptoms of irritation. 

Corpora Quadrigemina and Crura Cerebri.— Diseases of the corpora quadri- 
gemina are infrequent, and usually, when they do occur, they are merely a part 
of more extensive lesions of the brain. They are therefore very rarely considered 
from a diagnostic point of view. 

The anterior tubercles are certainly connected with the fibers of the optic nerve. 
If both of the anterior tubercles are destroyed, total blindness is inevitable, while 
if only one is disorganized, hemiopia is to be anticipated. Still, these symptoms 
are, of course, too ambiguous ever to be regarded as pathognomonic of localized 
disease of the anterior corpora quadrigemina. Another point to be considered, 
whenever the corpora quadrigemina are diseased, is the position of the nuclei of 
the nerves which preside over the motions of the eyeball, and in particular of the 
oculo-motor nerve. This explains why unilateral, or even bilateral, paralysis of 
the oculo-motorius has been repeatedly observed in connection with lesions of the 
corpora quadrigemina, as have also nystagmus and immobility of the pupil. 

Should the crura cerebri become involved in the disease, the resulting symptoms 
are often very characteristic of the locality affected ; there is paralysis of one side 
of the body (arm, leg, facial nerve), and, at the same time, a crossed paralysis (that 
is, one situated upon the opposite side) of the motor oculi. A glance at Fig. 64 
(page 504) will explain this phenomenon. Thus, a circumscribed lesion on the 
right side would destroy the fibers of the third nerve on that side, and, therefore, 
produce a right-sided paralysis of the oculo-motor nerves, and at the same time, if 
extensive enough, the lesion would involve the pyramidal fibers of the right crus, 
and thus occasion left hemiplegia. That disease of the tegmentum would neces- 
sarily entail sensory disturbances may be taken for granted, although there is as 
yet very little clinical proof of it. 

5. The Cerebellum. 

Quite extensive destruction of the cerebellum may take place without any 
symptoms to indicate it. In such cases, however, the disease is almost invariably 
confined to the hemispheres ; but, if the central portion or vermiform appendix is 
attacked to any great extent, peculiar symptoms almost always result, pointing in 
many instances with considerable certainty to disease of the cerebellum. 

There are two especially characteristic symptoms — a peculiar uncertainty of 
gait (cerebellar ataxia), and troublesome vertigo. 



684 



THE DISEASES OF THE BRAIN. 



Cerebellar ataxia affects only the trunk and lower extremities. Both standing 
and locomotion are interfered with. When the patient is lying in bed, he can 
move his legs almost as well as ever, and with normal vigor; but as soon as he 
gets up, the characteristic motor disturbances become very evident. Even while 
standing still, the whole body can usually be plainly seen to sway back and forth. 
This becomes more marked if the patient brings his heels together. If he stands 
with his legs widely apart, the trouble is less noticeable. Closing the eyes, as a 
rule, does not aggravate the swaying, inasmuch as the cutaneous and muscular 
sensibility of the lower limbs remains normal in uncomplicated cerebellar disease. 
When the patient tries to walk, he sways and totters, precisely as if he were deeply 
intoxicated, but usually in a very different way from that seen in locomotor ataxia. 
Instead of the uniform stamping and pitching gait of the latter, cerebellar ataxia 
causes a real staggering of the whole body, so that in severe cases the patient loses 
entirely the ability to walk straight, bat seems to fall forward, as it were, in a zig- 
zag line, now to the right and now to the left. Sometimes, but by no means inva- 
riably, it is noticed that, in walking, the body sways principally in one particular 
direction, either forward or backward, or to one side. Such peculiarities, however, 
do not enable us, with our present knowledge, to determine with certainty just 
what position in the cerebellum the lesion occupies. The most we can do is to 
surmise, in such a case, that the middle peduncles of the cerebellum {vide infra) 
are involved. It is worthy of note that, with few exceptions, the ataxia does not 
involve the upper extremities. Many a patient who can scarcely walk unaided is 
still able to perform the most delicate manipulations with his hands. This shows 
that it is only in maintaining the bodily equilibrium — essential to standing and 
locomotion — that the function of the cerebellum is important. 

As already stated, this cerebellar ataxia is in most cases attended with pro- 
nounced vertigo. There is not, however, a complete correspondence between the 
locomotor disturbance and the dizziness. Exceptionally one symptom may be 
present without the other. The vertigo is usually felt only when the patient 
stands or moves about, being almost always absent when he lies quietly in bed. 
We are as yet ignorant just how it is produced. Vertigo is quite frequently pro- 
duced by other cerebral diseases. It can not, therefore, be regarded as indicating 
disease of the cerebellum unless it is very persistent and decided, and is associated 
with the characteristic cerebellar gait. 

Little is known about other symptoms of disease in the cerebellum. There 
may be some diagnostic value in persistent occipital headache, particularly if 
other cerebellar symptoms are present. If they do not exist, the headache is too 
ambiguous to be of much value ; and, besides, an affection of the cerebellum may 
exceptionally be attended by pain in the side of the head or in the forehead. Vom- 
iting is of still less value. It is, to be sure, frequently occasioned by chronic 
disorders of the cerebellum, and by tumors in particular, but may be equally well 
the result of disease elsewhere. Tumors of the cerebellum are very apt to cause 
disturbances of vision ; but it is certain that these are not a direct result of the 
cerebellar lesion, but are occasioned by the development of a choked disk (vide 
chapter on cerebral tumors). 

We must add in conclusion a few words about diseases of the middle pedun- 
cles (crura ad pontem). Usually it is an irritation of these which causes those 
peculiar symptoms known as forced movements and forced positions. Thus, in 
such a case, the patient always lies upon one particular side in bed. He may be 
quite conscious or in a state of complete unconsciousness. If he is put in any 
other posture, he at once involuntarily reassumes his former position. Not infre- 
quently this forced position of the trunk is accompanied by a corresponding forced 
position of the head and eyeballs, while the extremities are seldom affected. 



THE LOCALIZATION OF CEREBRAL DISEASES. 685 



Genuine forced movements are seen far less often. They produce either often- 
repeated rotations of the body on its longitudinal axis, or, if the patient is able 
to walk at all, involuntary circular movements (" circus . movements "), etc. It is 
not possible, even by minute analysis of these symptoms, to determine in which of 
the two peduncles the source of irritation exists. In a few very rare cases of brain 
disease these same symptoms have been observed, although no affection of the 
middle peduncles of the cerebellum could afterward be detected. 



For convenient reference we subjoin a summary of the most important facts 
bearing upon the localization of cerebral diseases. 

1. The most frequent cause of ordinary hemiplegia is a lesion of the pyramidal 
tract in the posterior limb of the internal capsule. If the hemiplegia is persistent, 
then this tract is actually destroyed ; if temporary, the tract has been functionally 
deranged for a time by focal disease in neighboring parts of the brain. 

2. Monoplegic cerebral paralysis is usually due to affections of the cortex of 
the brain, that is, the central convolutions and the paracentral lobule. Mono- 
plegia of the face and tongue is the result of lesions in the lower extremity of the 
anterior central convolution. Monoplegia of the arm is referable principally to 
some lesion of the middle third of the anterior central convolution. Monoplegia 
of the lower extremity implies some affection of the paracentral lobule. 

3. Hemiplegia or monoplegia, if associated with epileptiform convulsions affect- 
ing either one half or one particular portion of the body, are almost always 
caused by cortical lesions. These same symptoms of motor irritation without 
accompanying paralysis are likewise ascribable to some irritation of the above- 
mentioned regions of the cortex. 

4. Hemiplegia with crossed paralysis of the oculo-motor nerve indicates a lesion 
of the crura cerebri. 

5. Hemiplegia with crossed facial paralysis implies, with an approach to cer- 
tainty, that the lesion is situated in the pons. 

6. Post-hemiplegic chorea {vide infra) seems to occur especially when there 
is focal disease in the neighborhood of the optic thalamus or of the posterior part 
of the internal capsule. 

7. Hemiansesthesia (of the skin and of the organs of special sense) seems to 
result principally from lesions of the most posterior portion of the internal cap- 
sule. 

8. Hemiopia may be due to a lesion of the occipital lobe. Probably, also, a 
lesion of the posterior extremity of the internal capsule may cause it, in which 
case it is usually associated with hemianaesthesia. Finally, it may be produced 
by affections of the posterior tubercle of the optic thalamus, or of one of the 
anterior corpora quadrigemina, or of one of the optic tracts. 

9. Genuine motor aphasia indicates disease of the third left frontal convolution. 

10. Word deafness seems to be due to disease of the first left temporal convolu- 
tion. 

11. Difficulty in articulation implies disease of the medulla, as does also dys- 
phagia. 

12. Staggering gait and vertigo are the most constant symptoms of cerebellar 
disease. Forced positions and forced movements are seen chiefly in connection 
with lesions of the crura cerebelli ad pontem. 



688 



THE DISEASES OF THE BBAIN. 



CHAPTEE III. 
CEREBRAL HEMORRHAGE. 

JEtiology. — The cause of cerebral haemorrhage should always be sought in 
some disease of the coats of the minute cerebral arteries. In 1868 it was first 
shown by Charcot and Bouchard that in almost every case of cerebral haemor- 
rhage there are miliary aneurisms of the small arteries of the brain-substance, 
some one of which has burst and allowed the blood to escape. All later investi- 
gators have confirmed their statements about the occurrence and importance of 
these miliary aneurisms. The aneurisms may attain a diameter of a millimetre 
or more. They usually appear like spindle-shaped dilatations of the entire cir- 
cumference of the vessel, although sometimes the bulging is confined to one side 
of it. So far as has yet been learned, the process of development starts with dis- 
ease of the intima. This layer presents at first proliferations and also a fatty 
degeneration of the endothelium. Later on, however, the intima atrophies, just 
as the muscular coat does. Inasmuch as the intra- cerebral arteries possess almost 
no true adventitia, it is easy to see that these vessels are especially predisposed to 
aneurismal dilatation. It has been affirmed that the disease of the vascular wall, 
which leads to the formation of these aneurisms, is identical with ordinary arterio- 
sclerosis (vide page 308) or atheroma. Charcot denies it ; but the later investiga- 
tions of Eichler make it seem very probable. Indeed, we very often, although not 
invariably, find that cerebral haemorrhage attacks persons who present either a 
general arterio-sclerosis or a more limited atheromatous disease of the cerebral 
arteries ; and most of the factors which are said to promote cerebral haemorrhage 
are the same as favor the development of arterio-sclerosis. 

It has long been recognized that age has an important bearing on these cases. 
Although exceptionally a younger individual may be attacked, the majority of 
sufferers are over fifty years old — that is, at the time of life when arterio-sclerosis 
usually becomes most fully developed. Again, cerebral haemorrhage is decidedly 
more frequent in men than in women, which is also true of atheroma. Alco- 
holism, syphilis, and gout are also reckoned among the aetiological factors of both 
disorders ; and in both a hereditary predisposition is not very rarely demonstra- 
ble. What is called the " apoplectic habit " also deserves brief mention. Although 
there is no variety of constitution which exempts its possessor from the possibility 
of cerebral haemorrhage, yet it can not be denied that often the victims of apo- 
plexy do exhibit a certain " habit." Such persons are not very tall, but are corpu- 
lent, broad-chested, with a short, thick neck and round face. They have not been 
disinclined to the pleasures of the table and the bottle, and sometimes they suffer 
from emphysema, moderate hypertrophy of the heart, and general arterio-sclero- 
sis, as the condition of the radial and temporal arteries may disclose even during 
life. 

Granting, therefore, that disease of the arteries, and more particularly miliary 
aneurisms resulting from chronic endarteritis of the smaller cerebral arteries, 
must be regarded as the chief cause of cerebral haemorrhage ; then, on the other 
hand, the question suggests itself whether an abnormal elevation of the blood- 
pressure may not have some part in determining the haemorrhage. If the coats 
of the arteries are normal, surely they would not be torn, no matter how great the 
arterial tension became ; but if aneurisms have already been developed, then 
there can be no doubt that a persistent or even a temporary elevation of the blood- 
pressure must favor the bursting of the vessels. In this sense a cerebral haemor- 
rhage, occurring in patients with certain forms of cardiac hypertrophy (contracted 



CEREBRAL HAEMORRHAGE. 



687 



kidney, idiopathic hypertrophy, etc.), combined with disease of the vessels, may be 
referred in part to the increased arterial tension ; but it is most of all with regard 
to many exciting causes, which are immediately followed by a cerebral haemor- 
rhage, that increased blood-pressure assumes great importance. Here it is tem- 
porary. Cerebral haemorrhage may, for example, follow excessive muscular 
exertion, the ingestion of a large amount of food, indulgence in alcohol, taking a 
cold bath, or violent mental excitement. In all such cases, however, the change 
in the arteries is a necessary prerequisite. 

It should be mentioned, in conclusion, that quite considerable haemorrhage 
may also take place in the course of such general diseases as are associated with 
impaired nutrition and a consequent diminution in the resisting power of the 
vascular walls. Cerebral haemorrhage under these circumstances is merely symp- 
tomatic of a general haemorrhagic diathesis, as we find it in leukaemia, pernicious 
anaemia, and those affections which are called, in a stricter sense, haemorrhagic 
diseases, such as scurvy and purpura haemorrhagica. The grave infectious dis- 
eases, including septicaemia, typhus or typhoid fever, and variola, may occasion 
haemorrhage into the brain as well as into other organs. The haemorrhages are 
generally, however, from capillary vessels, and are very rarely extensive. 

Pathology. — The miliary aneurisms do not develop in all the cerebral arteries 
with equal frequency, and accordingly we find certain regions particularly liable 
to cerebral haemorrhage, being very much oftener affected by it than others. It is 
the large central ganglia in the neighborhood of the lateral ventricles that suffer 
most frequently — namely, the optic thalamus, caudate and lenticular nuclei, and 
also the adjacent white matter of the internal capsule and centrum ovale. Haem- 
orrhages in other portions of the brain are much less frequent — such as haemor- 
rhages into the convolutions, the pons, the cerebellum, the crura cerebri, or the 
medulla. If the blood escapes into the neighborhood of a ventricle, it may burst 
into the latter. Likewise, in rare instances, an effusion of blood near the cortex 
may make its way out upon the surface of the brain. 

An extensive collection of blood in one of the hemispheres may exercise so 
decided a pressure upon surrounding parts that the results of increased tension 
upon the affected side are at once recognized when the skull is opened. The dura 
on that side is more tightly stretched, the falx is crowded over to the opposite 
side, the convolutions on the convexity seem flattened, and the furrows are shal- 
low. Exceptionally, when there is a very large effusion reaching nearly to the 
surface, we may even detect fluctuation. 

On cutting through the brain-substance we find the seat of haemorrhage, and are 
enabled to determine its position and extent. Its size, of course, varies considerably 
in different cases ; it may be small, or it may occupy a large part of an entire 
hemisphere. The wall of the effused mass is made up of ragged and torn cerebral 
tissue, and the mass itself contains debris of the nervous elements entangled in 
the coagulated blood. The blood-clots are almost always very dark-colored when 
fresh. Later on, the mass changes to a chocolate-colored or more brownish-yellow 
pulp, composed of the disintegrated remnants of the nervous substance and the 
clotted blood. The microscope reveals, particularly in the immediately sur- 
rounding tissues, numerous fatty granular cells. These are white blood-cor- 
puscles which have absorbed the fat resulting from the decomposition of the 
myeline substance. There is also always an abundance of haematoidine crystals, 
due to the disintegration of the red blood-globules. At a greater distance from 
the effusion the tissues present a yellowish tinge, from the imbibition of such blood- 
pigment as has reached them in a state of solution ; and there is also usually an 
cedematous softening of the parts not too far removed from the haemorrhagic focus. 

If the patient survives, the mass is gradually absorbed. It slowly diminishes 



688 



THE DISEASES OF THE BRAIN. 



in size, and the surrounding parts tend to reassume their normal relations. The 
final result in many cases is a cavity filled with serous fluid and bounded by 
smooth walls. This "apoplectic cyst" remains stationary. In some instances, 
however, and particularly if the effusion is rather small, the walls approach each 
other, as more and more of the fluid is absorbed ; there is a great hyperplasia of 
connective tissue ; and so, finally, there is nothing left but a so-called apoplectic 
scar, usually of a yellow color, due to vestiges of the blood-pigment. The position 
and dimensions of the permanent lesion determine, of course, the question of 
secondary descending degeneration (vide page 641), as well as the nature and 
extent of the persistent clinical symptoms. 

Clinical History. — The symptoms of cerebral haemorrhage agree closely with 
the anatomical lesions just described. The miliary aneurisms themselves, even 
when numerous, seldom excite any symptoms. Sometimes, however, it is possible 
that the slight circulatory disturbances they occasion produce the mild headache 
and similar annoyances which often precede, for a longer or shorter time, the 
occurrence of cerebral haemorrhage. 

As soon as an aneurism bursts, however, and blood escapes into any part of 
the brain-substance, there is immediately seen a group of grave cerebral symp- 
toms, collectively termed an apoplectic attack, or ""shock." As the blood escapes 
under a pressure nearly equal to the general arterial pressure, and doubtless 
much greater than that to which the soft substance of the brain is normally 
exposed, the affected portion of the brain is at once subjected to a considerable 
increase of tension, which is transmitted for various distances in all directions. 
It need not be said that the destructive influence of the haemorrhage may vary 
exceedingly, and that therefore the symptoms are by no means equally severe in 
all cases. The larger the rent in the blood-vessel, and the more rapid and abun- 
dant the consequent haemorrhage, the worse is the apoplectic attack. Bleeding 
from larger vessels is, therefore, usually attended by graver symptoms than from 
the minute arterial twigs. An extensive cerebral haemorrhage sometimes causes 
the patient to fall down suddenly in complete unconsciousness, while smaller 
haemorrhages may occasion only a temporary attack of vertigo and slight cloudi- 
ness of intellect. If the tear in the wall of the artery is very small and narrow, 
permitting the blood to escape but slowly, then there may be no sudden attack at 
all, the phenomena requiring a certain length of time for their development. 

There is also an important relation between the location of the haemorrhage 
and the severity of the apoplectic attack. The chief symptom of these cases is loss 
of consciousness (about which we shall soon speak at length) ; and, as this cer- 
tainly is due to an interruption of the functional activity of the cerebral cortex, 
it is plain (1) that the nearer the cortex is to the haemorrhagic focus, the more apt 
are the symptoms to be serious. It is confirmatory of this that haemorrhage into 
the more deeply situated portions of the brain, like the crura cerebri or the pons, 
quite often occasions comparatively slight symptoms. But (2) there is a fact about 
the circulation in the brain that often causes the shock from haemorrhage into the 
brain-stem to be greater than the shock following haemorrhage into the cortex or 
the white substance of the hemispheres. The explanation is that the brain-stem 
has comparatively much larger arteries than the other parts just mentioned, which 
contain only minute blood-vessels. Furthermore, as Buret and Heubner have 
shown, the blood-vessels are so distributed that the arterial tension in the brain- 
stem is not a little higher than in the other portions. This renders intelligible the 
clinical phenomenon that haemorrhages in the territory of the main arteries, beside 
being, as we have said, the most frequent of any, produce apoplectic symptoms 
even when the effusion is comparatively small ; while sometimes haemorrhages of 
about the same size in the cortex or white substance may not be noticed. 



CEREBEAL HEMORRHAGE. 



689 



The clinical phenomena of the apoplectic attack will now be considered in 
detail. The onset is sometimes absolutely without warning, but in other cases it 
is preceded for a greater or less length of time by certain prodromata. These are 
either the result of the disturbance of circulation caused by the disease of the 
blood-vessels in the brain, and then, as already stated, they comprise occasional 
headache, vertigo, tinnitus aurium, spots before the eyes, languor, and muscular 
weakness ; or they are caused by minute haemorrhages, which seem not infre- 
quently to precede a greater one. In such a case, the friends relate that of late 
the patient has had one or more slight and brief attacks, characterized by faint- 
ness, temporary trouble in speaking, sudden but temporary weakness of an arm 
or leg, and similar symptoms. The prodromata may extend over several days 
or even weeks and months preceding the severe attack. 

In other cases there are no such premonitory symptoms. The apoplexy occurs 
unexpectedly and suddenly. In the midst of apparently vigorous health the 
patient sinks down, "as if he had been struck." In still other cases there are 
indeed no prodromata, but the symptoms do not at first appear in all their severity, 
and occupy some hours or even a whole day in their gradual development. This 
is due to a slow and gradually increasing haemorrhage, and is termed a slow or 
delayed apoplectic attack. The patient grows confused, anxious, and delirious (a 
case of our own had pronounced hallucinations of sight) ; the arm and leg on one 
side become paretic, and gradually more and more completely paralyzed ; and 
after a few hours complete unconsciousness comes on. 

The attack may be rapidly fatal. In such cases the abnormal pressure prob- 
ably involves the medulla oblongata and paralyzes the cardiac and respiratory 
centers there situated. Usually, however, there is merely a complete loss of con- 
sciousness, more or less rapidly developed. Sometimes the patient has time to 
lie down. He usually sinks back in his chair or falls to the floor, and becomes 
deeply comatose. The face is often noticeably flushed, and the pulse full and 
tense, but not infrequently somewhat slow, because of the increased cerebral 
pressure. The respirations are deep, noisy, stertorous, and likewise often slow. 
The relaxed cheeks and lips are often drawn deeply in at every inspiration, and 
puffed out at every expiration. The temperature is usually subnormal at first, 
later regaining the normal, or even a higher point. In a rapidly fatal case, how- 
ever, the temperature remains depressed till death. It is not very rare in severe 
cases to observe a peculiar position of the head and eyeballs — they being all turned 
in one direction. This phenomenon is termed by Prevost conjugate deviation 
{deviation conjuguee) of the eyes and head. It is generally temporary, and is 
said by Landouzy to be connected principally with a lesion of the lower temporal 
lobe. There is no perfectly constant relation between the lateral deviation and 
the half of the brain affected. Apparently in most cases the eyes are directed 
toward the injured side, and so to a certain extent 14 look toward the lesion " and 
away from the paralyzed side of the body (vide infra). The pupils present no 
constant peculiarities. Often they are of normal size. In other cases they are 
contracted, dilated, or unequal. No definite diagnostic conclusions can be drawn 
from them. In the worst cases the pupils will not react to light ; in other cases 
they react, but often sluggishly. 

During the deep apoplectic coma the extremities generally lie completely 
motionless and limp. In the worst cases reflex action is wholly suspended ; but 
sometimes the vigorous thrust of a pin or the pinching of the skin will excite 
an occasional slow reflex twitch, or a motion as if to ward off the tormentor. 
Whether the apoplexy has caused hemiplegia at all, and if so on what side, can 
not always be easily determined during the initial coma. Still, it is often to be 
observed, even now, that one angle of the mouth hangs down lower than the 
44 



690 



THE DISEASES OF THE BEAIN. 



other, and that the corresponding cheek is more puffed out during- expiration 
than is the other ; that the extremities of one side are even more completely 
relaxed and limp than those on the opposite side of the body, and that the reflex 
action and defensive movements are almost absent upon one side (the paralyzed 
side), while they can be clearly demonstrated on the other. 

In contrast to the usual laxness of the arms and legs during the apoplectic 
coma, is the tonic rigidity sometimes seen in the extremities, particularly on the 
side opposite to the haemorrhage. This symptom seems to be especially, although 
not exclusively, connected with a bursting of the escaping blood into a lateral 
ventricle. It is rather exceptional for cerebral haemorrhage to be attended with 
general or unilateral epileptiform convulsions, a symptom which, as we have 
seen, is referable to irritation of the motor regions of the cortex. 

It should be mentioned that in many cases of cerebral haemorrhage the urine 
passed after the attack has been found to contain small amounts of albumen or 
sugar. This symptom is usually ascribed to compression of the medulla from the 
effusion. There is usually retention of urine ; in other cases there is involuntary 
micturition. 

A certain number of patients never awake from the initial coma. Death may 
not be immediate, but they remain completely unconscious ; the respirations 
become more rapid and irregular (sometimes of the Cheyne-Stokes character); 
and there is a rattling in the throat, because mucus aud saliva run down into it ; 
the pulse, which was at first retarded, now becomes accelerated ; the face grows 
paler and more and more sunken ; the eyes are deep in their sockets ; the cornea 
becomes opaque ; and at last, after the coma has lasted some hours, or even 
one or two days, death occurs, often attended by a considerable rise of tempera- 
ture. 

This termination is, however, by no means the usual one. More frequently 
the patient survives the attack. The bleeding ceases, the clot contracts, and 
begins to be disintegrated and absorbed. At the same time the pressure exerted 
upon surrounding parts grows less and less, the more distant parts of the brain 
gradually recover from the shock, and consciousness slowly returns. The patient 
begins to open his eyes when he is spoken to in a loud tone ; he raises his hand to 
his head, sighs, and yawns ; gradually the intellect clears up, he tries to talk, or 
to express himself by signs ; memory returns, and he recognizes those about him 
once more. Exceptionally, recovery is interrupted by a fresh and perhaps a 
fatal relapse. This may result from a renewal of the haemorrhage. Generally, 
however, improvement persists, the patient fully regains his consciousness at the 
end of a few days, and it now becomes possible for the first time to "estimate 
the damages." 

The symptoms thus far described belong to severe apoplectic attacks. There 
are also, as we have said, cases of all degrees of mildness, as regards the first onset. 
In these there is no deep and persistent coma. The patient loses consciousness 
only temporarily, if at all. He is seized with vertigo, or with sudden headache, 
and is for a time stupefied. Nausea and vomiting are of quite frequent occurrence, 
just as in ordinary syncope. Yet cases presenting these comparatively slight 
early symptoms, and with few even of these, may exhibit the genuine focal 
symptoms referable to the haemorrhage, such as hemiplegia, in all their severity. 
These latter phenomena must now be considered. 

Among the symptoms of impairment of function resulting from cerebral 
haemorrhage, only those are to be regarded as direct focal symptoms which are 
caused by the actual destruction of a regiou of the brain. Where the haemorrhage 
takes place, we have seen that a larger or smaller extent of the brain-substance is 
completely destroyed by the sudden and forcible escape of the blood. The dimen- 



CEREBRAL HEMORRHAGE. 



691 



sions of this lesion are represented later by the apoplectic scar or cyst, and its 
position by the nature and extent of the persistent, and for the most part irrepar- 
able, loss of function (Ausfallserscheinungeri). But there are, in addition to these 
direct symptoms, other indirect focal symptoms, which outlast the apoplectic shock, 
and vary with the locality of the haemorrhage. These do not, however, correspond 
to the territory actually destroyed. They are due to the influence exerted for a 
certain length of time by the haemorrhagic focus upon the immediately surround- 
ing structures. The pressure of the effusion, the disturbance of circulation 
resulting from it, the collateral oedema, and perhaps also the imbibition of the 
soluble products of disintegration, are the chief factors in exciting these indirect 
symptoms. They do, indeed, outlast the initial shock, but are, nevertheless, 
temporary, vanishing sooner or later, at the end of several days or weeks, or even 
months. 

Even if the character of the initial attack and the symptoms still exhibited 
have been minutely determined, yet we are unable to say, at first, whether the 
existing focal symptoms are direct or indirect. We can decide about this only 
after further observation. If the early symptoms disappear within the next few 
days or weeks, or after the first two or three months, we can then affirm, retro- 
spectively, that they were indirect. Such as outlast the first six months are to 
be regarded as direct, and not destined to improve much. From a practical 
point of view, this distinction is of extreme importance. We shall revert to the 
subject when considering the course of cerebral apoplexy. 

A minute description of all the focal symptoms which might occur after cere- 
bral haemorrhage, and of the light thus thrown upon the location of the haemor- 
rhage, need not be attempted here, for it would necessitate a repetition of all the 
facts enumerated in the preceding chapter. It is only requisite to describe, in 
detail, the chief and by far the most frequent result of a cerebral haemorrhage — 
ordinary cerebral hemiplegia. 

It has been mentioned that most of these haemorrhages occur near the lateral 
ventricles. Hence, in a majority of instances, the motor pyramidal tract, as it 
traverses the internal capsule, is either directly destroyed, or at least indirectly 
affected. Consequently, most patients who survive the apoplectic shock present 
a paralysis of that half of the body which is opposite the seat of haemorrhage. 
On minute examination we usually find, in the first place, that even in the 
distribution of the facial nerves there is a distinct difference between the two 
sides, the lower division of the facial (which supplies the muscles of the cheek, 
nose, and mouth) being evidently paralyzed on one side, while its upper division 
(going to the eyes and forehead) is entirely, or almost entirely, intact. The fore- 
head can be wrinkled on one side as well as on the other ; but, if the patient tries 
to turn up his nose, or alter the shape of his mouth, the paralysis becomes evident. 
Often, indeed, while the face is quiet, it can be noticed that one naso-labial fold 
is obliterated, or that one corner of the mouth hangs down. It is an interesting 
fact that the paresis of the lower division of the facial is much more noticeable 
during voluntary efforts, as in showing the teeth, than when the patient smiles 
involuntarily. A patient will sometimes try in vain to draw back the corner of 
his mouth, then begin to laugh at his own awkwardness, and thereupon open 
his mouth in an almost perfectly normal manner. Why there is such a difference 
between the upper and lower divisions of the facial nerve in cerebral hemiplegia 
is not certainly known. Possibly it has some connection with the fact that the 
muscles supplied by the upper division (frontalis, corrugator supercilii, and to a 
certain extent the orbicularis) are very seldom exercised upon one side alone, but 
always bilaterally. Perhaps both sides receive nervous fibers from each cerebral 
hemisphere, so that, if a single center is intact, it alone answers for the muscles on 



692 



THE DISEASES OF THE BRAIN. 



both sides.* Sometimes, however, careful examination shows a slight paresis of 
the frontalis muscle on the paralyzed side. In the distribution of the lower divis- 
ion of the facial, also, ordinary cases of cerebral hemiplegia present almost always 
a more or less marked paresis, and only exceptionally a complete paralysis. 

There is quite often a slight impairment of the hypoglossus in addition to the 
paresis of the facial nerve. If the patient puts out his tongue, its tip deviates 
toward the paralyzed side. This is a result of paresis of one of the genio-hyo- 
glossi. When both these muscles contract, they may be said to push the tongue 
forward. If this thrust is more vigorous on one (the healthy) side, the tongue is 
deflected toward the other (abnormal) side. In ordinary cerebral hemiplegia this 
is almost always the sole way in which the movements of the tongue can be seen 
to be impaired. Sometimes, however, the slight paresis of half of the tongue, 
combined with the facial paresis, entails a noticeable difficulty in articulation. 
This, to be sure, is not great, and is often appreciated by the patient alone, who is 
conscious that an effort is required in order to speak. 

The soft palate is rarely much affected. It may, however, hang rather lower 
down on the paralyzed than on the unaffected side, and move less. The uvula is 
inclined sometimes toward the healthy and sometimes toward the paralyzed side. 
There are no special disturbances of function as a result of these changes. 

The trapezius is the only muscle of the trunk which is ordinarily much 
affected in cerebral hemiplegia. As a result of the paresis of this muscle, the 
shoulder sags and can not be raised as high as on the normal side. If the patient 
tries to take a very deep breath, it is in some cases possible to see that the para- 
lyzed side lags behind a little in respiration, which is undoubtedly due to a pare- 
sis of the respiratory muscles on that side. It is perhaps due to this that the 
pulmonary diseases which attack hemiplegic patients frequently develop in the 
lung on the affected side, where respiration is deficient. 

The most important element in the hemiplegia is the paralysis of the extremi- 
ties. Immediately after the haemorrhage, it is often so complete that even the 
slightest voluntary motion in the affected arm and leg is impossible. Other cases, 
however, exhibit only a more or less severe paresis (hemiparesis) from the first ; 
or the complete paralysis at any rate is confined to certain groups of muscles, the 
others still retaining vestiges of their normal contractility. Even when there is 
total hemiplegia at first, some of the muscles usually regain a certain amount of 
their old power later on (vide infra). 

The behavior of the reflexes is comparatively constant in nearly all cases. 
Almost invariably there is increased tendon reflex on the paralyzed side. If, 
however, the initial shock is very severe, there may at first be no tendon reflex 
whatever. In all cases of any duration it is always exaggerated, and often very 
much so. A tap upon the tendons and bones (periosteal reflex) of the arm, as 
well as of the leg, excites the most vigorous and manifold contractions. Very 
often a persistent ankle clonus can be obtained. It is noteworthy that even on 
the normal side, particularly in the lower extremity, it is almost always possible 
to demonstrate an exaggeration of the tendon reflex, although less pronounced 
than on the paralyzed side. Many have expressed the opinion that the increased 
tendon reflex upon the paralyzed side is a result of the secondary degeneration of 
the pyramidal tracts in the spinal cord. In our judgment, this view is entirely 



* There is a remarkable general rule which should he mentioned here, and which is, perhaps, to be 
explained in the same way, namely, that those muscles which are usually called into play in pairs are 
never completely paralyzed in cerebral hemiplegia. Furthermore, it is impossible for us to contract 
most of these singly, on one side alone, or at least not without special practice ; this applies, for 
instance, to the corrugator supercilii, the frontalis, the motores oculi, and the muscles of mastication 
and respiration. 



CEKEBRAL HEMORRHAGE. 



693 



unfounded, inasmuch as the exaggeration of the tendon reflex often appears 
within a few days, or even hours, after the apoplectic attack — that is, before a 
secondary degeneration in the spinal cord is to be thought of. We would rather 
seek to explain the phenomenon as being due to the suspension of certain reflex- 
inhibitory influences because of the cerebral lesion. 

There is very often found, particularly in cases of long standing, affected with 
well-marked contractions, an increase of " direct mechanical excitability " in the 
paralyzed muscles, such that a tap upon them causes them to contract vigorously. 
We are, however, of opinion that, in part at least, this is also a reflex symptom, 
to be referred to the mechanical irritation of the fascia of the muscles (fascial 
reflex). 

The skin reflexes in hemiplegia behave in precisely the opposite way from the 
tendon reflexes, being almost invariably decidedly diminished on the paralyzed 
side. In the paralyzed arm it is usually impossible to excite any skin reflex what- 
ever ; and in the corresponding leg there is either none, or at any rate a greatly 
diminished, reflex. The difference is seen especially well in the abdominal and 
cremaster reflexes (vide page 512) ; on the paralyzed side they are almost or quite 
absent, while they remain normal upon the opposite side. This contrast often is 
of service in determining the location of the hemiplegia when the patient is in a 
stupor or coma. 

Sensation is but little impaired in most cases of cerebral hemiplegia. It is 
usually possible, in a hemiplegia occasioned by this particular lesion (cerebral 
haemorrhage), to find at first, by careful testing, a slight blunting of cutaneous 
sensibility ; but this is seldom very great, and later on frequently becomes even 
slighter than at first. Slight paraesthesia is not infrequently complained of on 
the affected side, especially at first. Any marked disturbance of sensation indi- 
cates, as has been seen (compare page 682), that the posterior extremity of the 
internal capsule is involved. Such cases are rare. In them we may observe a 
complete cerebral hemiansesthesia combined with the hemiplegia. According to 
Gowers, a temporary hemiopia is often present directly after the occurrence of a 
cerebral haemorrhage. Nor is it very exceptional to find a persistent hemiopia 
associated with hemiplegia; but as yet little is known about the pathological 
anatomy of such cases. The most likely thing would seem to be some lesion of 
the fibers of the optic nerve in the internal capsule or in the posterior tubercle of 
the optic thalamus. The muscular sense is not usually affected in hemiplegia. 
Lately it has been affirmed that paralysis of cortical origin invariably causes 
anomalies in the muscular sensibility of the parts which are paralyzed ; but the 
statement lacks confirmation. Our own observations would certainly lead us to 
doubt whether it is universally true. 

Turning now to the further course of hemiplegia, we find a new group of 
important symptoms. First of all should be considered the changes in the para- 
lyzed muscles. If the hemiplegia is incomplete, even from the start, almost the 
normal degree of motility may, in a comparatively brief period, be regained by 
the affected side. At most there will persist a certain slight amount of weakness 
and stiffness ; and even these will gradually diminish. From what has been 
already said, it is evident that in these cases the initial paresis is an indirect focal 
symptom, and accordingly vanishes as soon as the effusion ceases to affect the 
tissues not immediately involved. 

But even where there is a complete hemiplegia it is exceptional for this condi- 
tion to remain unabated throughout the entire region affected. After a few weeks, 
or even a few days, one part and another of the paralyzed half of the body begin 
to recover their former motility. The improvement goes on slowly, and in the 
most favorable cases the paralysis may for the most part have vanished at the end 



694 



THE DISEASES OF THE BKAIN. 



of some months. Usually, however, the improvement never becomes more than 
partial. It is noteworthy that the lower extremity almost always improves more 
than does the upper. Many patients gradually become able to walk alone once 
more, perhaps with the aid of a cane, although the arm remains almost useless. 
It must be confessed that the gait is seldom perfectly natural. The patient takes 
short steps, drags the affected limb more or less, and in many cases does not move 
it straight forward, but with an outward sweep. In the arm, the chief improve- 
ment is usually in the fingers and the elbow-joint, the movements of the shoulder- 
joint recovering least. 

The explanation of this improvement during the first few months is not fully 
ascertained. Probably it is largely true that only the persistent paralytic symp- 
toms are direct focal symptoms, while the temporary motor disturbances are only 
an indirect result of the haemorrhagic focus, and vanish when once the pressure, 
oedema, etc., have ceased. It is, however, not absolutely impossible that gradu- 
ally new tracts (perhaps originating in the sound hemisphere *) assume vicari- 
ously some of the functions which are at first arrested. That fibers which have 
been destroyed are ever actually regenerated is very improbable ; and, as has been 
mentioned already, there is not much improvement after the first six months. 

The permanently paralyzed muscles become very often contracted later on. 
The appearances produced exhibit considerable uniformity. The arm, which suf- 
fers more from paralysis than the leg, is also usually more contracted. The 
fingers are almost invariably flexed ; the forearm contracted in a position of 
pronation, and usually flexed rather than extended ; and the upper arm adducted 
(the pectoralis major being chiefly affected). These contractures correspond to 
the natural positions which the paralyzed arm almost always assumes, if left to 
itself. This, taken alone, is a reason for ascribing the contractures chiefly to the 
fact that the arm moves less than normal, and that, as a necessary sequel, certain 
muscles become permanently shortened. This view would make the changes " pas- 
sive contractures." Another argument in its favor is that the deformity can to a 
certain extent be prevented by the persistent use of passive motion, which renders 
any permanent shortening of the muscle impossible. Nevertheless, Charcot and 
his pupils, including Bouchard, hold an entirely different opinion — namely, that 
the contractures are due to the secondary degeneration of the pyramidal tract. 
In defense of their position no fact can be adduced, save that fatal cases exhibit- 
ing hemiplegic contractures do invariably present the secondary degeneration 
mentioned ; but of course this is no proof that the two things have any causa- 
tive relation to each other. A contracture occurs only in connection with persist- 
ent paralysis ; a persistent paralysis never is seen unless the pyramidal tract is 
destroyed; and if it is destroyed, a secondary degeneration must result. The 
contractures and the secondary degeneration are therefore two sequelae, inde- 
pendent of each other. And that the degeneration should " irritate " the fibers, 
and thus excite muscular contractions, is extremely improbable ; for, according to 
all analogy, fibers which are undergoing degeneration can not be stimulated, and 
can not therefore transmit any sort of stimulus to the paralyzed muscles. 

If the contractures become marked in the lower limb, they may involve either 
the extensors or flexors. In the leg a moderate contracture of the calf is the most 



* As has been already stated (page 691 ), it seems proper to assume that certain musqles enjoy a double 
innervation — that is, from each hemisphere. This applies particularly to such muscles as usually are 
exercised in pairs. We might perhaps in this way explain why the lower extremity is capable of 
more improvement after hemiplegia than is the arm. The legs have to be used simultaneously or con- 
sentaneously, as in walking, much more than the two arms. Another fact deserves brief mention ; on 
careful examination, it is sometimes possible to make out a slight paresis in the sound side, which may 
perhaps be referable to lesion of the direct motor fibers (Pitres). 



CEREBKAL HEMORRHAGE. 



695 



frequent condition. Hitzig has called attention to a remarkable fact, which is 
that often the contractures are very slight in the morning, when the patient first 
wakes up, becoming aggravated after he has moved about a little. Hitzig refers 
this phenomenon (which has not yet been at all satisfactorily studied) to abnor- 
mal " associated movements " of the paralyzed muscles. Such associated move- 
ments do occur : movements of the sound side excite associated movements in the 
opposite members; and efforts to move the paralyzed parts excite in their turn 
associated contractions of the normal muscles. Sometimes also involuntary 
movements of the lower limb on the paralyzed side are observed when the patient 
exerts himself to move his corresponding arm all he possibly can. 

Another peculiar phenomenon must be mentioned here. It is what Weir 
Mitchell has termed post-hemiplegic chorea. Some time after the paralysis begins 
the parts affected by it exhibit involuntary movements, reminding one of chorea 
or athetosis {vide page 509). Sometimes these movements are continuous, some- 
times they occur only as associated movements in connection with voluntary 
motions of the paralyzed, or even of the sound, side. Hemiplegia due to cerebral 
haemorrhage very seldom exhibits this phenomenon. It is said to occur chiefly in 
focal disease of the posterior extremity of the internal capsule, and of the optic 
thalamus {vide infra chapter on encephalitis). 

It is interesting to observe the trophic and vaso-motor changes in the paralyzed 
parts. At first the skin may be somewhat redder and warmer on the paralyzed 
than on the sound side. Nothnagel has shown that, even in the distribution of 
the cervical sympathetic, symptoms of vaso-motor paralysis occur. They are 
partly temporary and partly persistent, and comprise increase of temperature and 
color in the paralyzed side of the face, swelling of the eyelids, and contraction of 
the pupil; but they are usually slight. We very frequently find, especially on 
the back of the hands, more or less puffiness, which is likewise usually regarded 
as of vaso-motor origin. It should, however, be considered that the natural move- 
ments of any part of the body greatly promote the nervous and lymphatic circu- 
lation, and that the quietude of paralysis may therefore have much to do with 
the oedema. In hemiplegia of some duration the extremities upon the paralyzed 
side are always cooler than normal, and the hand in particular is very often 
deeply cyanotic. The skin sometimes becomes harsh and fissured, and often is 
thickened. The internal surface of the hand, in case of contracture, is frequently 
quite damp with perspiration. 

Among the specific trophic symptoms of hemiplegia, Charcot includes " acute 
malignant decubitus." This sometimes develops with extreme rapidity within a 
few days after the shock, and usually occupies the buttock on the affected side. 
There appears a circumscribed redness with the formation of vesicles, which is 
soon succeeded by a deep-reaching necrosis of the soft parts. We have ourselves 
never met with this in a case which has been properly nursed, and can not, there- 
fore, help thinking that its development is not wholly due to trophic disturbance, 
but to pressure and to the penetration of septic matter below the skin. Of course, 
patients long confined to bed with hemiplegia are as liable to bed-sores as are 
any others similarly situated. 

The permanently paralyzed muscles gradually atrophy somewhat in the course 
of years; yet, in uncomplicated cases of cerebral hemiplegia, this atrophy is 
never of the degenerative sort, nor is it usually very great. The paralyzed mus- 
cles, therefore, continue to react perfectly to faradism (see page 522). The joints 
of the paralytic extremities, and in particular the knee and shoulder, may excep- 
tionally become inflamed. The arthritis is sometimes acute, and sometimes more 
of a chronic variety. Its cause is not evident. Charcot thinks that it is probably 
a neurotrophic symptom, and he is of the same mind with regard to the rarely 



696 



THE DISEASES OF THE BEAIN. 



seen swellings of the peripheral nerve-trunks of the paralyzed side (" hypertrophic 
neuritis "). 

Mental symptoms are rare, except the initial loss of consciousness. There is 
sometimes, however, a persistent general uneasiness of mind, accompanied by 
great excitability and wakefulness. In a large number of cases of persistent hemi- 
plegia there finally come on, in the course of years, constantly increasing indica- 
tions of mental weakness. The patient grows dull and forgetful. Very often he 
exhibits a peculiar tendency to weeping, bursting into tears at the slightest provo- 
cation. But frequently he is subject to quick alternations of feeling, weeping and 
laughing in the same minute. 

The general nutrition is often good for a long while. Sometimes there is even 
a decided tendency to corpulence. In other cases, and especially in the bedridden, 
marasmus gradually comes on, and hastens the fatal termination, particularly if 
there be some intercurrent trouble, like a bed-sore or bronchitis. 

We have detailed the peculiarities of hemiplegia somewhat minutely, because 
the statements will apply to all cases of cerebral hemiplegia, no matter in what 
place the pyramidal tract is interrupted, or by what sort of a lesion. It is needless 
to enter into the diverse symptoms which are caused by diversity in the exact loca- 
tion of the haemorrhage. The hemiplegia itself is the same, whether the effusion 
be in the cortex, internal capsule, cms cerebri, or pons. It is easy to infer from 
the preceding chapter what the accessory symptoms are which would enable us 
to localize the trouble. We need here mention only the frequent combination of 
right hemiplegia and aphasia. This occurs when there is a large effusion in the 
left hemisphere, extending from the internal capsule to the neighborhood of the 
third frontal, or possibly the uppermost temporal (compare page 680) convolution. 

Diagnosis. — The diagnosis of cerebral haemorrhage rests on the sudden onset of 
the apoplectic symptoms, and on the later symptoms (if there be any) of impair- 
ment of the cerebral f mictions. The diagnosis can scarcely ever be made with 
absolute certainty, for cerebral embolism may exhibit almost identical phenomena ; 
the differential diagnosis between the two will be given in the following chapter. 
Occasionally there may be danger of mistaking other cerebral affections for a 
haemorrhage, like meningitis and tumors. The same may be said of a suddenly 
developed uraemia, and of constitutional sepsis. In these cases the rapid onset of 
grave cerebral symptoms of a general nature, such as unconsciousness, simulates 
the apoplectic coma. 

Prognosis. — The first question is, whether the patient will survive the initial 
shock. The answer depends upon the severity of the early symptoms. The deeper 
and more persistent the unconsciousness, the more deficient the respiration and 
pulse, the less the prospect of recovery ; but we can never decide absolutely. If 
the patient has withstood the first onset, and is hemiplegic, then the possibility of 
improvement hinges on the question whether the paralysis is a direct or an indi- 
rect focal symptom. Inasmuch as there are no means of knowing about this at first, 
we must speak very guardedly. It should never be forgotten that the haemorrhage 
may recur. The predisposing disease of the blood-vessels renders individuals who 
have had one stroke liable to be visited, sooner or later, by another. 

Treatment. — The treatment of the apoplectic shock demands, first of all, rest 
in bed, with the head and shoulders elevated. To avoid bed-sores, it is very 
important to maintain cleanliness, and to watch attentively that portion of the 
skin which is pressed against the bed by the weight of the body. An ice-bag 
should be put upon the head, and particularly over that side on which the haemor- 
rhage is supposed to be. Bleeding was formerly universally practiced, but of late 
its usefulness is doubted. It is not indicated unless the deep congestion of the 
face, the violent pulsation of the carotids, and the full, slow pulse show increased 



CEREBRAL HEMORRHAGE. 



697 



arterial tension. In such a case, if the patient seems otherwise robust, we may 
bleed at the commencement of an attack, in the hope of checking the now of blood 
by lowering" the intra-arterial pressure. In similar conditions experience shows 
that the local abstraction of blood from the temples is sometimes advantageous. 
The bowels should be well emptied by enemata, and later on by drastic purgatives. 
If the respiration and pulse fail, we may try stimulants (ether, camphor), but very 
likely they will be without success. 

When the patient is safely over the shock, our resources for aiding him in the 
further stages of his trouble are very limited. As long as headache and symptoms 
of fever persist, the application of ice to the head should be kept up, and other 
disturbances should be treated symptomatically. For uneasiness and wakefulness, 
small doses of morphine or chloral are given. Treatment of the hemiplegia must 
be deferred for the first three or four weeks, until all the initiatory symptoms of 
irritation are over. Then electricity plays the chief role. Local galvanization 
should be tried, the current being made to pass transversely through the head, 
with as much regard as possible to the position of the hsemorrhagic focus; the 
current should be feeble, and the application should occupy two or three minutes. 
With this may be combined galvanization of the sympathetic nerve on the side of 
the haemorrhage. Nor should galvanization (stroking with the kathode) and fara- 
dization of the paralyzed muscles and nerves be neglected. If favorable changes 
take place, it is, however, uncertain how much should be ascribed to treatment ; 
since, as has already been stated, there is often improvement without treatment. 

Passive movements and massage of the paralyzed limbs are very important as 
a prophylaxis against contractures. They should be commenced promptly, and 
be methodically continued. Massage, and later on systematic and appropriate 
gymnastic exercises, may contribute much to the restoration of voluntary motions. 
The same object is also promoted by rubbing in spirits of camphor, chloroform 
liniment, etc. 

Internally, potassic iodide is frequently given, out of regard for its " absorbent " 
properties. We may also try the effect of strychnine; it is most adapted for cases 
of some duration. 

As to baths, they should not be too warm— that is, not over 90°-93° (26°-27° 
R.). Moderately warm baths, medicated with common salt if it seems desirable, 
and employed three or four times a week, seem to be beneficial. If it is thought 
best to send the patient to a regular bathing-place, Wildbad, Ragaz, Teplitz, Wies- 
baden, or Rehme may be chosen. At the first-mentioned places none but the 
cooler springs should be used. 

Hemiplegic paralysis often lasts so long that the physician must repeatedly 
change the details of treatment, so as to support the courage and patience of the 
sufferer. Particular care should, be given to regimen, in order that any recur- 
rence of the haemorrhage may, if possible, be avoided. The diet should be simple ; 
any large amount of alcohol should be forbidden ; and there should be no severe 
bodily exertion or mental excitement. 



698 



THE DISEASES OF THE BRAIN. 



CHAPTER IV. 

CEREBRAL EMBOLISM AND THROMBOSIS. 

{Softening of the Brain from Embolism or Thrombosis.) 

JEtiology and Pathology. — Occlusion of the cerebral arteries is one of the most 

frequent injuries inflicted by embolism. Usually the emboli originate in the left 
side of the heart, from thrombi in the left auricle, or from the thrombotic deposits 
which form in chronic endocarditis (mitral or aortic disease) upon the valves of 
the left ventricle. Chronic arterio-sclerosis may also lead to thrombosis in the 
larger arteries, particularly the aorta ; and in case the cerebral arteries themselves 
are extensively atheromatous, the larger vessels at the base of the brain may fur- 
nish material for embolism of the smaller cerebral arteries. 

Thrombosis of the arteries of the brain is always due to primary disease of the 
blood-vessels, the most common cause being the chronic arterio-sclerosis just men- 
tioned. Wherever the atheroma has altered the normal structure of the intima, 
deposits of fibrine may take place. Their development is further promoted by 
the subnormal elasticity of the arteries, and by the occasional narrowing of their 
lumen ; for thus the flow of blood is rendered slow, if not even completely 
checked. It is easy to understand that thrombosis and embolism may each give 
rise to the other. From every thrombus an embolus may be detached ; and every 
firmly lodged embolus may form a nucleus for thrombosis. 

Next to arterio-sclerosis, the most frequent cause of a cerebral thrombus is 
syphilitic endarteritis. In the chapter on cerebral syphilis this subject will be 
minutely considered. Whether thrombi ever form here independently of disease 
of the vessels is doubtful. An apparently spontaneous thrombosis is now and 
then seen in patients who are cachectic or severely ill (cancer, grave typhoid or 
typhus fever, pneumonia) ; in such instances the cardiac weakness, and possibly 
also an abnormal tendency of the blood to coagulate, are regarded as either the 
causes, or at least the predisposing factors, of the thrombosis. 

In whatever part of the arterial system complete occlusion has been produced 
by an embolus or thrombus, the results depend upon the possibility or impossi- 
bility of blood reaching by collateral channels the region thus deprived of its 
ordinary supply. If the collateral circulation prove efficient, no harm is done ; if 
not, the tissues must perish and undergo "softening." It is thus a matter of the 
greatest practical import that the perforating arteries of the brain-stem (Arterien 
des Hirnstammes), and particularly the branches of the middle cerebral artery 
in the fissure of Sylvius, which supply the great central ganglia and internal cap- 
sule, are all "terminal," in Cohnheim's sense — that is, they form few anastomoses 
with neighboring vessels. Now, the middle cerebral artery and its branches are 
known from experience to be peculiarly liable to embolism, above other cerebral 
arteries. Hence we see why the region they supply suffers so severely and so very 
frequently from emboli. It is noteworthy that the left middle cerebral artery 
is more frequently plugged by emboli than is the right. In the centrum ovale 
and cortex there is more opportunity for collateral compensation than in the cen- 
tral ganglia; but even here the supply of blood often proves insufficient, as is 
shown by the not infrequent occurrence of spots of softening in the cortex and 
the white substance of the cerebrum. On the other hand, embolic foci are much 
rarer in the crura cerebri, pons, and cerebellum. 

The various steps in the process which begins with embolic or thrombotic 
occlusion and ends in softening of the brain-substance are essentially the same as 
occur in other organs (compare chapter on pulmonary embolism, page 229). The 



CEREBRAL EMBOLISM AND THROMBOSIS. 



699 



tissues which are deprived of their arterial blood perish, become disintegrated, and 
are transformed into a soft homogeneous mass. Into the empty portion of the 
artery, beyond the embolus, blood flows in the reversed direction from the veins, 
and, if the anatomical relations permit, from the minute arteries in the neighbor- 
hood ; but the supply is not sufficient to nourish the tissues. The walls of the 
blood-vessels become abnormally permeable and delicate, so that some red glob- 
ules invade the disintegrating region by diapedesis, and others in the way of 
minute but genuine ecchymoses. Actual infarctions are, however, never formed 
in the brain, perhaps because, as Weigert suggests, the nervous structures swell so 
much as to exclude any large amount of blood. But the little punctiform ecchy- 
moses are in many instances so abundant that the whole softened spot seems dis- 
tinctly reddish or yellowish. This red or yellow softening is also due in part to 
the tissues being stained by the dissolved pigment of disintegrated blood-globules. 
If the discoloration is not very striking, then we speak of a white softening. 

Fresh foci of softening are seen through the microscope to be composed of drops 
of myeline, bits of swollen nerve-fibers, numerous fatty granular cells, and free 
fat globules. The minimum time required for these changes is one or two days. 
If within that period a compensatory collateral circulation is set up, the nervous 
structures may be restored and resume their functional activity. If not, the tis- 
sues perish and become disintegrated. The white blood-corpuscles and leucocytes 
(and possibly also the endothelial cells of the blood-vessels, and the neuroglia and 
ganglion-cells) absorb the fatty detritus thus made, and come to form the fatty 
granular cells above mentioned. If the patient lives, the dead and disintegrated 
tissue is gradually absorbed, and may even finally be replaced by a cyst not differ- 
ent in appearance from those which occur after cerebral haemorrhage. A minute 
focus of softening may sometimes also be replaced by indurated cicatricial tissue. 
If portions of the surface of the brain become softened, quite a deep depression 
often results. This is filled up in part with serous fluid and in part by hyperplasia 
of the pia mater. Sometimes the convolutions are still recognizable in places ; 
but they are atrophied, of a yellowish color, and of a greatly increased consistence, 
due to the growth of cicatricial tissue. 

Clinical History. — The occurrence of cerebral embolism is attended with almost 
precisely the same sort of shock as is cerebral haemorrhage. We do not need 
to enter into the particulars again here, but will refer to the preceding chapter 
(vide page 688). In embolism also, the intensity of the shock varies ; it ranges 
between extreme mildness, when it occasions only transitory confusion of intel- 
lect or slight vertigo, to the greatest severity, when there is deep and persistent 
coma. One chief factor in determining the nature of the case is the size of the 
occluded artery ; another is its position, according as the embolism has taken 
place in the hemispheres or toward the base of the brain. In general, the shock 
of embolism is not often so severe and long continued as that of haemorrhage ; 
and embolism does not so frequently give rise to symptoms of cerebral compres- 
sion, including slowing of the pulse. On the other hand, epileptiform convul- 
sions are seen more often in embolism than in haemorrhage. Embolism again 
may have a rather slow onset, where there is at first a small embolus and this 
becomes the nucleus of a gradually formed thrombus. 

It is not easy to explain why there should be a shock at all in case of embolism. 
Perhaps the main reason is the diminution of pressure which the embolism 
occasions in the region directly affected and in its neighborhood. The portion of 
the artery beyond the plug becoming empty, not only causes a draught upon the 
blood and lymph, but subjects all the soft surrounding structures to a diminution 
of tension and to a certain amount of strain (Wernicke). It is not impossible, 
however, that the disturbance of circulation occasioned in the surrounding blood- 



700 



THE DISEASES OF THE BRAIN. 



vessels by sudden embolism of a good-sized artery is of itself enough to account 
for the symptoms of shock. 

With regard, also, to the persistent symptoms of embolism we may be equally 
brief, inasmuch as they very closely resemble those which follow a cerebral 
haemorrhage. As has been said, it is only when a compensatory collateral circu- 
lation is developed within the first forty-eight hours that the early symptoms of 
focal disturbance can entirely vanish. After this period, the tissues which have been 
deprived of their normal blood-supply must undergo necrosis ; although there is 
still room for hope that some of the symptoms will prove indirect, and therefore 
capable of improvement, so that embolic hemiplegia, like that from haemorrhage, 
may improve decidedly in the course of the first few weeks. 

Inasmuch as the middle cerebral artery is by far the most frequent seat of 
cerebral embolism, and inasmuch as this artery supplies the internal capsule as 
well as the great central ganglia, the most frequent focal symptom of embolism of 
the brain is ordinary cerebral hemiplegia, all the features of which have been 
depicted in the preceding chapter. Aphasia is associated with it with comparative 
frequency, for, as already mentioned, the left middle cerebral artery is especially 
apt to suffer. Less frequent is paralysis of a single member, due to cortical embol- 
ism, or an occipital lesion with hemiopia. 

Where softening is the result of thrombosis, the symptoms are but seldom 
abrupt in their onset. Usually the focal symptoms and the more general ones 
(like unconsciousness) are developed rather gradually. This is most often 
seen in so-called senile softening of the brain, a disorder almost always caused by 
sclerosis of the cerebral arteries. The various symptoms generally come on under 
cover of repeated relapses and fresh aggravations of the disease. A severe initial 
shock seldom occurs ; but almost invariably there is a gradual and progressive 
dementia. 

The further course and the final termination of cerebral softening vary as do 
those of cerebral haemorrhage. Embolism of a larger artery may cause speedy 
death. If, however, the first shock passes away, the impairment of function 
which may be left behind may last for years without seriously affecting the 
general health. There is always danger of a recurrence when the source of the 
embolism continues unchanged, as in cardiac disease or atheroma. 

Diagnosis. — Both the onset and the persistent focal symptoms are so much alike 
in haemorrhage and embolism that in many cases it is utterly impossible to decide 
which caused the apoplexy and hemiplegia. The following are factors in making 
a differential diagnosis, if one can be made : 1. It is very important whether there 
is any source for an embolus. Thus, if the patient have valvular cardiac disease 
(particularly mitral), embolism is more probable than haemorrhage. 2. A young 
person is, on the whole, more apt to have embolism than haemorrhage. At a later 
period of life one is about as probable as the other. 3. When the shock is severe 
and persistent, with red face, strong pulsation of the carotids, and signs of cerebral 
compression (slow pulse), we would think of haemorrhage rather than embolism, 
in which latter the initial symptoms are sometimes comparatively slight {vide 
supra). 4. Finally, it is sometimes possible to obtain support for a diagnosis of 
cerebral embolism by demonstrating embolism elsewhere, as in the fundus oculi, 
by means of the ophthalmoscope. 

In rare instances, also, tumors of the brain, into the substance of which haemor- 
rhage takes place, may induce symptoms closely simulating a primary apoplec- 
tic shock, as may also abscesses which have been previously latent, and then sud- 
denly burst into a ventricle. In such cases a correct diagnosis is seldom possible. 

Softening due to a thrombus is the most readily diagnosticated in those cases 
where there is cerebral syphilis (q. v.). Senile softening is inferred from the age 



INFLAMMATION OF THE BEAIN. 



701 



of the patient, the signs of general arterio-sclerosis, the abrupt advances of the dis- 
ease from mildness toward severity, and the developing dementia. 

For the prognosis and treatment of cerebral embolism we may refer simply to 
what was said in the preceding chapter. 



CHAPTER V. 

INFLAMMATION OF THE BRAIN. 

(Acute and Chronic Encephalitis.) 

1. Abscess of the Brain (Suppurative Encephalitis). 

iEtiology.— In most cases of cerebral abscess it is possible to demonstrate with 
certainty that infectious material, capable of exciting suppuration, has penetrated 
to the encephalon. This is particularly true of those not very rare abscesses which 
follow injuries of the scalp, cranium, or brain (traumatic abscess of the brain). 
Here the wound is almost always an open one, affording free ingress to the virus. 
It is not essential that the bones should be injured, for experience shows that, even 
where the soft parts alone are wounded, suppuration may extend to the brain. 
The manner in which this extension takes place determines the question whether 
a suppurative meningitis (q. v.) or an abscess shall be developed. Not infrequently 
we find the two combined. Another source of traumatic cerebral abscess is foreign 
bodies which penetrate into the brain (for instance, through the orbit), and thus 
carry septic matter into the very substance of the organ. Some exceptional cases 
have been reported of traumatic cerebral abscess without any open wound ; as yet 
they are beyond our comprehension. Possibly there is even in these some minute 
wound invariably present but overlooked. 

Analogous to the above causes is suppuration in neighboring parts, which may, 
by direct extension, occasion cerebral abscess. The same processes are prominent 
in this connection which we have already found to excite purulent meningitis (vide 
page 659) — particularly suppuration (caries) in the middle ear and in the petrous 
bone. In such a case the most frequent position of the abscess is naturally the 
temporal lobe or the cerebellum. Abscesses also occur in the anterior part of the 
brain, from suppurative processes in the nasal cavity and the ethmoid bone ; but 
this mode of origin is much less frequent. 

In yet a third class of cases the morbific agents are conveyed from foci of 
disease situated in distant parts of the body. These are metastatic or embolic 
abscesses. They occur, for instance, in pyaemia and ulcerative endocarditis. 
Abscesses of this sort, however, are usually small, and seldom are conspicuous in 
modifying the grave general disease. Of more importance are cerebral abscesses 
connected with certain suppurative affections of the lungs and pleura. These are 
not so very rare. They are oftenest associated with fetid bronchitis, pulmonary 
gangrene, and empyema. Purulent meningitis (q. v.) may occur in the same way. 
There can be no doubt that virus is in some way conveyed to the brain, but just 
how is not yet known. 

In some few cases of cerebral abscess no certain aetiology can be made out. 
To these the term idiopathic is applied. We met with several of them just at the 
time of an epidemic of cerebro-spinal meningitis ; and it therefore seems reason- 
able to suspect that possibly many apparently spontaneous cerebral abscesses are 
referable to the same poison as is epidemic meningitis. 

Pathology. — The pathological anatomy of abscess of the brain is precisely the 



702 



THE DISEASES OF THE BRAIN. 



same as that of abscesses in other organs. The size varies from minute foci 
hardly as large as a lentil to great cavities occupying nearly the whole of one 
lobe. Not infrequently several abscesses appear simultaneously in different parts 
of the brain. The pus is usually greenish yellow. It may be odorless or offen- 
sive. Sometimes remnants of the destroyed (" melted ") nervous tissue and red 
blood-globules are mixed with it. The walls of the abscess often bulge out irregu- 
larly. The cerebral parenchyma around the abscess for a greater or less distance 
exhibits white softening. This is due partly to the pressure and partly to the 
spread of the inflammation. An abundance of granular cells is generally to be 
found in the tissues near the abscess. 

If the abscess is very large and reaches near to the surface of the brain, it may 
sometimes be recognized during life by a distinct bulging and fluctuation. The 
convolutions on the surface of the affected hemisphere are almost always flat- 
tened. If the abscess extends clear to the surface of the brain, purulent menin- 
gitis is excited. Abscesses which are centrally situated not infrequently burst 
into a lateral ventricle. An abscess of long standing may finally become encap- 
sulated — that is, become incased in a smooth, firm layer of connective tissue, 
which prevents further extension of the process. The pus inside gradually 
becomes thick and cheesy. Apparently, however, it is very seldom entirely 
absorbed. 

Clinical History. — Small abscesses, and even large ones, may for a long while 
have scarcely any symptoms. This is particularly true of idiopathic abscesses, 
and of those which develop very slowly and insidiously after apparently insig- 
nificant injuries of the head or in connection with chronic inflammation of the 
middle ear. 

In cases following more extensive injuries, the symptoms are more violent 
from the start ; which is also true of many abscesses which develop acutely and 
enlarge rapidly. The symptoms can hardly be distinguished from acute menin- 
gitis. The patient is dull, or grows delirious ; he has violent headache and fever. 
Sometimes the temperature repeatedly rises to a high point. The loss of conscious- 
ness becomes more and more complete ; and in a comparatively brief time (one or 
two weeks) there may be profound coma and death. Rarely the violent symp- 
toms abate, and the acute passes into a chronic stage. 

The symptoms of cerebral abscess, when it pursues a chronic course, may be 
divided into (1) the general symptoms and (2) the focal symptoms, resulting from 
the special position of the abscess. There is no other localized cerebral disorder 
in which the focal symptoms are so often absent, either for a long while or even 
throughout the illness. This is partly because the abscesses are often situated in 
parts of the brain, injury to which does not occasion any demonstrable focal 
symptoms. Such localities are the white matter of the frontal lobe, and the hemi- 
spheres of the cerebellum. A second reason is that an abscess seldom excites indi- 
rect focal symptoms by affecting the parts around it. 

Among the general symptoms, the most important is a persistent, deeply situ- 
ated, dull headache. For a long while it may be the only symptom, especially 
when the abscess is gradually developed after an injury to the head or after aural 
disease of long standing. The pain is referred mainly to the seat of the abscess; 
but the exceptions to this rule are not infrequent. Another frequent symptom is 
vertigo ; and in many cases there is vomiting, either after meals or entirely inde- 
pendently of food. Another valuable symptom in diagnosis is the irregular fever, 
sometimes slight, and sometimes exhibiting great elevations with intervals 
between them ; but in many cases also, particularly where the abscess is encap- 
sulated, there may be no fever whatever. An important negative point is that 
choked disk is much rarer in cerebral abscess than in case of tumors (q. v.). 



INFLAMMATION OF THE BRAIN. 



Y03 



The general health, may be but slightly disturbed. Usually, however, there is 
decided indisposition. The patient is pale, has no appetite, and loses flesh. 

As to the focal symptoms, we need add here little to what is contained in 
Chapter II of this section. Abscesses involving the motor region of the cortex 
have been repeatedly found to cause limited epileptiform attacks and paralysis of 
some one limb. It is particularly characteristic that, as the abscess grows, one 
symptom of paralysis is added to another, and that often the advance of the 
paralysis is ushered in by epileptiform convulsions. Abscesses in the occipital 
lobe have repeatedly been observed to cause hemiopia, and abscesses in the tem- 
poral lobe word deafness ; and these facts have been used in making a diagnosis 
of the location of abscesses. Abscesses in the cerebellum may remain unsuspected 
for a long while ; or the above-mentioned general symptoms may occur in especial 
severity in such cases. 

The duration of chronic cerebral abscess varies greatly. In most cases it lasts 
months ; and sometimes it has certainly lasted years. Particularly where the 
abscess gives rise to no symptoms, or merely to slight and indefinite ones refer- 
able to the head, it may last a very long while. It is quite often the case that 
there are separate attacks of the severe symptoms, like headache, vomiting, and 
fever, and that in the intervals of variable duration between these paroxysms 
the patient feels pretty well. 

The final termination of cerebral abscess is almost always fatal. Recovery is 
not impossible, but has been seen with certainty in only a very few instances. 
Death either comes on gradually, where, as the abscess grows larger, all the symp- 
toms become correspondingly aggravated ; or it may happen quite suddenly. 
Sometimes it is brought about by the abscess bursting into a lateral ventricle, or 
by the supervention of meningitis. Often a cerebral abscess terminates in a sud- 
den and unxepected death, where no immediate cause for the event can be found. 

Diagnosis. — Although it is often possible to make a correct diagnosis of cerebral 
abscess, yet there is usually a good deal of difficulty in arriving at such a conclu- 
sion, and entire certainty is seldom attainable. The most important points in 
diagnosis are : (1) The demonstration of some cause like trauma, chronic otitis, fetid 
pulmonary diseases, or empyema. (2) The presence of general cerebral symptoms, 
such as headache, vertigo, and vomiting; and the fact that these are sometimes 
better and sometimes worse. To aid in excluding tumor, we have (3) the febrile 
symptoms frequently caused by abscess, but rare in case of tumor; and (4) the 
extreme rarity of choked disk, winch is very frequently occasioned by tumors. 
The focal symptoms, if there be any, are not characteristic. They grow worse 
by fits and starts in tumor just as in abscess. One fact, however, is of value, 
namely, that while tumors {vide infra) frequently cause disturbances in the area 
of distribution of the nerves at the base of the brain (like paralysis of the motores 
oculi), an abscess does this only exceptionally. It is often quite impossible to 
make a differential diagnosis between acute abscess and purulent meningitis, 
unless focal symptoms are developed. These can be caused by a circumscribed 
lesion alone, and therefore point to abscess. 

Treatment. — The only possible way in which to cure an abscess is by opera- 
tion; the skull is trephined and the abscess laid open. It can be readily seen that 
such a procedure is feasible in but few instances. "We need to be certain that 
there is an abscess and where it is located, and, finally, that it is so located as to 
render operation permissible. Under the present antiseptic modes of procedure, 
the dangers of an operation need not be over-estimated. For particulars we must 
refer to works on surgery. 

If operation is not justifiable, nothing but purely symptomatic treatment is left 
us. Ice to the head, narcotics, potassic bromide, electricity, and sometimes also 



704 



THE DISEASES OF THE BKAIN. 



the local abstraction of blood, are the main remedies beyond general hygienic 
measures. 

2. Acute and Chronic Non-suppurative Encephalitis. 

While the spinal cord is quite frequently affected by idiopathic circumscribed 
inflammation (transverse myelitis), analogous cerebral disease is much more 
exceptional. The scanty information which we possess upon the subject is as fol- 
lows: 

1. Idiopathic (Inflammatory) Softening of the Brain.— In rare instances there 
are found in the brain quite extensive foci of softening, the pathological anatomy 
of which is almost identical with that of embolic softening, and yet the afferent 
blood-vessels do not furnish any explanation of the condition. They have accord- 
ingly been termed "foci of inflammatory softening." The mode of their produc- 
tion is unknown. The symptoms resemble closely those of softening from 
thrombus. 

2. Curable Form of Encephalitis. — In certain cases pronounced symptoms of 
focal disease exist for a time, and suggest a tumor or the like ; but after some 
months, or even a still longer time, the symptoms gradually abate, and finally 
there is complete recovery. Such cases undoubtedly occur. They are usually 
explained by assuming that there has been a localized inflammation, followed by 
a restoration to the normal state. The nature of the symptoms, as we have 
observed them, would seem to imply that the lesion is generally in the neighbor- 
hood of the cortex, for there is usually paresis of some one part of the body, often 
associated with certain symptoms of irritation and impairment of speech. Possi- 
bly the recovery of these cases may be assisted by electricity and potassic iodide ; 
but we should never venture upon an absolutely favorable prognosis. 

3. Diffuse Cerebral Sclerosis. — Diffuse sclerosis of the brain is a peculiar disease, 
which is usually classed as a chronic inflammation. The whole brain may be 
involved, or the disease may be confined chiefly to a large part of one hemisphere. 
There is a very marked increase in the consistency of the brain-substance, so that 
it cuts like a tough piece of leather. The microscope reveals in many cases, but 
not in all, diffuse hyperplasia of the neuroglia. In a case which we recently 
examined there was a decided atrophy of the nervous fibers lying in the white 
substance of the brain. The disease is rare, and its characteristic symptoms can 
not yet be stated absolutely. They are developed slowly. The most constant 
among them seem to be hemiplegia without much change in sensation ; symptoms 
of motor irritation, such as epileptiform convulsions (sometimes general and some- 
times unilateral), or single twitchings, which may be rhythmical or like those of 
chorea ; and, lastly, dementia. Where both hemispheres are involved, there are 
usually marked spastic symptoms in the lower limbs. 

The disease has been observed in children and in elderly people. Possibly 
chronic alcoholism sometimes acts as an setiological factor. Treatment can be 
only symptomatic. 

Multiple sclerosis of the brain is almost always associated with the same affec- 
tion of the spinal cord. We have, therefore, already described the disease in the 
preceding section (page 592). 

4. The Acute Encephalitis of Children. (Cerebral Paralysis of Children. 
Spastic Infantile Hemiplegia of BenediM.) — Children not infrequently suffer 
from a definite form of hemiplegia, which deserves a brief special description. 

The patient is usually between one and four years old. The commencement 
of the symptoms is almost always acute. Having been previously healthy, the 
child is suddenly attacked with malaise and fever. Very often there is nausea 
and vomiting, speedily or at once followed by grave cerebral symptoms. There is 



INFLAMMATION OF THE BKAIN. 



705 



stupor, and convulsions are particularly frequent. This condition may last but 
one or two days ; or it may continue, perhaps with unabated severity, for two or 
three weeks. Then the acute symptoms abate, and the child recovers compara- 
tively fast; but it is noticed by the parents to be paralyzed: and this paralysis 
seldom entirely disappears, although it may diminish. 

If such children come under observation after the paralysis has lasted some 
time, as is usually the case, their condition is generally as follows : The cranial 
nerves, as a rule, are but little affected. The main change is in the extremities of 
one side ; and the arm is almost always worse than the leg. The affected parts 
betray an arrest of development, more or less impairment of motion, in many 
cases a marked exaggeration of the tendon reflexes, and almost invariably con- 
tractures of more or less severity. The muscles, although generally somewhat 
atrophied, never exhibit the reaction of degeneration. Sensation, as a rule, is 
unimpaired. Motor symptoms of irritation are found upon the affected side with 
striking frequency : the commonest are movements like athetosis or chorea (hemi- 
athetosis, hemichorea) ; and associated movements are also not infrequent. The 
constant movements of the fingers resulting from the athetosis sometimes render 
the articulations so lax that it is possible to make the fingers assume an angle of 
ninety degrees or even less with the back of the hand, at the metacarpo-phalangeal 
joint. The child may keep making motions with its paretic arm while walking. 
It is ii ot very rare for epilepsy to be developed later. There are convulsive attacks, 
which usually begin on the paralyzed side, but which may later affect the whole 
body. The intellectual development of many such children is tolerably normal. 
Others, however, are more or less demented, or betray defective moral sense. 

The whole course of the disease suggests very strongly an acute encephalitis. 
The process is probably in most cases more or less completely limited to the motor 
region of the cortex, and has hence been called " poliencephalitis. " * It reminds 
one forcibly of the acute poliomyelitis of children, with a difference merely in the 
localization of the disturbance. It is not impossible that the two diseases have a 
very similar, if not identical, aetiology. They can hardly be differentiated in their 
initial stage ; but when further developed they could not be confounded, because 
the cerebral disease causes unilateral paralysis, leaves the electrical reaction unim- 
paired, and frequently causes exaggeration of the tendon reflex. It deserves men- 
tion that precisely similar phenomena may be presented by children during 
recovery from measles, scarlet lever, and other acute infectious diseases. 

The pathological conditions of the early stage have not yet been studied. Long 
after the process has run its course, the affected portion of the cerebrum presents 
marked atrophy with cicatricial coutraction. If the surface of the brain has been 
affected, a corresponding depression is to be noticed ("porencephalia"). At these 
places the pia is thickened. Sometimes limited cystic formations are found. The 
pyramidal tract exhibits a secondary descending degeneration. It is thus evident 
that the process is, from an anatomical point of view, precisely like the atrophy of 
the anterior cornua occasioned by poliomyelitis. 

The treatment at first is to be governed by the same rules as in the initial 
period of acute poliomyelitis (q. v.). The hemiplegic symptoms which persist 
after the first few months will never improve much. The most we can do will be 
by means of electricity, massage, and cold baths with friction ("cold rubbing"). 
For the epileptic attacks large doses of bromide of potassium are decidedly bene- 
ficial. 



[* This name, however, has been previously applied by Wernicke to that form of external ophthal- 
moplegia due to changes in the nerve nuclei m the pons (vide page 651). — Trans.] 
45 



706 



THE DISEASES OF THE BEAIN. 



CHAPTER VI. 

INSOLATION. SUNSTROKE. HEAT PROSTRATION. THERMIC FEVER. 

[JEtiology and Pathology. — Under exposure to undue heat, either in the direct 
rays of the sun, or, during hot weather, in engine-rooms, laundries, and the like, 
marked effects may be produced on the human organism, manifesting themselves 
in a widely different manner in different cases. The liability to these effects is 
much greater with us than m most portions of Europe or in Great Britain, and is 
enhanced by a moist atmosphere which tends to prevent evaporation from the 
surface of the body. Attacks may come on at night and under cover as well as 
by day. While excessive heat is the sole and sufficient exciting cause of the 
changes and symptoms to be described, exhaustion due to muscular exertion or 
other cause plays a very important secondary role. A vigorous person, however, 
of regular and temperate habits, can stand much greater heat and exertion than an 
individual who is debilitated or addicted to the use of stimulants. The frequency 
of attacks after a full meal has been noted. Those newly arrived in the country 
are, other things being equal, more likely to succumb than natives or those who 
have become accustomed to the climate. That high temperature due to solar or 
artificial heat, or a combination of the two, is the ijrime causative condition has 
been clearly shown by experiments on animals. 

Pathological Anatomy. — In cases of sudden death from shock there are no con- 
stant and peculiar lesions. The blood is dark, imperfectly coagulated, and col- 
lected in the veins ; ecchymoses are frequently found. 

After death due chiefly to abnormally high temperature — that is to say, 
in cases of thermic fever — the heart, and especially the left ventricle, is firmly 
contracted from post-mortem coagulation of its myosin ; the lungs are apt to be 
much engorged with dark fluid blood, and may be the seat of haemorrhage ; extrava- 
sation of blood under the skin is more or less marked, and haemorrhage into and 
about the cervical sympathetic ganglia has also been observed. The membranes 
of the brain and cord are often greatly congested, and there may be evidences of 
commencing meningitis. The blood-corpuscles are crenated and show a diminished 
tendency to the formation of rouleaux. Rigor mortis is marked and early in the 
voluntary muscles as well as in the heart, and is attributable to the same cause. 
Parenchymatous degeneration of the organs is sometimes found. 

Symptoms and Course. — The onset of the attack is usually sudden, though there 
may be slight premonitions, such as dizziness, pain, or uncomfortable sensations 
in the head. 

It will, perhaps, add to clearness to distinguish three leading forms of attack, 
it being understood that Nature does not always classify cases as sharply as is 
done here. The first of these comprises cases of heat prostration, denoted by faint- 
ness, syncope, nausea, and sometimes vomiting, with marked muscular and general 
weakness. The surface of the body is cool, the pulse rapid and feeble. The great 
majority of these cases are mild, and the symptoms pass away more or less quickly 
on placing the patient in the recumbent posture in a relatively cool and quiet 
place with free ventilation. After a few hours the patient can be removed to his 
home, and in a day or two has recovered perfectly, except for some sensitiveness to 
heat or the sun's rays. There may be transient insensibility, or, on the other hand, 
the case may terminate fatally very soon from general exhaustion and cardiac 
failure. 

The second form includes cases with respiratory as well as circulatory failure, 
due especially to the exhaustion of the nerve-centers presiding over these func- 



INSOLATION. SUNSTROKE. HEAT PROSTRATION. 707 



tions. Under this head come cases of true sunstroke — patients suddenly losing 
consciousness while exposed to the sun. The skin is cold and the pulse is feeble ; 
death may quickly ensue or recovery may follow, especially if prompt and suit- 
able treatment is instituted. The after-effects of the attack may be very slow to 
pass away, and may never disappear entirely. 

The most striking- characteristic of the third form is the great increase in the 
temperature — a symptom which has given rise to the term thermic fever. 
In this form premonitions are more common than in the others. The ther- 
mometer may register 110° or even more ; the skin is burning hot and generally 
dry ; the pulse is slow and full, or quick and jerking ; the respiration is quick- 
ened, sighing, or even stertorous ; the pupils at first are usually contracted ; 
there may be great restlessness ; coma and convulsions sometimes occur ; vomit- 
ing is common ; and, toward the close of life, the sphincters are sometimes 
relaxed. A fatal result is due to apncea and asthenia combined. What was said 
with regard to recovery from the second form holds good also for the third. 

Diagnosis. — This is seldom difficult. The circumstances under which the at- 
tack comes on are generally patent ; and the hyperpyrexia, if present, is distinct- 
ive. Acute alcoholism and meningitis are the chief affections which might lead 
to error. 

Prognosis. — The mortality rate of the severer forms of the disease is very high, 
but the prognosis depends much on the possibilities of securing prompt and skill- 
ful treatment. Under this many a case recovers from a seemingly desperate con- 
dition. The tediousness and imperfection of recovery have been already alluded 
to. For long periods in some cases the mental and physical powers are much 
impaired, and great care has to be exercised as regards exertion, high temperature, 
and the sun's rays. Insanity is sometimes a sequel. 

Treatment. — In the first place, much may be done by preventive measures to 
obviate the necessity for any treatment. A regular and temperate life will do 
much ; and special precautions of an obvious nature should be taken during hot 
weather by those whose occupations involve a liability to exhaustion and exposure 
to unusual heat. It would be well if it were generally known that there is com- 
paratively little danger of sunstroke as long as perspiration is free. Many an 
attack might be averted by noting the activity of the skin and seeking rest and 
shelter as sweating diminishes. A considerable responsibility rests upon militia 
surgeons and others in similar positions during hot weather. 

Mild cases of heat prostration seldom require other measures than those 
already indicated in describing the symptoms. If it seems desirable to give stimu- 
lants, and there is nausea, they are better given under the skin or by the rectum. 
The clothing should be loosened ; the cold douche and other refrigerating meas- 
ures are not indicated unless there is fever, and they should then be used with 
caution. 

For true sunstroke, treatment should be active and energetic, the indications 
being to reduce the temperature of the overheated centers and to stimulate their 
activity. If a cool or shady spot is near at hand, the patient should be removed to 
it and largely stripped of clothing ; if not, no time should be lost before resorting 
to the cold douche on the head and body while stimulants are administered by 
enema or subcutaneously. External stimulation by mustard or flagellation, and 
purgative enemata, are said to be sometimes useful. The use of cold externally 
should not be prolonged in these cases unless there is fever. Nervous exhaustion 
is the prominent symptom, and all depressing measures are out of place. 

The case is widely different with the third form of the attack. Here the imme- 
diate danger is from the hyperpyrexia, which must be combated by rubbing the 
patient with ice, placing him in a tub of water with lumps of ice, or similar meas- 



708 



THE DISEASES OF THE BEAIN. 



ures, until the temperature in the rectum is reduced nearly but not quite to the 
normal point. In the application of the refrigerating measures the head must not 
be neglected. The sole indication at first is the reduction of the temperature. 
Antipyrine subcutaneously has been given in a few cases in the Boston City Hos- 
pital, and also in Brooklyn, with good results. After a reduction of the tempera- 
ture, any symptoms of collapse or exhaustion demand stimulants. 

With regard to the employment of blood-letting there is considerable differ- 
ence of opinion. That cases occur in which this procedure is indicated is 
undoubtedly true, but they are exceptional ; they are characterized by the evi- 
dences of great cerebral congestion without hyperpyrexia. 

The subsequent management of convalescents from any form of sunstroke is 
often very important. Prolonged rest, and sometimes change of climate, may be 
demanded. A symptomatic and common-sense treatment is in place. It has 
seemed to the editor that quinine, especially in solution with a moderate excess of 
sulphuric acid, is distinctly useful in those suffering from mild or moderate after- 
effects of undue heat.] 



CHAPTEE VII. 
TUMORS OF THE BRAIN. 

iEtiologfy.— The precise causes which lead to the development of tumors in the 
brain are no more certainly known than in regard to other organs. In most 
cases the new growths are formed insidiously and gradually in persons previously 
healthy, without ascertainable cause. A circumstance which deserves mention is 
that sometimes the first symptoms come on immediately or a short time after 
some injury to the head ; but whether this is a matter of cause and effect, or of 
coincidence, can very seldom be determined. 

The sufferer from cerebral tumor is usually in middle life. Certain forms of 
tumor, however, particularly solitary tubercles, are comparatively frequent in 
children. Sex seems to exert a decided influence : men are much oftener 
attacked than women. 

Varieties of Cerebral Tumor.*— The most important forms of tumor seen in the 
brain are as follows : 

1. Glioma. — Glioma is a kind of tumor peculiar to the central nervous system, 
but seen much oftener in the brain than in the spinal cord (vide page 638). 
Apparently the new growth always originates in the neuroglia, which is the con- 
nective-tissue frame- work of the true nervous matter. As seen under the micro- 
scope, a glioma is made up of fibers and cells, the latter being precisely like the 
normal cells of the neuroglia, while the fibers seem to consist mainly of the 
numerous cell-processes. Klebs maintained that the ganglion-cells also take an 
active part in the new growth ; but this has not yet been proved. It is character- 
istic of gliomata that they are seldom sharply defined, but shade off gradually 
into the healthy tissue. The affected portion of the brain is usually enlarged, but 
yet maintains pretty nearly its original shape. On cross-section, the glioma 
presents a gray or reddish-gray surface. It is usually rather soft, and almost 
always is very vascular. This great vascularity is not without clinical impor- 
tance, for variations in the fullness of the blood-vessels, and, above all, sudden 



* From a clinical standpoint, the term "cerebral tumor" usually is meant to include also such 
tumors as originate in the neighborhood of the brain (as in the base of the skull), if they finally 
involve the brain itself. 



TUMORS OF THE BRAIN. 



709 



haemorrhages into the interior of the new growth, which not infrequently occur, 
may produce marked symptoms. 

Gliomata are most frequent in the white substance of the cerebral hemispheres, 
but they are also found in the central ganglia, cerebellum, and elsewhere. They 
are usually single, seldom multiple. 

2. Sarcoma. — It is very seldom that any form of sarcoma originates in the 
brain-substance. It usually commences in the connective tissue of neighboring 
parts, in the dura mater, the periosteum of the cranium, or the cranium itself 
(osteo-sarcoma). The sarcoma is most often found at the base of the skull, in the 
form of a circumscribed tumor of varying consistency. By pressing upon neigh- 
boring parts, or by involving them in the diseased process, it may cause the 
gravest disturbances. Histologically, we have here such varieties as round- 
celled, spindle-celled, fibro-sarcoma, etc. 

3. Gumma and Solitary Tubercle. — Both gumma and solitary tubercle are 
very prone to attack the brain. We shall revert to gumma in the chapter on 
cerebral syphilis. Solitary tubercles may grow to the size of a cherry or larger. 
They may be single or multiple, and may occupy any part of the brain. They 
are most often found in the cortex, and in the cerebellum and pons. 

Solitary tubercles and gummata, upon cross-section, have a yellowish, cheesy 
appearance, and are usually distinctly defined. Histologically, they are composed 
of granulation tissue. It was formerly no easy matter to distinguish gumma from 
tubercle in all cases; but now complete certainty is attainable by determining 
the presence or absence of tubercle bacilli (and likewise of syphilis bacilli). 

4. Carcinoma. — Carcinoma completes the list of such cerebral tumors as have 
much clinical importance. They are here almost always secondary. It has been 
our experience that secondary cancer of the brain is principally associated with 
primary cancer of the breast, or of the lungs and pleura; which fact bears a 
remarkable analogy to the occurrence of secondary cerebral abscess after primary 
empyema, pulmonary gangrene, etc. 

5. Among the rarer varieties of tumor are psammoma, which usually starts 
from the meninges, is hard, generally comparatively small, and therefore often 
harmless, and contains calcareous matter, so that it grates under the knife; 
cholesteatoma, a rare tumor which has the brilliancy of mother of pearl; lipoma; 
and angioma. 

The General Symptoms of Cerebral Tumors. —As is the case with all focal dis- 
eases of the brain, some of the symptoms of cerebral tumors are connected with 
the special localization of the new growth. There are definite focal symptoms, 
varying with the part destroyed, or at any rate functionally impaired ; and it is from 
these symptoms alone that we are enabled to determine the position of the tumor. 
But, in addition to these focal symptoms, there are certain general symptoms com- 
mon to almost all cerebral tumors of any size. They are in large part referable to 
the general compression of the brain due to the enlargement of the new growth. 
In the first place, numerous clinical facts, which will be immediately enumerated, 
indicate that whenever there is a tumor of any great size, a large part of the 
entire encephalon is subjected to pressure ; and, secondly, the anatomical appear- 
ances of almost every brain affected by a large-sized tumor lead to the same con- 
clusion. The convolutions are flattened and obliterated, the dura mater is 
crowded against the cranium, and perhaps thinned or even perforated because of 
the persistent pressure, or, on the other hand, thickened as a result of chronic in- 
flammation. Now and then the effects of pressure are visible even in the bones of 
the skull : they are worn thin, or even perforated, or their sutures are loosened. 
Another result of the general intra-cranial tension, through its effect upon the 
venous trunks of the brain, is serous effusion into the ventricles (internal hydro- 



710 



THE DISEASES OP THE BRAIN. 



cephalus), which, occurs very frequently. The largest effusions are caused by 
tumors in the posterior cerebral fossa, which directly compress the venae Galeni. 

The symptoms of cerebral tumors, referable to the effects of general compres- 
sion, are as follows : 

1. Headache is one of the earliest and most constant symptoms. It is usually 
persistent, although subject to temporary exacerbations and intermissions. The 
patient describes it as dull, deeply seated, and stupefying. Although it affects the 
whole head, it is sometimes (not invariably) referred mainly to the neighborhood 
of the tumor. It is particularly true of persistent occipital headache that it indi- 
cates a new growth in the posterior fossa. Sometimes also it is possible, by tap- 
ping upon the skull, to find a hyperaesthetic region. Considerable caution, how- 
ever, should be used in drawing diagnostic conclusions from such observations. 
The headache usually lasts to the close of the disease, and, even after the patient 
has become completely comatose, the persistence of the pain is still evident, from 
his low groans and the way in which his hand seeks his head. 

2. Next in frequency to headache are intellectual and mental disturbances. 
Even the facial expression may be somewhat characteristic, being peculiarly lan- 
guid, apathetic, and dull. The patient talks slowly, often having to think a long 
while before knowing what to say. Memory becomes impaired, especially with 
regard to the most recent events. The interest of the patient in those about him, 
and the things he used to care for, grows less and less. He has a sleepy, dazed 
look, and grows careless and untidy. Of course, individual cases present various 
deviations from this outline ; but in general, cases are a good deal alike, although 
the degree of mental disturbance may vary from a slight dullness to complete 
dementia. 

If unusual fullness of the blood-vessels, a haemorrhage into the new growth, or 
some similar cause, induces a sudden temporary increase of tension, there may be 
such marked symptoms as syncope or an apoplectiform shock. 

3. Other general cerebral symptoms are vertigo, slowing of the pulse, and 
vomiting. If, however, vertigo is a very prominent symptom, it implies that the 
cerebellum is especially encroached upon by the tumor. The retardation of the 
pulse is a frequent symptom, and not without diagnostic value. It has already 
been mentioned as one result of general compression of the brain, in connection 
with cerebral haemorrhage. The rate may be put at about 50 to 60, or even lower. 
The pulse is sometimes also slightly irregular. Cerebral vomiting may be one of 
the earliest and most troublesome symptoms. It frequently occurs independently 
of the ingestion of food, especially in the morning, and is not infrequently asso- 
ciated with dizziness. 

4. Epileptiform convulsions are sometimes excited by cerebral tumors, al- 
though many patients are free from them. Such attacks in all probability origi- 
nate invariably in the cortex of the cerebrum ; and it is, therefore, natural that 
they should be seen most frequently (as they are) in connection with tumors in 
the cerebral hemispheres. This rule, however, is not without exceptions. If the 
convulsions are not general, but are unilateral or confined to distinct portions of 
the body, they are to be regarded rather as focal than as general symptoms, and 
may be utilized for the approximate localization of the lesion {vide page 672). A 
certain amount of information in the same direction may also be got from those 
attacks which begin unilaterally or in one particular limb, and then quickly 
involve the entire body. 

5. Choked disk is one of the most important general objective symptoms of 
cerebral tumor. We should never omit to make an ophthalmoscopic examination 
of the fundus oculi in a case of chronic cerebral disease. Some differences of 
opinion yet exist in regard to the special pathology of choked disk ; but we may 



TUMOES OF THE BRAIN. 



Ill 



regard it as extremely probable tbat the main factor in its production is the purely- 
mechanical one, of general compression of the brain. The original view of Von 
Graef e was that the increased intra-cranial pressure obstructs the venous return 
through the vena centralis retinae into the cavernous sinus. The opinion which 
prevails at present is that advanced by Schmidt and Manz — namely, that the 
increased tension forces the cerebro-spinal fluid into the lymph-sheath of the optic 
nerve (Schwalbe), and that the " hydrops vagince nervi optici " thus produced 
compresses the nerve and the blood-vessels which traverse it. At any rate, choked 
disk is not a focal symptom. The tumor occasioning it may have any position, if 
only it gives rise to general compression of the brain. 

Disturbances of vision may or may not be entailed by choked disk ; the 
patient may have amblyopia, defects in the field of vision, or even total blindness. 
In some few instances, amblyopia has been one of the earliest symptoms of cere- 
bral tumor, insomuch that the patient has applied first of all to an oculist. Usu- 
ally the sight is preserved for quite a long while, in spite of the abundant object- 
ive evidences of choked disk. The latter consist of swelling of the disk, marked 
distention and tortuosity of the veins, possibly haemorrhages (from passive con- 
gestion), and cloudiness of the disk, although the retina still exhibits its normal 
transparency. It is not until the long-continued congestion impairs nutrition 
to such an extent as to cause atrophy of the optic nerve that vision is much 
impaired. 

6. The last general symptom to be mentioned is general loss of flesh and strength. 
This often appears comparatively early. It is in large part due to the small 
amount of food taken, vomiting, and wakefulness ; but it is not impossible that the 
grave cerebral disorder itself exerts a direct and unfavorable influence upon all 
the processes of nutrition. There is in most cases, also, a tendency to obstinate 
constipation. 

Tumors in the different Parts of the Brain— their Focal Symptoms— The symp- 
toms above discussed indicate the existence of a tumor, but not its particular loca- 
tion. Other phenomena are necessary to enable us to localize the disease, but it is 
not exceptional to have none but the general symptoms. Tumors in the white 
matter of the frontal lobe, or such as affect the corpus striatum, as well as others, 
may run their course without any focal symptoms ; but most cases afford evi- 
dence which points with more or less certainty to the exact position of the tumor. 
Almost all of these focal symptoms have already been fully discussed in Chapter 
II of this section, and their interpretation follows the rules for all focal lesions of 
the brain. We may, therefore, be brief here. It is necessary only to emphasize 
the fact that with regard to cerebral tumors, as well as other lesions, focal symp- 
toms should be divided into the direct and the indirect. Direct focal symptoms 
are the immediate result of the destruction of nervous tissue by the new growth, 
while the indirect are excited by the pressure exerted by the tumor upon the parts 
closely surrounding it. This pressure varies with the amount of blood in the ves- 
sels of the new growth, and therefore the indirect symptoms may undergo tempo- 
rary exacerbations and remissions. An intermediate position is occupied by those 
focal symptoms which occur in many cases as the result of certain anatomical 
changes secondary to the new growth. Not infrequently there is white softening 
of the substance of the brain around the tumor proper. Probably this condition 
is generally the result of a compression of the minute blood-vessels surrounding 
the new growth, but sometimes it is the sequel of an obliterative endarteritis 
(Friedlander). The latter cause is especially operative where the tumor is a gum- 
ma or a solitary tubercle. 

1. Tumors of the cerebral hemispheres generally lead to the gradual develop- 
ment of hemiplegia — a focal symptom which is to be regarded as partly direct and 



712 



THE DISEASES OF THE BRAIN. 



partly indirect. Since the new growth is often situated near the cortex, symptoms 
referable to that region are especially frequent with tumors of the cerebrum. It 
is therefore not infrequently the case that the hemiplegia is the result of the suc- 
cessive paralysis of single portions of the affected side ; for instance, first there is 
only facial paralysis, then, in addition, paralysis of an arm, then of the lower limb. 
Very often the extension of the paralysis is accompanied by convulsions, which 
either are confined to one limb or one side of the body, or are universal. There 
may be still other focal symptoms, varying with the exact location of the tumor. 
Thus, there is hemianaesthesia, if the parietal region or the posterior part of the 
internal capsule is affected ; hemiopia, if an occipital lobe suffers ; aphasia, if the 
neighborhood of the left island of Reil is involved, and so on. 

2. Tumors at the Base of the Brain. — The base of the brain is a very favorite 
place for new growths. The symptoms are in a majority of cases quite character- 
istic. Some of the tumors spring from the base of the skull ; among these are many 
sarcomata and syphilitic growths ("gummoas periostitis'"). Other tumors origi- 
nate in the meninges, especially the dura ; and still others from the brain itself. 
Of these last, it is remarkable that some spring from the pituitary gland. The 
exact starting-point is very seldom of much clinical importance ; for all the parts 
mentioned are in such close proximity to one another that there is no great differ- 
ence in the symptoms produced. We can only decide that there is a tumor in this 
or that place at the base of the brain. 

Tumors at the base of the brain owe their characteristic clinical stamp to the 
frequency with which the cranial nerves at the base are involved. The anatomi- 
cal relations are such that these nervous trunks are often compressed by the new 
growth or actually incorporated in it. Of the symptoms thus occasioned, the 
most frequent is paralysis of the motores oculi (oculo-motor and abducens). This 
is at first usually unilateral, but may later affect both sides. If one of the optic 
tracts is involved, hemiopia may result, and pressure upon one optic nerve may 
produce unilateral choked disk with unilateral disturbance of vision. Tumors of 
the pituitary gland are especially prone to cause symptoms referable to the optic 
nerve at an early period. Lesions of the trigeminus not infrequently cause dis- 
turbances of sensation in the face, and occasionally also paralysis of the muscles 
of mastication. The trunk of the facial often suffers. The facial paralysis thus 
occasioned throws considerable light upon the diagnosis, for there is usually to 
be found in the paralyzed muscles the reaction of degeneration, showing that the 
paralysis is peripheral. We have therefore reason to assume that the lesion is 
situated at the base of the cranium, rather than central. Another factor is 
almost always present to support the idea of a peripheral lesion — namely, the fron- 
tal muscles are involved {vide pages 529 and 691). Peripheral paralysis of the 
hypoglossal nerve may also be produced by tumors at the base of the brain; 
but this is much rarer than facial paralysis. Whether other nerves of special 
sense beside the optic are disordered is a question about which we possess little 
information as yet, but probably careful examination will not infrequently reveal 
changes in them. 

As might naturally be expected, various degrees and forms of paralysis in the 
extremities are often found in combination with the above disturbances of the 
cranial nerves. Such conditions are most frequent where the crus cerebri, with 
its pyramidal tract, is affected. There is no need of enumerating all the possible 
varieties of symptoms. We must consider them all carefully in each individual 
case, and then, by bearing in mind the anatomy of the parts, we shall, in a major- 
ity of instances, be enabled to determine with some approach to accuracy the 
place at the base of the brain where the new growth must be. Sometimes, but 
not often, we may be led into error by tumors which, though situated in the brain- 



TUMORS OF THE BRAIN. 



713 



substance and at a comparative distance, yet by their pressure give rise to indirect 
symptoms referable to the cranial nerves at the base. 

3. Tumors of the Cerebellum. — We shall refrain from describing the symp- 
toms which may be excited by tumors in other parts of the brain, with a single 
exception. Tumors of the cerebellum are comparatively rather common, and 
deserve a brief notice. The direct focal symptoms of cerebellar lesions, such as 
the peculiar pitching gait and the vertigo, have been discussed at page 683. But 
cerebellar tumors generally occasion also very strongly pronounced general symp- 
toms — namely, headache, mainly occipital; sometimes a spasmodic and persist- 
ent stiffness of the neck ; vomiting ; and visual disturbances, mainly due to the 
frequent existence of choked disk. Analogous to this last symptom would seem 
to be disturbances in other nerves of special sense. Thus, where the general 
intra-cranial pressure is elevated, the acoustic or olfactory nerves seem liable to 
passive congestion. Tumors in the posterior fossa have several times been found 
to occasion bilateral anosmia and deafness ; and they should always be considered 
where such a condition is found. 

General Course of Cerebral Tumors— The symptoms of these growths almost 
always cover a long period of time. Exceptionally a tumor remains latent till a 
haemorrhage or some similar event takes place in it, giving rise to sudden and 
grave symptoms, and possibly to an equally sudden termination. The rule is, 
however, for the phenomena to develop gradually. According to the location of 
a new growth, either the general or the focal symptoms may come first into 
prominence. They generally occur in the order named. First of all is an ill- 
defined, deeply seated headache ; and by degrees all the other general and focal 
symptoms follow after. The symptoms may vary repeatedly and greatly in 
severity, a fact due mainly to the varying pressure of the tumor on neighboring 
parts. Repeated mention has already been made of the sudden exacerbations 
which may come on, especially in case of the vascular gliomata. 

The entire duration of the disease is usually at least some months, and may be 
one or two years or more. The termination is almost invariably unfavorable. 
Death may be rather sudden, or it may not come till after a long period of wretch- 
edness. Fortunately, however, the lameness, blindness, and marasmus are fre- 
quently made less terrible to the patient because of his mental debility. Recovery 
is possible only where the growth is syphilitic. It is indeed possible that solitary 
tubercles may also end favorably, but the matter is still in doubt. 

Diagnosis. — The main points in support of a diagnosis of cerebral tumor would 
be the gradual onset and continuous slow increase of the general symptoms above 
detailed — namely, headache, vertigo, vomiting, convulsions, dementia, etc. The 
most constant of these symptoms is the headache. They all indicate the develop- 
ment of some chronic brain trouble, a tumor being the most probable if there be 
no definite aetiology to suggest some other process, such as traumatism resulting 
in abscess, or syphilis. Much stress may also be laid on the choked disk, which 
is much less often seen in case of abscess or softening than of tumor. 

The general symptoms indicate that a tumor of the brain exists ; but, in order 
to learn the position of that tumor, we have to rely mainly upon the focal symp- 
toms. Their gradual development and the way in which one new symptom is 
slowly added to another, also give further ground for the opinion that some 
continuously progressive disease exists, and most likely a cerebral tumor. Of 
diseases with a similar course, abscess is recognized by the absence of choked 
disk (an important point), frequently by febrile symptoms, and by its aetiology 
(trauma). Inflammatory and thrombotic softening, if they come on slowly, 
usually produce less general disturbance than do tumors, they seldom cause a 
choked disk, and (unless of syphilitic origin) are much rarer before middle age 



714 



THE DISEASES OF THE BRAIN. 



than tumors of the brain. Sclerosis sometimes simulates cerebral tumor; but 
here also there is no choked disk ; the disease lasts much longer (five or ten years, 
or more), and, inasmuch as the sclerosis is usually multiple, there is frequently 
too great a complexity of symptoms to warrant the assumption of one solitary 
lesion. 

Certain rare cases of chronic circumscribed meningitis can not be differen- 
tiated from a tumor. They generally occur at the base, lead to a considerable 
thickening of the tissues, and may simulate all the symptoms of a new growth in 
this region. Occasionally, also, chronic hydrocephalus is confounded with tumor 
of the brain. "We met with a case of dropsy of the fourth ventricle which pre- 
sented during life a perfect picture of tumor of the cerebellum. 

As to the nature of a new growth, we can not go beyond surmises. If the 
focal symptoms indicate that the tumor is in the substance of the brain itself, our 
first thought would be of a glioma, because it is by far the commonest sort of 
growth in that situation; and, as has been stated, certain peculiarities in the 
course of the disease (especially, if new symptoms add themselves abruptly) 
would make glioma probable. If, on the other hand, the tumor is at the base, it is 
most apt to be sarcoma, which is the most frequent form of new growths here. 
When symptoms referable to the optic nerve occur noticeably early, a tumor of 
the pituitary gland is to be thought of. In all cases, and especially in tumors at 
the base of the brain, we should bear in mind the possibility of syphilis. The 
previous history and the entire body of the patient should be closely searched 
with this point in mind ; its therapeutic importance need not be dwelt on. 

One special form of tumor deserves a brief mention here — namely, large 
cerebral tubercles. The growth may be single or solitary, or it may be multiple. 
It is seen chiefly in childhood, and any chronic cerebral disorder in a child should 
suggest the possibility of such a growth. It is rendered all the more probable by 
the co-existence of the signs of tuberculosis elsewhere, as in the lymph-glands, 
lungs, or bones. The symptoms are analogous to those produced by other tumors. 
Among the most frequent phenomena are headache and convulsions. The latter 
are often unilateral. There may also be all sorts of focal symptoms, according to 
the locality of the lesion. 

Prognosis. — Except gummata, all tumors of the brain have a very unfavor- 
able prognosis. It is said that in very rare instances tubercular growths have 
been arrested or cured ; but in practice we can never rely upon any such result. 
In all other cases recovery is next to impossible. The time intervening between 
the appearance of the first symptoms and death varies greatly, as has been said. 
We should therefore be very cautious in predicting the duration of the illness. It 
seldom, however, exceeds one or two years, and sudden death without any warn- 
ing may occur at any time. 

Treatment. — Inasmuch as the nature of the tumor can not be determined with 
absolute certainty in any instance, antisyphilitic treatment should always be tried. 
Forty to seventy-five grains of mercurial ointment (grm. 3-5) should be used by 
inunction, and thirty to seventy-five grains (grm. 2-5) of potassic iodide should be 
given internally each day. If the new growth is syphilitic, much benefit may be 
done in this way. It must be confessed that the treatment is generally of little 
avail, because the tumors are of a different character ; although it may be that 
iodide of potassium sometimes has a temporary good effect upon these. A long- 
continued course of arsenic has also been recommended, in order to check the 
growth of the tumor. This remedy particularly deserves a trial where there is a 
suspicion of solitary tubercle. 

Beyond what has just been indicated, treatment must be symptomatic. The 
headache is combated with ice-bags and narcotics ; the convulsions require bro- 



CEREBRAL SYPHILIS. 



Y15 



mide of potassium or the inhalation of chloroform ; the vomiting is lessened by- 
rest in bed, opium, and bits of ice. The general care and nursing of the patient 
are very important, so that bed-sores and the like may be avoided if possible. 

APPENDIX. 

HYDATIDS OF THE BRAIN. 

It was stated on page 413, that the cysticercus cellulosse, which originates 
from the taenia solium, may occur in great numbers in the brain. The cysticerci 
most frequently occupy the pia mater, but generally project downward into the 
cortex of the brain. The meninges not infrequently exhibit signs of chronic 
inflammation, and may present haemorrhages, which are not always minute. If 
there are numerous cysticerci in the neighborhood of the ventricles, a varying 
degree of internal hydrocephalus usually develops. The individual cysticerci are 
usually enveloped in a capsule of connective tissue, but may be entirely devoid 
of such a covering. 

No characteristic clinical sketch of hydatids in the brain can be drawn, because 
the symptomatology of each case differs according to the number and position of 
the parasites. Sometimes cysticerci produce absolutely no symptoms, and are dis- 
covered incidentally at the autopsy. In other instances they cause a long and 
tedious illness. Epileptiform convulsions seem to be the most frequent symptom, 
and must be due to the position of the cysticerci in the cortex of the brain. There * 
may also be general cerebral disturbances, similar to those of cerebral tumor, and 
including persistent headache, vertigo, and mental disorder. Focal symptoms are 
likewise possible, but on the whole are rare. 

The diagnosis can never be made with absolute certainty. The presence of 
cysticerci in the brain may be suspected when the above-mentioned symptoms 
occur in a butcher or other person who is from his calling especially exposed to 
infection, or who is known to have had or still to have a tape-worm, or in whom 
cysticerci have been demonstrated in some other part of the body, like the skin. 

We know of no remedy capable of destroying the cysticerci. Treatment, there- 
fore, can be only symptomatic. 



CHAPTER VIII. 

CEREBRAL SYPHILIS. 

JEtiology. — The importance of syphilis as an setiological factor in many chronic 
diseases of the nervous centers has been repeatedly adverted to in preceding chap- 
ters. Although with regard to its influence upon the spinal cord in exciting loco- 
motor ataxia and certain forms of myelitis there is still some obscurity, the brain 
presents with comparative frequency disorders unmistakably referable to constitu- 
tional syphilis. 

Cerebral syphilis is almost always a tertiary symptom. It is only in excep- 
tional instances that cerebral symptoms are produced by the end of a year from 
the date of the initial lesion. Usually the interval is several years, and it may be 
ten or even twenty. 

Liability to the disease does not seem to be essentially influenced by age or sex. 
Even hereditary syphilis has been proved to cause diseases of the nervous system. 
But it can not be denied that a predisposition to cerebral syphilitic disease is often 



716 



THE DISEASES OF THE BRAIN. 



engendered by those influences which are apt to promote cerebral disease in gen- 
eral. Just as the position of syphilitic cutaneous lesions is often determined by 
external irritation at some one place on the skin, so the disease seems more liable 
to attack a brain which is exposed to certain unfavorable conditions than one 
which is perfectly normal and vigorous. Such conditions are inherited tendency 
to nervous diseases, various injurious mental influences, poisons, in a broad sense, 
and traumatism. It need hardly be said that even a previously sound brain does 
not enjoy immunity from the affection. 

Pathology. — As far as has yet been ascertained, there are two chief forms as- 
sumed by syphilis in this organ : (1) a circumscribed syphilitic tumor, the gumma, 
and (2) a disease of the arteries of the brain, which is usually quite extensive. 
There is no essential difference underlying these two varieties. They may also 
occur in combination with each other. The disease of the blood-vessels is really 
a syphilitic new growth affecting the walls of the arteries. 

The circumscribed syphilitic tumors are yellowish or grayish-red, and fre- 
quently cheesy in the center. Their most frequent seat is the dura mater or the 
subarachnoid spaces, whence they spread to the brain-substance ; but exceptionally 
they may originate in the substance of the brain itself. Histologically they are 
made up of granulation tissue of varying degrees of vascularity, and presenting 
yellow spots usually visible to the naked eye. These spots are of firmer consist- 
ency than the rest of the growth, and have undergone coagulation-necrosis (have 
become cheesy) . Circumscribed gummata in the brain which have become cheesy 
» do not differ essentially in microscopic appearance from a collection of tubercles 
(see preceding chapter). The new growth sometimes takes on a more diffuse form 
in the meninges, particularly at the base (gummous meningitis). Often the 
originally delicate granulations become transformed into a firm connective tissue, 
forming extensive cicatricial induration. 

The syphilitic disease of the arteries was first fully appreciated by Heubner, 
who has described it accurately. It is usually most pronounced in the arteries of 
the base of the brain, aud especially in the middle cerebral artery and its branches. 
Even the unaided eye detects a grayish opacity in the arteries. They feel firm 
and stiff, and on cross-section their walls are found to be thickened, either uni- 
formly or in some places more than in others. This causes no inconsiderable nar- 
rowing of the lumen, or even its obliteration, particularly if the last gap is closed 
by the formation of a thrombus. The microscope shows that the new growth 
originates chiefly in the intima of the vessel, where there is a hyperplasia of the 
endothelium, and a gradual transformation of it into a firm connective tissue. 
But the adventitia also undergoes a gradual thickening of considerable extent. 
Syphilitic endarteritis presents no distinctive histological characteristics. Entire 
certainty that the inflammation is due to syphilis can be attained only by discov- 
ering other evidences of syphilis, whether in the brain or elsewhere, or from the 
personal history and the previous course of the disease. 

The great clinical importance of syphilitic endarteritis is due to its cutting off 
the normal supply of blood from the regions supplied by the diseased arteries. If 
the occlusion be complete, cerebral softening is inevitable, as in ordinary embolism 
and thrombosis of cerebral arteries ; and, inasmuch as the middle cerebral artery 
is particularly liable to the disease, syphilitic softening is most often found in the 
region supplied by this vessel. 

Clinical History. — The variety of the pathological processes and of their loca- 
tion produces a corresponding variety in the symptoms of cerebral syphilis. We 
shall, therefore, be obliged to limit ourselves to a brief description of some few 
types of the disease which are oftenest met with (Heubner). 

1. The group of symptoms may be mainly that of a cerebral tumor. Here 



CEREBRAL SYPHILIS. 



711 



there is a circumscribed new growth, situated either at the base or upon the con- 
vexity of the brain (and in the meninges). If at the base, the symptoms are analo- 
gous to those discussed on page 712. The focal symptoms are often preceded 
for a certain length of time by general cerebral symptoms, such as persistent head- 
ache, worse at night, wakefulness, mental depression, and impairment of mem- 
ory. Then paralysis of the nerves at the base of the brain comes on : the nerves 
controlling the motions of the eyeball suffer the most frequently, but the facial 
and other nerves may also be affected. 

In the second subdivision, where the syphilitic new growth is mainly upon 
the convexity of the brain, the picture is a tolerably characteristic one. Often in 
this case, also, prodromata similar to those just enumerated precede the severer 
symptoms. Then appear violent epileptiform convulsions. These often come on 
very suddenly, and may recur at considerable intervals or in quick succession. 
There are usually still other symptoms of cortical disturbance, especially paresis 
of one limb or even of one half the body ; very frequently slight disturbance of 
speech (stumbling over syllables), referable to the cortex, and indications of men- 
tal impairment. Many of these cases reach a fatal termination comparatively 
early. The epileptiform convulsions become more and more frequent, and uncon- 
sciousness increases into a deep coma ending in death. But it is in cases of 
just this sort that prompt and energetic treatment may accomplish a great deal. 

2. Another common variety of cerebral syphilis is characterized chiefly by 
syphilitic arteritis. Not infrequently there is a prodromal stage ; then, as a result 
of the occlusion of some vessel, which often occurs quite suddenly, there is a pro- 
nounced apoplectic attack, followed in most cases by hemiplegia. The intensity 
of the initial shock may vary greatly ; sometimes there is only a slight dizziness, 
sometimes there is a coma that lasts for days. Sometimes the shock is succeeded 
by a peculiar condition of mental confusion and dullness, which may persist for 
weeks. In severe cases, death is speedy, and is usually ushered in by a great rise 
of temperature. Other patients improve more or less rapidly, especially under 
proper treatment. 

Apoplectic attacks of this sort may recur after temporary improvement has 
taken place, and may be associated with all sorts of nervous symptoms. 

3. In a third class of cases, cerebral syphilis assumes the form of a diffuse 
chronic disease of the brain, closely resembling multiple sclerosis or certain types 
of progressive general paralysis of the insane. Perhaps it would be more correct 
to say that certain cases of cerebral syphilis are identical with general paralysis. 
There are gradual impairment of memory and of speech, and various motor symp- 
toms (tremor, ataxia, paralysis of single members). The intellectual powers grow 
less and less, and, after passing years as a physical and mental wreck, the patient 
at last dies, unless indeed he has the good fortune to be carried off earlier, in 
some apoplectiform or epileptiform attack. These cases often present compara- 
tively slight objective lesions. Probably there are changes in the minuter blood- 
vessels, or in the interstitial tissue, or in the parenchyma, which in part escape 
our present powers of investigation. 

Diagnosis. — While some few of the phenomena produced by cerebral syphilis 
are rather characteristic — we refer, for instance, to the intense prodromal head- 
ache, the epileptiform convulsions, and the apoplexy — still these symptoms alone 
are never sufficient to establish the diagnosis, for they may be precisely simu- 
lated in cases of tumor, softening, haemorrhage, multiple sclerosis, and other cere- 
bral diseases. The most important diagnostic criterion is in every case the demon- 
stration of the aetiology — that is, a previous infection with syphilis. We can not 
here describe in detail the methods of determining this fact. The history of the 
patient and the objective signs on other parts of his body are the two sources of 



718 



THE DISEASES OF THE BRAIN. 



information. There may be scars on the skin or raucous membranes, enlarged 
glands, ulcers, tibial periostitis, or changes in the testicles. Age is also impor- 
tant : thus an apoplectic attack in a young person would suggest syphilis, because 
the other causes of such an attack operate chiefly upon the aged. The results of 
treatment often throw considerable light upon the diagnosis. As there is nothing 
to lose and much perhaps to gain, we should always give specific remedies in 
doubtful cases. If they prove successful, the diagnosis of syphilis receives strong 
confirmation. 

Prognosis and Treatment. — There are few severe and dangerous diseases where 
timely and appropriate treatment may be attended with the success achieved in 
many cases of cerebral syphilis. In order, however, both to understand the favor- 
able results, and not to be misled by the failures, we need to gain a clear idea of 
the way in which antisyphilitic remedies can be of benefit. They can accomplish 
this only by causing the dissipation and absorption of the new growth — that is, 
the gumma or the swelling of the intima. If this is effected, the surrounding 
parts are, of course, relieved from pressure, and the circulation becomes unim- 
peded. If the tissues still retain functional power, they resume their duties and 
all symptoms of disease vanish. But, when the tissue has already been consider- 
ably impaired by the compression, or by the scanty blood-supply, the results are 
quite different. Even then the nervous trunks at the base of the brain may gradu- 
ally become regenerated ; but such parts of the true cerebral parenchyma as have 
undergone softening have lost their functional capacity for ever. In this case, 
antisyphilitic treatment is unavailing. 

It is, therefore, obvious that the first essential of success is to begin treatment 
as early as possible. The sooner a correct diagnosis is reached, the sooner will 
existing symptoms be relieved, and farther danger be averted. The method of 
treatment which will probably accomplish all that can be accomplished, and in 
the shortest possible time, is energetic mercurial inunction. At least a drachm 
(grm. 3-5) of mercurial ointment must be rubbed in every day at first, according to 
the ordinary method. We should not venture to restrict the diet unless the patient 
be well nourished and " full blooded." If he is anaemic and feeble, a generous 
regimen is demanded. Usually the internal administration of iodide of potassium 
is combined with the inunctions ; we should give thirty to forty-five grains (grm. 
2-3), or, in severer cases, even a drachm or a drachm and a half (grm. 4-6), daily. 
And the same remedy should also be given afterward, for a long time, in smaller 
doses. Where there is no benefit at all after twenty or thirty inunctions, there is 
little prospect of any appreciable improvement. In favorable cases, the mercury 
often begins to produce some effect after the fifth or sixth inunction ; and it may 
cause astonishingly rapid improvement. Potassic iodide alone is sufficient for the 
milder cases only, where there is merely headache, trigeminal neuralgia, or paraly- 
sis confined to the motores oculi. 

In many cases, some symptomatic treatment is also required. Narcotics, appli- 
cations to the head, electricity, baths, etc., are employed, as in other chronic cere- 
bral diseases, and they often supplement very efficiently the specific remedies. 



PROGRESSIVE GENERAL PARALYSIS OF THE INSANE. 719 



CHAPTER IX. 

PROGRESSIVE GENERAL PARALYSIS OF THE INSANE. 

{Paralytic Dementia. Paretic Dementia. General Paresis.) 

Preliminary Remarks. — Although the description of mental diseases is not 
properly a part of the plan of this book, we must, nevertheless, make an exception 
of one disease of the sort, namely, the so-called progressive general paralysis of 
the insane, or paralytic dementia, which, in medical parlance, is often abbreviated 
into u general paralysis." We consider it advisable to make this exception, 
because a great part at least of the symptoms of general paralysis are purely of 
a physical nature, and also because a knowledge of this disease, which is so com- 
mon and so fatal in its results, is of the greatest importance for the general prac- 
titioner. 

We must thank the French alienists Boyle (1822) and Calmeil (1826) for the 
first clinical descriptions of general paralysis, by which it was more sharply dif- 
ferentiated than previously from other diseases which run a like course. A more 
accurate knowledge of the different symptoms, and the anatomical changes to 
which the morbid symptoms must be referred, has, however, only of late years 
been rendered possible, by the introduction of better methods of investigation. 
Accordingly, we must now say that general paralysis is a disease which may attack 
the most diverse portions of the whole central nervous system * — the brain and 
spinal cord — at the same time or successively, but in which, of course, we can 
make out certain rules as to the predisposition of individual portions to disease, and 
in the order of the symptoms. General paralysis begins most frequently in those 
regions of the cerebrum which have an immediate relation to the regular course 
of the psychical and certain psycho-motor processes. Mental and motor symptoms 
accordingly form the introductory features of the disease in most cases. More 
extensive regions of the central nervous system are gradually involved in the 
morbid process, which goes hand in hand with a progressive degeneration of all 
the higher intellectual existence, while at the same time many physical disturb- 
ances, dependent upon the nervous system, constantly become more extensive. 

JEtiology. — General paralysis is a common disease, and apparently demands a 
heavier quota from the better and more highly educated classes than from the 
lower classes. We may assume that, on the average, one tenth of all patients 
committed to the insane asylums are general paralytics. In most patients the 
beginning of the disease falls in the period between the thirtieth and fiftieth year. 
The disease is much rarer in advanced life. In young people under twenty it has 
hardly ever been observed. There is no doubt but that the male sex is much 
more frequently affected than the female, but the number of cases of general 
paralysis among women is not very small. 

What is. the special cause of general paralysis ? A generally acceptable answer 
can not be given ; but the theory is constantly gaining ground, and we agree to 
it, from our own experience, that by far the most important causal factor lies in 
the existence of a previous syphilitic infection. Such an infection can be made 
out in at least seventy-five per cent, of all general paralytics. In this regard pre- 
cisely the same conditions exist, and, of course, the same difficulties in the inter- 
pretation of this relation are to be considered, as we have previously mentioned 



* At present hardly anything is known in regard to a primary implication of the peripheral nerves 
in the whole process of general paralysis. No theoretical objection can be raised to the supposition 
of such an implication. 



720 



THE DISEASES OF THE BEAIN. 



in the account of the dependence of locomotor ataxia on syphilis (see page 597), a 
circumstance which again is not without significance, since intimate points of con- 
nection are to be found between locomotor ataxia and general paralysis (vide 
infra). If we consider that general paralysis depends upon a previous syphilis, 
we have an easy explanation of most of the other peculiarities in the onset of the 
disease, especially the above-mentioned influence of age and sex, the decidedly 
common occurrence of the disease in persons in certain callings — like artists and 
officers — the frequency of the disease in large cities in distinction from its rarer 
occurrence in the country, etc. 

Beside the setiological factors named, which, in our opinion, are the most 
important, all other " causes " of general paralysis may well be regarded as merely 
predisposing. Mental over-exertion has the greatest significance, especially if it 
be associated with psychical irritation. In merchants, civil officers, etc., who 
suffer from general paralysis, such a previous over-exertion can often be made 
out. In some cases injuries to the head or insolation is claimed to be the cause. 
Hereditary predisposition to nervous diseases plays perhaps a certain part in the 
origin of general paralysis, but by no means a very large one. 

Clinical History. — General paralysis usually begins so slowly and gradually 
that a definite period for its beginning can hardly ever be given. In addition, it 
is often clear, at a period when the disease is already fully developed, that 
certain early symptoms, whose nature was at first not correctly recognized, ought 
to have been regarded as the initial symptoms. 

The first symptoms of the disease in the psychical domain usually consist of 
the gradual appearance of a change in the whole nature and in the mental indi- 
viduality of the patient; wherein, however, the mental disturbance usually shows 
from the start the character of weakness — that is, of a lessened capability of psy- 
chical exertion. The patient's ordinary mental work no longer goes on as easily 
as before. His memory is uncertain, and there are marked f orgetfulness and inat- 
tentiveness, which were previously quite impossible for him to exhibit. The patient 
is often disorderly in his dress, and violates the ordinary social rules of decency and 
morality. Since his judgment as to the value and significance of things is uncertain, 
he commits purposeless actions, wastes money, commits crimes, is dissolute, etc. In 
these respects, too, the increasing mental dullness often appears, since the patient 
becomes incapable of any higher intellectual, aesthetic enjoyment, and since the 
nobler sway of feeling finally becomes dulled, and can no longer exert any lasting 
influence upon his actions. Beside all these signs of beginning mental weakness, 
we often notice, on the other hand, an abnormal irritability. The patient easily 
becomes agitated, or gets angry ; but these humors rapidly pass away without 
leaving a lasting impression. We easily understand how this change in the whole 
personality of the patient must distress and alarm his family, since the relatives 
at first can not understand at all why the patient is now " so different from what 
he was." 

In the first period of the disease a subjective feeling of illness is very often 
present. The patient notices himself that his mental capacity, especially his mem- 
ory, is diminished, and he very often becomes extremely anxious on this account. 
It often happens that certain subjective sensations are also noticed, a feeling of 
confusion in the head, pressure in the head, dizziness, rheumatoid pains, etc. The 
sleep is disturbed, as a rule, and also the appetite and the digestion. If such a 
patient comes to the physician with his complaints, it unfortunately only too 
often happens that he is in the beginning regarded as "neurasthenic," and 
treated accordingly. 

Careful observation, however, may even now usually discover the disease with 
certainty. The beginning mental disturbance is usually more apparent to the 



PROGRESSIVE GENERAL PARALYSIS OF THE INSANE. Y21 



family than to the physician, who has not known the patient before, and sees him 
only cursorily, but it can usually easily be confirmed on a somewhat more search- 
ing examination of the patient. We generally succeed best by making the patient 
reckon ; he often makes the greatest mistakes in simple examples in multiplica- 
tion ; especially does he forget to add numbers carried in the mind, etc. 

Certain motor symptoms, however, which usually come on in the early stages 
of the disease, are of the greatest diagnostic significance, especially peculiar dis- 
turbances of speech and hand- writing. The paralytic disturbance of speech shows 
itself first in the form of stumbling over syllables (Silbernstolperri), or literal 
ataxia. The individual sound (in distinction from bulbar paralysis) can be pro- 
nounced quite correctly, but the combination of different sounds in the whole 
word causes increasing difficulties. It is a good plan, in order to recognize 





Fig. 101.— Examples of hand- writing in general paralysis. Attempts made by patients in the Danvers 
Lunatic Hospital to write "God save the Commonwealth of Massachusetts." Beside the motor dis- 
turbance, the frequent omission of certain letters will be noticed, e. g., " Masschuetts " for " Massachu- 
setts.'' 1 In 3 and 4 the hand- writing is almost wholly illegible. 

the first beginnings of this difficulty, to have the patient pronounce a few difficult 
words, such as "third riding artillery brigade," "representative government," 
" initiative," " electricity," etc. We often hear " artralleriry " instead of " artillery," 
and like blunders. In the later stages of the disease the speech is sometimes 
almost wholly incomprehensible. We also observe other more complicated apha- 
sic disturbances, like paraphasia, persistent repetition of the same word, etc. In 
such cases the patients are sometimes no longer able to read any sentence 
correctly. They at times put in entirely different words, so as to make utter 
nonsense — but they do not notice it themselves. The abnormal associated move- 
ments of the facial muscles on speaking are also often to be observed, and are 
very characteristic. The voice of general paralytics often loses its power of 
modulation and becomes weak and rough, symptoms which depend upon a 
46 



T22 



THE DISEASES OF THE BRAIN. 



defective innervation of the vocal cords. The change in the hand-writing, to 
be observed in general paralytics, is even more characteristic than the disturbance 
of speech (see Fig. 101). This is at first purely of a motor nature; the letters are 
uncertain, irregular, and tremulous. A psychical factor, however, also shows itself ; 
single letters are omitted, the dot on the i and the marks of punctuation are for- 
gotten, the patient ceases to keep on the lines, or leave a free margin, etc. If the 
disease advances, the disturbance in the hand- writing gradually increases, so that 
the writing may finally become wholly illegible, and may consist merely of sense- 
less scratches. 

Beside the changes in the speech and the hand-writing, which we have just 
briefly described, other physical disturbances are often quite early symptoms, and 
prove in how many parts of the nervous system at once the disease may begin its 
work of destruction. The condition of the pupils especially is of importance in 
diagnosis. They are often unequal, and also show a reflex immobility (see page 
606) in a large number of cases, especially in those in which other tabetic symp- 
toms develop {vide infra). Transitory ocular paralyses are at times early symp- 
toms. Not infrequently we find quite early changes in the tendon reflexes, either 
absence of the patellar reflex (a tabetic symptom) or an increase (beginning spastic 
paralysis of the legs). In the distribution of the sensory nerves we may mention 
as repeatedly observed symptoms, neuralgia, attacks of migraine, and finally 
optic atrophy, the latter usually as one symptom of a co-existing locomotor 
ataxia. 

We can not give a generally applicable account of the further course of general 
paralysis, since it may differ decidedly in this respect. In what follows we can 
point out only the main features of the different types of the disease, and, in 
particular, we will sketch only very briefly the groups of mental symptoms. 

We often say that those cases belong to the u classical form " of general paraly- 
sis where an initial " stage of depression " with a melancholy tendency is followed 
by a second stage of " maniacal exaltation. 1 ' This is the stage where the delusions, 
which are already quite pronounced, assume more and more the character of 
"grand ideas," and thus exhibit the " delusions of grandeur" which have for a long 
time been generally regarded as ominous. The first signs are often found in the 
patient's statements that he is now much better, that he is " very well," that he 
feels "very strong," etc. These delusions, however, often assume gradually a 
more exaggerated form ; the patient considers himself enormously rich, he owns 
thousands of palaces, millions of dollars, has made the greatest inventions, con- 
siders himself the Emperor Napoleon, Christ, a " higher God," etc. Any judgment 
as to the absurdity of these ideas, and as to the sad contrast between his claims 
and the reality, has already become impossible to him ; but, of course, there are 
even now occasional remissions in this condition, when the patient is clearer and 
recognizes temporarily the morbid character of his delusions. 

We must not think, however, by any means, that the delusion of grandeur is 
necessarily an invariable symptom in general paralysis. In many cases (the so- 
called " depressive " form of general paralysis) the initial melancholic-hypochon- 
driacal condition continues. The delusions that appear possess the same coloring; 
the patient claims that he can no longer eat, that he is poisoned, that he no longer 
has a head or an arm, that he is very small (" delire micromaniaque "), etc. Some- 
times acute and severe conditions of anxiety come on. In other cases, again (the 
agitated or maniacal form of general paralysis), there are states of violent excite- 
ment, in which the patient raves loudly, cries, and tries to destroy whatever 
falls in his way. Such states sometimes alternate with delusions of grandeur. 
Finally, we not at all infrequently see cases which, in their mental relations, 
present simply the symptoms of a mental enfeeblement gradually increasing to 



PROGRESSIVE GENERAL PARALYSIS OF THE INSANE. 723 



complete dementia, without ever showing, in any notable form, states of excite- 
ment, the development of delusions, etc. 

While the intellectual life steadily goes to utter ruin in the ways just stated, 
the physical disturbances of the disease, as a rule, gradually advance in a more 
severe degree. In many cases ataxia of the extremities develops, and also loss 
of sensibility and vesical disturbances — in short, the symptoms of locomotor 
ataxia. In these cases the tendon reflexes are almost always lost, and the pupils 
are often immobile. In other rarer cases, however, there is actual paralysis, first 
in the lower and then in the upper extremities. In these cases the tendon reflexes 
are often increased, so that the picture of " spastic paralysis " develops. Again, in 
other cases bulbar symptoms appear, like disturbances in swallowing or mastica- 
tory paralysis, and also ocular paralyses, usually as a part of the tabetic symptom- 
complex, etc. 

Peculiar attacks, which are among the commonest and most characteristic 
symptoms of general paralysis, are, however, of special interest, and sometimes 
even of marked importance in diagnosis. These "paralytic attacks" in their 
milder degrees sometimes appear even in comparatively early stages of the dis- 
ease. Then they usually consist of attacks of vertigo, an obscuring of conscious- 
ness, or even a loss of consciousness, coming on quite suddenly, and lasting from 
a few minutes to half an hour or more, and they are very often associated with 
mild hemiplegic or monoplegic symptoms. We very often see, beside the vertigo, 
a temporary feeling of weakness in the right arm, associated with a marked apha- 
sic disturbance of speech. To this there is often added some slight twitching 
in the affected extremities or in the face. In the further course of the disease the 
attacks usually increase, and are termed apoplectiform or epileptiform paralytic 
attacks, according as the conditions of paralysis or spasm predominate. The epi- 
leptiform attacks may often be repeated with great frequency — thirty or forty 
attacks a day or more — during which time the patient remains in an unconscious 
state. If the patients gradually return to consciousness, sometimes only after a 
week or two, we very often see, as a result of such severe attacks, a permanent 
impairment of the general condition, an increase of the dementia, etc. 

The other organs, apart from the nervous system, are only secondarily impli- 
cated in the morbid process. It may be mentioned briefly here that formerly, for 
a long time, stress was laid upon certain changes in the pulse, the pulsus tardus 
especially being thought to be characteristic ; but the numerous investigations of 
the pulse have so far not given us any significant or sure results. 

The temperature as a rule is approximately normal, or often somewhat sub- 
normal, but very marked changes in the temperature occur in connection with 
the paralytic attacks — sometimes elevations and sometimes very deep declines. 

The whole duration of the disease is in some cases only a few months (the 
"galloping" form of general paralysis), usually it is two or three years, and some- 
times much more. The most rapidly fatal form is that in which there is very 
soon a marked emaciation and a rapid loss of strength as a result of the sleepless- 
ness, the constant unrest, and the refusal of food. In other cases death ensues 
from the gradual and general loss of strength, or in a paralytic attack; or, finally, 
frequently from the onset of secondary conditions, like severe bed-sores, pyelo- 
cystitis, tuberculosis, intestinal diseases, etc. 

Pathological Anatomy and Nature of the Disease.— Considering the great diffi- 
culty of an accurate microscopic examination of the brain, it is not strange that 
our knowledge of the pathological anatomy of general paralysis is still very defect- 
ive. If we except occasional immaterial changes in the skull, like hyperostoses 
and the like, or in the meninges, such as hsematoma of the dura or secondary 
thickening of the pia over atrophied portions of the brain, the first striking and 



724 



THE DISEASES OF THE BRAIN. 



most important anomaly at any rate seems to be the atrophy of the brain, which 
affects chiefly the anterior half, especially the frontal lobes. In this region the 
convolutions are very much diminished, and the fissures are wider ; the weight of 
the anterior portion of the brain may be reduced to one fourth or one third of the 
normal. If we examine the convolutions microscopically we find that the dimi- 
nution of the whole organ depends chiefly upon a loss of nervous elements. The 
cortex usually shows the greatest changes. In fresh cases we sometimes see the 
signs of a mild " inflammation " — that is, we find vascular dilatation and little 
disseminated foci of round cells about the vessels, but the changes in the nerv- 
ous elements themselves are far more important, and consist essentially in a degen- 
erative atrophy. We must mention especially that in the cortex of the frontal 
lobes, especially marked in the straight convolution, and in the island of Reil, and 
also in other portions, we can make out with certainty, by the aid of good meth- 
ods of examination, a very considerable loss of the fine medullary nerve-fibers, 
mainly those which run parallel with the surface, and hence are termed " associ- 
ation-fibers " (Tuczek) ; but signs of degeneration and atrophy are very often to be 
seen in the ganglion-cells themselves. The destruction of the nervous elements is 
regarded by many investigators as secondary, since they lay the chief stress upon 
the marked changes in the interstitial tissue, such as increase of the connective 
tissue, numerous spider-cells, or thickening of the vascular walls, which are almost 
always to be found in old cases, and hence they speak of an interstitial encephalitis 
(Mendel). We ourselves, with Tuczek, Wernicke, and others, are much more in- 
clined to the theory that we have to do mainly with a primary process of degen- 
erative atrophy of the nerve-fibers and nerve-cells, to which the increase of the 
connective tissue is only a secondary addition. 

The anatomical affection in general paralysis, moreover, is by no means limited 
to the cerebral cortex. We can often make out the loss of fibers in the deeper 
parts also, in the white substance, and the central ganglia. The co-existing 
changes in the spinal cord, first accurately described by Westphal, and since then 
recognized as almost constant, are of especial interest. They usually consist of 
fascicular systemic degeneration of the lateral columns (the pyramidal tract), or 
the posterior columns. A large part of the physical disturbances of general 
paralytics, like tabetic symptoms or spastic paralysis (vide supra) , is certainly due 
not to the cerebral disease, but to these accompanying changes in the spinal cord. 

Accordingly, we believe that, according to our present knowledge, we can 
best conceive the nature of general paralysis in the following way : By the action 
of certain injurious influences, which usually seem to stand in some connection 
with syphilis (see page 596), there is a gradually progressive destruction of nerve- 
tissue in the most diverse portions of the nervous system. The clinical symptoms 
must naturally differ according to the significance and function of the affected 
fibers or cells. As a rule, certain cortical regions of the cerebrum are first dis- 
eased. The disturbances of speech are probably dependent upon the loss of fibers 
in the left island of Reil, the disturbances of intelligence upon the destruction of 
fibers in the frontal lobes. We may also make out corresponding anatomical 
changes, either cerebral or spinal, as an explanation of the later motor, tabetic, and 
other symptoms ; but in many cases the order in which the different sections are 
affected varies considerably. We have seen in a previous section (see page 609) 
that the whole process may begin with a spinal disease, especially locomotor 
ataxia, to which the paralysis is " added" later; but we must understand that the 
two conditions are wholly analogous to and co-ordinate with each other. Both 
are parts of the same degenerative process, which can accomplish its work of 
destruction in the most diverse regions of the nervous system. 

No coarse anatomical lesions can be made out, as a rule, to explain the 



PROGRESSIVE GENERAL PARALYSIS OF THE INSANE. 725 



paralytic attacks, but it is very probable that they depend, at least in great part, 
upon the changes in the motor central convolutions. 

Diagnosis. — Since the diagnosis of beginning general paralysis is of the great- 
est practical importance, we will once more mention briefly all those symptoms 
which are especially to be considered in diagnosis: Striking alteration in the 
behavior, rapid and motiveless change in the disposition, disturbances of mem- 
ory, loss of intelligence (failures in reckoning, etc.), the characteristic changes 
in the speech and hand-writing, and finally the somatic symptoms which often 
co-exist: difference in the pupils, immobility of the pupils, loss, or, more rarely, 
increase of the tendon reflexes, and mild paralytic attacks, like vertigo, disturbance 
of speech, temporary disturbance of motion in one arm, etc. 

We would also mention, as especially common and disastrous mistakes, that 
the symptoms of general paralysis are often misunderstood at first, and are regarded 
as the signs of immorality, the failure of the sense of duty, etc. It also fre- 
quently happens that general paralysis is at first regarded as simple neurasthenia 
or hypochondriasis, and treated accordingly. 

As a rule, general paralysis can be certainly distinguished from other organic 
nervous diseases by careful attention ; but of course we must add that in some 
cases cerebral tumors, syphilis of the cerebral arteries, and especially certain cases 
of multiple sclerosis, may show a type of disease very like general paralysis. 

Prognosis. — The prognosis of general paralysis, like that of all chronic degen- 
erative conditions of the central nervous system, is very unfavorable. At present 
we know of only a small and decreasing number of actual recoveries, but there are 
many cases where there is a temporary improvement in the condition, a " remis- 
sion," sometimes of a considerable degree and lasting a long time. The earlier the 
patient comes under proper care and treatment, the sooner may we hope for such 
a favorable turn. Of course, as we have said, relapses of the affection almost 
always come on later. Those cases especially are to be regarded as unfavorable 
in which frequent paralytic attacks come on early, in which other physical symp- 
toms, especially of a spinal nature, soon set in, and in which the whole nutrition 
of the body rapidly suffers. 

Treatment. — As soon as the disease is recognized, the first and imperatively 
necessary injunction must be to remove the patient from all physical and intellect- 
ual exertion as well as from all mental excitement. The patient must, therefore, 
if possible, withdraw from business, which, up to that time, he may have tried to 
carry on. His methods of life and his diet must be regulated, and every excess 
must be forbidden. For the cases which even at first are associated with states of 
great mental excitement, the commitment to a proper asylum is often most 
urgently to be recommended, while for cases that during their course show simple 
mental weakness, care at home is often sufficient. 

In regard to the treatment of the disease itself, we should advise inunction with 
mercurial ointment, especially if we can discover a previous syphilitic infection. 
As a rule, we ought not to expect much success from this any more than in loco- 
motor ataxia (see page 611), but we may perhaps check the advance of the disease. 
We should, therefore, try the anti-syphilitic treatment chiefly in the initial stages 
of the disease. We may combine the internal use of iodide of potassium with the 
inunction. 

Furthermore, we should try tepid baths, with cool sponging, and also a cautious 
application of electricity (galvanization of the head and spinal cord), and, of inter- 
nal remedies, ergotine especially. We need not go more fully here into the 
numerous symptomatic details. 



726 



THE DISEASES OF THE BEAIN. 



CHAPTER X. 
CHRONIC HYDROCEPHALUS. 

iEtiology and Pathology. — Repeated mention has been made in iDreceding 
chapters of the occurrence of dropsy in the ventricles as a sequel to other cerebral 
diseases, like meningitis and tumors. Beside this " secondary hydrocephalus," 
a collection of fluid in the ventricles may be a symptom of an apparently 
idiopathic primary disease. This is observed most of all in the new-born, or at 
least in young children. 

Little is known with certainty about the causes of chronic hydrocephalus. The 
assumption is very frequently made that the condition is the result of an inflam- 
mation of the ependyma of the ventricle, which itself occurs either before birth or 
very soon after ; but the autopsy often fails to support this idea. There is equally 
slight objective evidence that there is a stasis due to mechanical obstruction. 
Syphilis and dipsomania have been regarded as predisposing causes ; whether 
justly or not, is uncertain. It has been repeatedly observed that the disease has 
attacked several children of a single family. 

The most important physical sign of hydrocephalus in children is enlargement 
of the head. The circumference of the skull may even in the first year of life be 
sixty to eighty centimetres. Usually the frontal bones and the parietal eminences 
are especially prominent. The cranium becomes gradually almost as thin and 
translucent as paper. The fontanelles and sutures gape widely. The brain is 
flattened out, so as to seem almost like a bag, filled with the hydrocephalic fluid. 
In well-marked cases the entire thickness of the hemispheres is frequently not 
more than an inch. The space within, containing the serous effusion, represents 
the enormously distended ventricles, particularly the lateral ventricles, although 
the third and fourth ventricles are quite often distended also. The walls of the 
ventricles are often strewn with minute granulations ; or they present a reticular 
hypertrophy. The hydrocephalic fluid usually has the appearance of colorless 
serum, and contains a very slight amount of albumen, if any. The specific gravity 
is about 1004 to 1008. The amount of fluid may be a quart or more ; but, of 
course, there is great variation in this respect in different cases. 

Congenital hydrocephalus is not infrequently associated with other peculiarities 
or defects in the structure of the brain, into the particulars of which there is not 
space to enter here. 

Clinical History. — Sometimes a child is born with hydrocephalus so far devel- 
oped as to occasion dystocia. Usually, however, the parents notice nothing pecu- 
liar about the child for some weeks. Then they are alarmed by the gradual swell- 
ing of the head. As a basis for determini ug abnormal size, we may mention that 
under normal conditions the circumference of the head at birth is about forty centi- 
metres, at the end of a year about forty-five centimetres, and from that age to puberty 
there is a gradual approach to a circumference of about fifty centimetres. The pos- 
sible dimensions in chronic hydrocephalus have been already stated. The increase 
in circumference is often quite rapid, amounting in a fortnight or three weeks to 
one or two centimetres. Usually the swelling is tolerably symmetrical; but some- 
times the greater increase is in the antero-posterior diameter, making the skull 
dolichocephalous. At times the rate of expansion may be particularly rapid, and 
then at other times it may seem to be suspended. That the fontanelles and sutures 
remain widely open has already been mentioned ; sometimes it is even possible to 
get fluctuation through them. An intra- vascular murmur can now and then be 
heard in the head, but it has no great importance with regard to diagnosis. The 



CHEONIC HYDROCEPHALUS. ?27 

veins are often so greatly distended as to form a bluish network underneath the 
scalp. The face remains small, in striking contrast with the great, heavy cranial 
portion of the head. The head almost always hangs over forward from its weight. 
The eyes generally look down, partly because the roof of the orbit is depressed, 
and partly because of impairment of the nervous supply to the motores oculi. 

A very important symptom is the defective intellectual development of hydro- 
cephalic children. They can not learn to talk well, if at all. If they play, it 
is in a silly manner. They can not concentrate their attention upon anything, 
and they are heedless and dirty. It must, however, be mentioned that sometimes, 
in spite of considerable hydrocephalus, the patient now and then evinces an unex- 
pected activity of mind — thus, he gradually becomes able to distinguish the differ- 
ent objects and individuals about him. 

There is almost invariably motor disturbance also. The legs, more rarely the 
arms, are decidedly paretic, or there may be even complete paraplegia. There are 
usually spastic symptoms and increased tendon reflexes. Few patients learn to 
walk or stand alone. The arms seldom present any great paresis, but their move- 
ments often betray an awkwardness and uncertainty suggestive of ataxia. It is 
noteworthy that sensation almost always remains intact. At least the patient 
reacts vigorously to the prick of a pin, etc. Of the special senses, sight is most 
frequently affected ; choked disk and atrophy of the optic nerve have been observed 
repeatedly. Symptoms of motor irritation are of very frequent occurrence, such 
as general convulsions and spasm of the glottis. General nutrition is pretty well 
maintained in many cases ; but, as a rule, hydrocephalic children are atrophic and 
ill developed. 

The chronic hydrocephalus of children almost always terminates unfavorably. 
Only a few patients survive the fifth year, although now and then striking excep- 
tions occur. Death is generally the result of marasmus ; or a convulsive seizure 
may prove fatal. The possibility of recovery has not yet been demonstrated. The 
progress of the disease may, however, be arrested, and the child continue for years 
in statu quo. 

Hydrocephalus in adults is a very rare, chronic, and apparently idiopathic dis- 
ease. Its cause again is assumed to be a chronic inflammation of the ventricular 
ependyma. The symptoms are sometimes very like those of a tumor of the brain, 
and sometimes there is a remarkable absence of characteristic cerebral disturbance, 
except that spastic paralysis of the extremities (compare page 626) is gradually 
developed. 

Diagnosis. — A pronounced case of congenital hydrocephalus can be recognized 
without difficulty, inasmuch as the excessive size of the head betrays the disease 
upon the first glance. Less extreme cases may indeed be somewhat obscure, and 
we have especially to avoid confounding the condition in question with rachitic 
enlargement of the skull. We should always, therefore, take into consideration 
the intellectual powers, the presence or absence of motor disturbances, and other 
similar symptoms, as well as the cranial peculiarities. In the hydrocephalus of 
adults there is often no enlargement whatever, so that a diagnosis can hardly ever 
be declared positively. 

Treatment. — So far, no remedy has been applied with success in chronic hydro- 
cephalus. The following may be tried: Applications of mercurial ointment and 
of tincture of iodine to the scalp, methodical compression of the skull, and iodide 
of potassium internally. The hydrocephalic fluid has often been drawn off, to a 
certain extent, by tapping, but with merely temporary benefit, if any. 

Most physicians, therefore, confine themselves to hygienic and symptomatic 
treatment. 



728 



THE DISEASES OF THE BRAIN. 



CHAPTER XI. 

MENIERE'S DISEASE. 

( Vertigo ab aure Icesa. Labyrinthine Vertigo) 

In 1861, Meniere, a Trench physician, first called attention to a peculiar affection 
which sometimes results from chronic aural disease and is characterized mainly 
by excessive vertigo and loud tinnitus aurium. At first the symptoms appear in 
distinct paroxysms. These are ushered in by a shrill ringing in the ears, which 
is often compared to the whistling of a locomotive, and which is perceived in but 
one ear. At the same time, or shortly after, comes on a very pronounced dizzi- 
ness, of a unique sort. The patient has a feeling as if his whole body were mov- 
ing, as if he were falling forward or were whirling around. Consciousness is 
unimpaired, but the patient feels very badly, the skin is pale and cool, and the face 
is bathed in cold perspiration. Frequently there is vomiting toward the close of 
the attack. The first paroxysms are of brief duration. 

As the disease progresses, the attacks become more and more frequent, and at 
last the vertigo may be constant, being extremely annoying to the patient and 
perhaps confining him to bed. Even now there are occasional paroxysmal exa- 
cerbations of the disorder, usually ushered in by the shrill tinnitus. The tokens 
of chronic aural disease on one side, or less frequently on both sides, also persist. 
Sometimes there is purulent otorrhcea ; often the aural speculum reveals lesions 
of the drum or of the middle ear ; and almost invariably there is more or less 
deafness on the affected side. This condition may persist for years, until finally 
it ceases of its own accord, after the deafness on that side becomes complete. 

We possess scanty information as to the origin of these subjective phenomena. 
That they are due to a disease of the internal ear (labyrinth) can scarcely be 
doubted ; and it is further probable that in every case the semicircular canals are 
involved. Numerous experimental investigations have demonstrated that these 
last-named structures bear a part in maintaining the equilibrium of the body. 
Acquaintance with this variety of vertigo is valuable to a nervous specialist, inas- 
much as Meniere's disease has been more than once confounded with epilepsy and 
disease of the cerebellum and other parts of the brain. 

Treatment is not wholly unavailing. Charcot has discovered that the persist- 
ent use of quinine almost always gives great relief, and may even completely cure 
the disease. Eight to fifteen grains (grm. 0*5-1) of quinine should be given daily v 
in two or three doses, and continued for at least several weeks. The particulars 
of such special treatment of the ear as maybe necessary must be sought elsewhere. 



EPILEPSY. 



729 



VI.— Neuroses without known Anatomical Basis. 



CHAPTER I. 

EPILEPSY. 

{Falling Sickness. Morbus sacer.) 

JEtiology. — Epilepsy is a peculiar disease of rather frequent occurrence, the 
main symptom of which is paroxysmal loss of consciousness. In typical cases 
the unconsciousness is associated with violent general convulsions ; but there are 
many anomalous and rudimentary forms of epilepsy without any symptoms of 
motor irritation. " Genuine epilepsy " is a functional neurosis — that is, with our 
present means of investigation we can discover no constant objective lesion of the 
nervous system as its basis. It is, indeed, true that attacks similar to those of true 
epilepsy not infrequently occur in the course of tumor, syphilis, and other diseases 
which do present an anatomical lesion; but such attacks are merely symptomatic, 
and are therefore termed " epileptiform," in distinction from the genuine epileptic 
paroxysms. 

Of the actual causes of epilepsy we know nothing. We are acquainted only 
with certain factors which are favorable to the development of the disease, and are 
to be regarded, therefore, as predisposing or exciting causes. Heredity is decidedly 
the most important of these. About one third of all cases of epilepsy occur in 
persons who have inherited a nervous diathesis, and one or more of whose blood- 
relations have suffered from diseases of the nervous system. It should not be 
understood that we must find other cases of genuine epilepsy in the family, in 
order to establish the fact of congenital predisposition. The question is merely 
whether the ancestors have exhibited a general tendency to nervous disease. The 
more accurate and careful our investigations, the oftener shall we find among the 
relatives of the patient instances of nervous trouble — sometimes genuine epilepsy, 
sometimes insanity, hysteria, or general u nervousness." Of course these " nervous 
families " present, beside those that are actually ill, others who are more or less 
peculiar and odd, and yet others who have extraordinary talents, although fre- 
quently somewhat ill-balanced. It is said that the children of parents who are 
related to each other are somewhat predisposed to epilepsy, as well as to other 
nervous diseases. But certainly this factor is very rarely of importance. Perhaps 
dipsomania in the parents is somewhat more prejudicial in this regard ; it is said 
to have been repeatedly observed that children begotten while the father was 
intoxicated became epileptic. 

There are other influences which are assumed to have setiological importance, 
but whether justly or not is difficult to decide. Alcoholic excesses can seldom act 
in this way (although epilepsy is said to attack absinthe-drinkers in France quite 
frequently). Venereal excesses, probably, have still less importance. It should 
also be borne in mind that not infrequently excesses in these directions are the 
result of neurotic tendencies already existing. Syphilis has no direct connection 
with genuine epilepsy. Epileptiform convulsions may, as we have seen, be symp- 
tomatic of syphilis, being due to the cerebral lesion caused (vide page 717) by this 



730 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



latter disease. Certain factors may determine the onset of epilepsy, although they 
can not be said to cause the disease. Such are over-exertion of mind or body ; 
repeated emotional disturbance ; certain general conditions of the system, like 
anaemia or malnutrition, on the one hand, and plethora on the other ; and, in 
particular, acute febrile diseases, like scarlet fever, measles, and gastritis. Another 
important point is that the first attack is sometimes brought on by great mental 
excitement, especially fright. But here, too, it is probable that the terror is merely 
the inducing cause — a tendency to the disease already pre-existing. We must also 
be on our guard against confounding genuine epilepsy with the convulsive form 
of hysteria (q. v.), which very frequently develops after fright. 

In some instances there is an evident connection between epilepsy and a pre- 
vious injury to the head, as from a fall, blow, or cut. At a certain interval after 
the trauma, attacks begin which seem precisely like those of genuine epilepsy. 
This is known as "traumatic epilepsy." But these are not cases of genuine epi- 
lepsy, inasmuch as there is really some anatomical lesion of the cortex cerebri 
which in some way, as yet unknown, causes irritation of the motor centers of the 
cortex (vide infra). It is often the case that this sort of epileptiform attacks is 
peculiar in that the convulsions are at first unilateral, or confined to a single limb, 
corresponding to the seat of the injury in the opposite cerebral hemisphere. 

" Reflex epilepsy " remains to be mentioned. This name is applied to cases 
where each convulsive attack seems to be excited by reflex influence, originating 
in some one part of the body. Most cases have followed traumatic injury of 
peripheral nervous trunks (retained splinters, or scars), and have ceased upon 
removal of the exciting cause. Other causes are new growths in the nerves, 
foreign bodies in the ear, otitis, intestinal parasites, and, apparently, diseases of 
the female sexual organs. But it seems probable that sufferers from these attacks 
have had a tendency to disease of the nervous system. We must hesitate to rank 
reflex epilepsy in the same class with the genuine form. 

Both the traumatic and the reflex varieties of epilepsy have repeatedly been 
the object of experimental investigation. Brown-Sequard has shown, by a great 
number of experiments, that epilepsy can be excited in rabbits by injuries to the 
medulla, the spinal cord, and the sciatic, as well as other peripheral nerves. A 
certain time after the operation, the animals undergo spontaneous convulsive 
paroxysms. These occur at frequent intervals for a long time, and may be volun- 
tarily excited at any time by irritation of a certain portion of the skin, called the 
" epileptogenous zone. " An interesting observation in this connection has been 
made by Brown-Sequard, which is that sometimes the progeny of these animals, 
who have been made epileptic, suffer from spontaneous epilepsy. Westphal 
induced epilepsy in guinea-pigs by blows upon the skull. Immediately after the 
blow general convulsions occurred, but soon entirely ceased. Afterward, how- 
ever, there were repeated epileptiform attacks. Westphal thought that the causa- 
tive lesion in these instances was the minute haemorrhages which were found in 
the upper part of the cervical division of the cord and in the medulla. 

Further experiments bearing upon the same subject will be discussed later on. 

Clinical History. — In describing the symptoms of epilepsy, we shall first con- 
sider the various forms of the epileptic paroxysm, and then describe the general 
course of the disease. 

1. The typical epileptic paroxysm is usually described, for the sake of greater 
clearness, as made up of several stages. First is the prodromal stage, or, accord- 
ing to Galen's expression, still in vogue, the stage of the epileptic aura [aura = 
breath). Not infrequently, however, there is no aura whatever, the convulsions 
coming on without warning. But in many cases the prodromata are well marked, 
and are repeated with remarkable regularity and similarity before each individual 



EPILEPSY. 



731 



attack, although the different cases of epilepsy differ greatly as to the special 
phenomena of the aura occurring in each. 

The best manner in which to distinguish the various forms of aura is accord- 
ing to the nature of the nervous phenomena, whether sensory, motor, vaso-motor, 
or psychical. Of these the most frequent is, beyond a doubt, the sensory. Here 
we have peculiar paresthesia?, beginning in an arm or leg, or perhaps in the 
region of the heart or stomach, and thence usually "mounting to the head." It 
is seldom that the peculiar sensation is actually like a " breath " or puff of air. 
The aura which proceeds from the epigastrium is sometimes associated with a very 
disagreeable feeling of oppression and anxiety, and often also with nausea and 
vomiting. The aura may be referred to the nerves of special sense. In certain 
instances the patient perceives an unpleasant odor, which he likens to some familiar 
one. An aura of taste also occurs, but it is very rare. An optical aura is much 
more frequent, consisting in a subjective sensation of color or light, in an apparent 
increase or diminution of the size of surrounding objects, or finally in actual hal- 
lucinations of vision, such as beholding all sorts of human or brute shapes. An 
auditory aura is not very rare: it produces a sudden feeling of deafness in one ear, 
or various subjective sounds, like whistling, humming, or roaring. 

The motor aura takes the form of mild premonitory contractions, affecting the 
head, face, arm, or leg. There may be aphasic disturbance at the same time ; or 
we may observe symptoms of irritation of the non-striated muscles (strangling, or 
a desire to go to stool). Sometimes there are prodromal vaso-motor phenomena, 
where the aura consists in a sensation of cold or warmth, often associated with 
excessive pallor or redness of the face or hands. An attack may be ushered in by 
chilliness, perspiration, or palpitation. 

Finally, the name of psychical aura is applied to an initial impairment of con- 
sciousness, with vertigo, confusion of thought, etc. A particularly frequent form 
for this to assume is excessive mental uneasiness and excitement. 

Various forms of aura are not infrequently seen in combination. 

The aura lasts sometimes only a few seconds. It may persist long enough for 
the patient, who knows from experience what is coming, to lie down or take other 
precautionary measures (vide infra). In some few cases the aura may last hours, 
and even days. This is especially true of the psychical variety. Sometimes the 
aura passes away without being succeeded by any true epileptic fit ; but it is 
usually followed by the second stage of the attack — the convulsive stage. 

The convulsions almost invariably begin abruptly. Perhaps there is no aura, 
or only a very brief one, before the patient falls suddenly to the ground, usually 
on his face, although sometimes on the side or back. Consciousness is entirely 
suspended. Insensibility is complete, and often the patient sustains severe 
injury from his fall. Some patients utter a loud "epileptic cry" at the com- 
mencement of the attack ; but they are already entirely unconscious. 

The convulsive stage begins with a brief period of general tonic spasm of the 
muscles. The head is usually strongly extended, the teeth are pressed firmly 
together, the trunk is curved backward in opisthotonos, the extremities are 
extended, and the fingers are clinched over the flexed thumb. Inasmuch as the 
respiratory muscles participate in the seizure, breathing stops, arid the original 
pallor of the face soon gives place to deep cyanosis. This general tonic convul- 
sion ordinarily is but brief, say fifteen to thirty seconds. It is followed by the 
second period of the convulsive stage — that of the clonic convulsions. The facial 
muscles now exhibit the most violent contortions ; the eyeballs roll, or occasion- 
ally present a conjugate deviation toward one side ; the tongue is thrust out and 
retracted convulsively ; the head beats violently against the floor ; and the mus- 
cles of the arms, legs, and trunk undergo the severest clonic spasms. The pupils 



732 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



are probably contracted for a short time at first, but during the convulsive stage 
they are widely dilated and do not react at all. The pulse is somewhat accel- 
erated, but not greatly. The temperature is normal, or elevated a small fraction 
of a degree. The cutaneous reflexes are still suspended directly after an attack ; 
but the tendon reflexes are generally somewhat exaggerated, although sometimes 
they also are diminished or absent. Not infrequently an involuntary dejection 
takes place during the fit, or the bladder is emptied ; and in men there may be a 
seminal emission. During these violent convulsions the body is often severely 
injured. The tongue is frequently bitten. The venous stasis is so extreme that 
sometimes minute haemorrhages occur into the conjunctiva, the skin of the face, 
and other parts. 

The convulsive stage usually lasts several minutes. Then the contractions 
cease, often after a deep, long-drawn sigh ; and the patient passes into the third 
stage, of post-epileptic coma. He lies unconscious, but his respiration grows quiet, 
and the cyanosis vanishes. Gradually the coma yields to slumber, which may 
persist for some hours ; but some patients remain only a very brief time in this 
stage, and recover from their attack with surprising rapidity. It is, however, not 
infrequently the case that for some days after-pains are felt ; there are headache, 
languor, and exhaustion, and mental despondency and irritability. For some 
time there may be severe pain in the muscles, particularly those of the trunk. 
There may be slight paresis of one limb or one side of the body after an attack ; 
but this speedily vanishes again in cases of pure epilepsy. In the urine first passed 
after the seizure is often found a trace of albumen, and perhaps a few hyaline 
casts. Not infrequently there is also decided polyuria for some time subsequent 
to the fit. 

2. The Milder, Rudimentary Forms of Epileptic Seizure. Petit Mai. — 
Beside these violent paroxysms just delineated (" grand mal "), there are very 
often witnessed in epilepsy milder attacks of so-called " petit TnaV Sometimes 
there is only a transitory dizziness, or slight faintness, or perhaps a brief 
loss of consciousness, but without accompanying symptoms of motor irritation. 
These milder attacks may or may not be preceded by an aura. Cases have been 
seen repeatedly where the patient suddenly pauses in the midst of conversation, 
card-playing, piano-playing, or other occupation, stares absently for a moment, 
and then, with equal abruptness, goes on with what he was doing, as if nothing 
had happened. In other instances the patient pursues his occupation during this 
brief suspension of consciousness. For example, if seized while upon the street, 
he walks on mechanically, but takes the wrong turning, or goes into a strange 
house, when suddenly he comes to himself and wonders to find himself where he 
is. Cases of " sudden somnolence " are also almost all of them ascribable to epi- 
lepsy. There are all sorts of transitional forms between the slight attack of vertigo 
and the typical epileptic fit. Not infrequently the patient falls down unconscious, 
but has only a slight twitching of the face or arm, and in a few minutes is entirely 
himself again. 

[The medico-legal bearings of epilepsy, in its mild as well as in its severe form, 
are very important, but can be only alluded to here.] 

3. Epileptoid Conditions. — Cases of petit mal are generally rudimentary forms 
of the typical epileptic paroxysm, and consist merely in a simple impairment of 
consciousness, possibly associated with slight motor symptoms ; but, in the epilep- 
toid state, the character of the typical epileptic attack is almost indistinguishable. 
The disturbance is paroxysmal, and it can often be shown to be connected with 
genuine epileptic seizures ; else, its undoubted relation to epilepsy would never 
have been recognized. The greatest practical importance attaches to Samt's 
"psychical equivalents of epilepsy." These are attacks of mental disturbance, 



EPILEPSY. 



733 



which either immediately succeed a typical epileptic fit (" post-epileptic insanity "), 
or occur independently. The patient is completely deranged, and may do the 
strangest things — may strip himself, steal, jump into the water, or commit incen- 
diarism. Here the mind may be said to be only clouded, as compared with other 
instances where there is violent psychical excitement, associated with terror, 
frightful hallucinations, and resultant maniacal excitement. Not infrequently 
the patient is led to acts of violence against those about him. In the young, the 
attack may take a peculiar form : the child runs about in a peevish way, collects 
all sorts of things together, makes strange motions, etc. Almost always the 
patient, on recovering consciousness, remembers nothing, or almost nothing, of 
what has happened. Numerous and valuable particulars upon this subject, and a 
consideration of its great medico-legal importance, must be sought in text-books 
on insanity. 

Another form of epileptoid attack is the epileptoid sweating of Emminghaus, 
a spontaneous outbreak of excessive perspiration in epileptics, which may or may 
not be associated with impairment of consciousness. 

General Course of the Disease. — In a large majority of cases epilepsy begins 
before the thirtieth year. Often the disease appears in early youth, and sometimes 
in even the earliest years. Many a child has u convulsions from teething," which 
later on are seen to have been epileptic. It is only in rare instances that the first 
appearance of trouble occurs in advanced life. 

It is impossible to give any general rule as to the frequency of the paroxysms. 
Different cases differ very much. There are persons who, during their whole life, 
have no more than three or four seizures, at intervals of ten or fifteen years, while 
in most cases there is an attack every two to eight weeks. In severe types the fits 
may even recur daily. One very often sees certain variations in the course of the 
disease — at some periods the intervals between the attacks will be longer, and 
at others shorter. In severe cases the patient may have for several days very 
frequent seizures, so that he does not regain consciousness at all between them. 
This is termed the epileptic state (etat de mat). The condition is quite rare. It 
is often fatal, death being ushered in by a great rise of temperature. 

External influences sometimes affect the frequency of epileptic attacks. Alco- 
holic or sexual excess, mental excitement, and physical over-exertion almost 
always exert a malign influence. An opposite effect is often experienced where 
a quiet life is led, with every attention paid to hygiene arid pure air. In women 
the appearance of the catamenia is not infrequently the signal for the occurrence 
of an attack. In many instances the disease begins with the first establishment of 
menstruation. Sometimes, however, epileptic girls grow better when they arrive 
at puberty. Pregnancy sometimes increases and sometimes diminishes the fre- 
quency of the paroxysms. Intercurrent diseases seem frequently to exert a bene- 
ficial influence upon the frequency of the attacks. 

There is a practical distinction between diurnal and nocturnal epilepsy. Many 
patients have attacks only during the day, while others again have them only at 
night. A case of purely nocturnal epilepsy may go on for a long while unsuspected, 
particularly if the patient sleeps alone. The latter seldom has, on the next morn- 
ing, the slightest recollection of his attack during the night. He usually perceives, 
however, from a confused feeling in his head, or from certain injuries, such as a 
bitten tongue, or from the disordered state of the bed, that something must have 
happened to him during the night. In some cases of nocturnal epilepsy the 
patient wakes up out of sleep before he enters into the epileptic state of uncon- 
sciousness. Probably he is aroused by the aura. Beside cases where the fits 
occur during the day or the night only, mixed forms are frequently seen. 

With regard to the occurrence of the different varieties of epileptic seizure, all 



734 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



sorts of combinations are possible. Many cases never bave any but tbe typical 
convulsions ; but in many others there are also a greater or less number of attacks 
of petit mal. The latter may even be for a long period the sole indication of the 
disease. Often there are no epileptoid conditions whatever, while in other 
instances the '* psychical equivalents " are the most prominent feature of the dis- 
order. 

During the interval between the individual attacks many epileptics seem per- 
fectly well, both physically and mentally. They are not infrequently, to be sure, 
somewhat peculiar and nervously excitable, or again dull and lethargic ; but this 
does not by any means apply to them all. Many epileptics, and particularly such 
as have comparatively infrequent paroxysms, are very capable ; and history 
furnishes numerous examples of eminent men who suffered from this disease— for 
instance, Caesar, Mahomet, Rousseau, and Napoleon I. 

Much effort has been devoted to the discovery of " signs of physical degener- 
ation" in epileptics. Relying upon numerous measurements, Benedikt believes 
that a majority of epileptics exhibit craniometric anomalies, such as asymmetry 
of the cranium, macrocephalia, or steepness of the vertex. It is also not unusual 
to meet with anomalies of the auricles, teeth, or hands * in such cases. And, 
indeed, all peculiarities of this sort are, in general, more frequently observed in 
neuropathic families than in healthy ones. 

When the disease has lasted some time, and particularly if the attacks come at 
very short intervals, the general condition of the patient often undergoes a 
gradual but marked change. This rule is by no means invariable. The mind 
becomes more and more affected. The intellect grows feeble, memory grows 
weaker, and occasionally there is at last dementia. In such cases the body also 
suffers. There are emaciation, paresis, tremor, and other persistent disturbances 
of cerebral origin. 

Duration. — Epilepsy must be termed a life-long disease. To be sure, it is no 
rare thing for the paroxysms to cease and not return for years. But one can 
never rest satisfied that all trouble is at an end ; some cause or other may excite 
another attack after a long interval. In general, an epileptic has a shorter life- 
expectancy than healthy persons, especially as he may be carried off by chronic 
pulmonary or other intercurrent disease. 

The prognosis is obvious from what has been already said. The individual 
seizure is only exceptionally dangerous of itself. Often the so-called " status epi- 
lepticus " ends fatally, as above stated. In general, those cases may be called the 
most favorable where the separate paroxysms are infrequent and mild ; but even 
here the disease may suddenly assume an aggravated form. With regard to the 
distinction between nocturnal and diurnal epilepsy, the nocturnal is, in our 
opinion, the milder of the two. 

Pathology. — The very fact that in the intervals between attacks the patient 
often betrays no sign of disease, shows that epilepsy can not be due to any per- 
sistent macroscopic lesion of the tissues. Indeed, in many cases nothing is found 
at the autopsy, or at most changes which can not be regarded as essential, such as 
osteosclerosis of the cranium or thickening of the cerebral meninges. Epileptic 
subjects who were during life decidedly demented, usually present atrophy of the 
hemispheres. Meynert states that changes in the pes hippocampi major are 
noticeably frequent in epilepsy ; but these changes are not at all constant, and 
their significance remains to be established. 

We must therefore, for the present, be content to assume that the cause of the 
epileptic seizure is an intermittent functional condition of irritation. A natural 



* We have lately seen an epileptic man who had six fingers on each hand. 



EPILEPSY. 



Y35 



question is, Where shall we locate this irritation, and what may be its nature ? 
The opinion was long current that the medulla oblongata must be regarded as the 
true seat of the disease. Schroder van der Kolk was the first to express this opin- 
ion. It afterward received support from the experimental investigations of Noth- 
nagel, who demonstrated that irritation of a particular spot (" convulsive center") 
in the pons, in rabbits, invariably excites general convulsions. Nevertheless, 
most pathologists have now abandoned this view, because experiment and clinical 
observation indicate with increasing distinctness that the origin of epileptic con- 
vulsions is to be sought in the cortex cerebri. The clinical evidence is the 
invariable combination of convulsions and impairment of consciousness ; the cir- 
cumstance that the milder and the masked forms of epilepsy, now known to be 
intimately related to the true epileptic convulsions, also, almost without exception, 
indicate psychical disturbance ; that attacks, the symptoms of which are perfectly 
analogous with those of epilepsy, are often found to be the result of anatomical 
lesions of the cerebral cortex ; and, finally, that these convulsions in man and the 
convulsions of " cortical epilepsy " {vide infra), experimentally produced in ani- 
mals, extend over the different groups of muscles in a way which corresponds pre- 
cisely with the anatomical position of the different motor centers in the cortex 
(Hughlings Jackson). For example, if the convulsion begins in the distribution 
of the facial nerve, it extends from this point to the arm before it affects the leg. 

There is also experimental evidence that epileptic paroxysms are of cortical 
origin. A great number of observers (Hitzig, Ferrier, Albertoni, Luciani, Franck, 
and Pitres) have proved that electrical irritation of the motor regions of the cortex 
in animals will produce epileptiform convulsions. Unverricht has made some of 
the latest and most thorough investigations in regard to this point upon dogs. He 
found that when a motor center is stimulated the convulsions spread from the 
corresponding group of muscles to others in a way which corresponds precisely 
to the anatomical position of the separate centers. If one of the centers in the 
cortex is destroyed, the convulsions of the corresponding muscles cease at once. 
This proves that the motor centers must be intact in order to render the occur- 
rence of epileptic seizures possible. Just how the stimulation extends from one 
center to another, we have as yet no certain information. Probably it travels 
horizontally through the cortex. 

We see, therefore, that in all probability the seizures in man also originate in 
the cortex of the brain. The phenomena of the aura are likewise referable to 
some stimulation of the cortex, probably of the sensory region in most cases, as in 
the optical aura. The manner in which the irritation is created is as yet entirely 
conjectural. Kussmaul and Tenner proved that epileptiform convulsions can be 
excited by a general cerebral anaemia ; and this fact was the main foundation for 
the assumption that the genuine epileptic convulsions are also due to a temporary 
cerebral anaemia, caused, it may be, by local vaso-motor constriction. Definite 
proof has not yet been furnished on this point. In the artificial epilepsy which 
Unverricht produced, and that also which Magnan excited by absinthe, the cortex 
of the brain was not strikingly anaemic. 

Diagnosis. — Most cases of epilepsy are easily recognizable. It needs only to be 
borne in mind that epileptiform convulsions may also occur as a symptom of cere- 
bral diseases which do have an anatomical basis, such as tumor, abscess, multiple scle- 
rosis, and hydatids. As a rule, however, such diseases are readily distinguished by 
the state of the patient between the seizures, or by the further course of the illness. 
It should also be understood that unilateral convulsions, or such as are confined 
to a single member (Jacksonian epilepsy, vide supra, page 675), are usually not 
true epilepsy, but symptoms of some circumscribed affection of the cortex. The 
differentiation from hysterical convulsions (q. v.) is seldom difficult. Weight 



736 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



should be laid on the general character of the attack, the complete loss of con- 
sciousness in epilepsy, the dilatation of the pupils, which do not react to light, the 
initial pallor not infrequently observed, and the late cyanosis of the face. It is 
mainly the same factors which will enable us to detect simulated epilepsy. Here, 
also, there is an absence of those bodily injuries, such as a bitten tongue, which 
are often so characteristic of the genuine disease. 

Treatment. — Although no remedy is capable of working a certain and perma- 
nent cure of epilepsy, yet a favorable influence can be exerted upon the disease in 
many ways, so as to lessen the frequency and severity of the paroxysms, and to 
avert many of their evil results. 

In the first place, regimen is of great importance. Any excessive exertion of 
mind or body must be forbidden. Temperance must be exercised in eating and 
drinking. Alcohol, strong coffee, and tea, can be used only moderately ; nor is 
too much smoking permissible. The diet should be simple and unirritating, and 
vegetable rather than animal. It is said that in some cases decided improvement 
has been brought about by confining the patient to milk and vegetables. In 
summer, the patient should live quietly in the country or the mountains. We 
have also the individual constitution to consider : a weak and anaemic person 
must have iron and abundant nourishment ; and a full-blooded, corpulent indi- 
vidual should drink the natural aperient waters, and live abstemiously. 

Proceeding to the treatment of the disease itself, we shall rarely find any cause 
to remove ; although, in a few cases of reflex epilepsy, the excision of old scars, 
the extraction of foreign bodies, or trephining the skull, where the disease has 
followed an injury, have brought about permanent recovery. In genuine typ- 
ical epilepsy we have no such indications to fulfill, and must have recourse to 
such treatment as experience shows can influence favorably the outward mani- 
festations of the disease. 

Among symptomatic remedies, potassic bromide has an undisputed right to 
the first place. It was first recommended by Locock in the year 1853. It should 
be the first thing tried in any severe case. Apparently it acts by directly lower- 
ing the sensitiveness of the motor centers of the cortex to irritation. Rather 
large doses are requisite. Beginning with about one drachm (grm. 4-5) a day, we 
may find it advisable to increase up to two or two and one half drachms (grm. 
8-10). It may be prescribed in water (1 to 10 or 15), or in powders which the 
patient himself is to dissolve in water, sweetened if desired. The remedy in 
almost all cases needs to be used for months and years, and it is therefore often 
advisable for the patient to buy a half-pound or a pound and weigh it out him- 
self into the proper doses. It should always be taken in a good deal of water, say 
half a tumbler or more, to avoid irritating the stomach. The total amount for 
the day is usually divided into two or three portions ; but the whole may be dis- 
solved in a large amount of water and drunk gradually through the day. The 
bromides of sodium and ammonium are also frequently employed. They have 
the advantage of disturbing the stomach less than does the potassium salt. It is 
a good way to combine the different bromides — for instance, bromide of sodium 
and bromide of ammonium, of each 10 parts ; distilled water, 200 parts : three 
tablespoonfuls a day in water. It is well to combine the various bromides. Er- 
lenmeyer strongly recommends a mixture of two parts of potassic bromide with 
one each of sodic and of ammonic bromide. 

In using the bromides, persistence is necessary for at least months, and often, 
with occasional interruptions, for years, if benefit is to be obtained. In case there 
are unpleasant symptoms due to the remedy, such as excessive acne, muscular 
lassitude and tremor, cardiac weakness, dyspepsia, impotence, or melancholy, we 
must diminish the dose, or even omit the medicine for a time. Many patients are 



EPILEPSY— INFANTILE CONVULSIONS. 



greatly annoyed by pustules due to the bromide ; this can sometimes be avoided 
by giving Fowler's solution at the same time. If the attacks are decidedly 
abated, the dose may be gradually diminished, to be increased again, however, if 
there be any tendency to a relapse. 

Recourse to other remedies is seldom had, unless potassic bromide fails, or for 
some cause must be discontinued. We may then try valerian in powder (8-30 gr. , 
grm. 0*5-2 several times a day), or as an infusion. It is a very good plan to give 
patients who are taking bromide a cup or two of valerian tea at bed-time. Bella- 
donna may also be exhibited, or a pill of atropine (gr. y£ ¥ , grm. 0*0005) three to 
five times a day; or zinc oxide in the dose of one to three grains (grm. 0*05-0.20), 
perhaps combined with a grain of extract of belladonna, and fifteen grains of 
valerian, as a powder three times a day. There are also many other remedies of 
doubtful efficacy : curare, hyoscyamine, the root of artemisia vulgaris, ammonio- 
cupric sulphate, nitrate of silver, and arsenic.* 

Electricity is apparently beneficial in occasional instances, and may be tried in 
connection with other remedies. The galvanic current should be cautiously 
applied to the head and the sympathetic nerves. Still greater benefit is some- 
times obtained from a carefully conducted cold-water cure. Cold sponging with 
friction at night helps most cases, and it is sometimes very advisable to send the 
patient in summer to some appropriate establishment for cold-water treatment. 

Treatment during the Paroxysm. — In most cases we can do little during the 
seizure except to take such precautionary measures as common sense suggests. 
We possess no means of suppressing an attack when once under way ; nor, 
indeed, is it often dangerous. In individual instances the patient finds out from 
experience some method to cut short the paroxysm during the aura. For 
instance, there are cases where tightly bandaging or vigorously rubbing the part 
in which the aura originates will avert the convulsions. A number of cases have 
also been known where the ingestion of a generous quantity of common salt dur- 
ing the aura (usually in these instances starting from the epigastrium) has had 
the same effect. A patient of our own, whose attacks began with a feeling of rectal 
tenesmus, maintained that she could almost invariably suppress the convulsions 
by promptly going to stool, if she had time and opportunity. It was formerly a 
frequent manoeuvre to seek to ward off the attack by compressing the carotids ; 
but this usually fails. Berger recommends the inhalation of nitrite of amyl at 
the commencement of the fit, having repeatedly seen benefit follow it. 

In the " status epilepticus," narcotics are the most deserving of trial, and in 
particular chloroform or ether given by inhalation. Amyl nitrite may also be 
of service. 

[It is sometimes desirable to withhold the knowledge that he is an epileptic 
from the patient, whose ordinary life should be interfered with as little as is pos- 
sible. 

Especially in cases characterized by headache and heat in the head, Brown- 
Sequard finds the application of ice directly to the back of the neck and between 
the shoulders useful.] 

APPENDIX. 

INFANTILE CONVULSIONS (ECLAMPSIA INFANTUM). 

Convulsions in childhood are of such frequency and importance as to justify 
brief special mention here. 

* [Borax in ten to fifteen grain doses (grm. 0*6-1 -0) three times a day has lately been used with 
success in cases where the bromides have failed. Belladonna and some carminative, like cardamom, 
should be given at the same time, to counteract its disturbing effect on the stomach. — Trans.] 
47 



738 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



Every practitioner learns from experience that the young are especially pre- 
disposed to convulsions. Probably this is partly due to excessive reflex excitability 
of the brain in childhood. Thus children not infrequently undergo convulsions 
under circumstances in which adults would very rarely have them. They some- 
times are seen in children in the beginning of acute febrile diseases, such as pneu- 
monia, scarlet fever, and measles. They also occur from indigestion, particularly 
when the stomach has been overloaded; sometimes on account of teething; or 
because of intestinal worms. Here they are in all probability of reflex origin. 

Convulsions may occur in very early life without ascertainable cause. In 
many cases they are really the commencement of epilepsy, as is seen afterward. 
Again they may be due to some actual lesion in the brain. For example, if one 
recalls the initial stage of the acute poliomyelitis and acute encephalitis of children 
{vide pages 630 and 704), it will not seem unlikely that many rapidly fatal cases of 
" convulsions " are really instances of the diseases mentioned. This point has not 
yet been at all satisfactorily investigated by pathologists. At any rate, it does not 
seem satisfactory to us to regard the " oedema of the meninges " found in such 
cases as an independent disease and the sufficient cause of death. Often convul- 
sions occur suddenly in children and then cease, never to recur, without our 
being able to find any explanation of the attack. Experience shows that rachitic 
children are especially liable to suffer from eclampsia — possibly because of cranial 
rachitic changes (?). 

The symptoms of the eclamptic attacks are on the whole analogous with those 
of epileptic paroxysms. The child's eyes become staring and fixed ; and there are 
tonic and clonic spasms of the face, trunk, and extremities. Such seizures may 
continue for days with brief intermissions. In such cases the prognosis is dubious, 
particularly if the child be weakly; but it is by no means absolutely bad. The 
cause and the significance of the convulsions can seldom be determined imme- 
diately. 

Symptomatic treatment consists in applying cold to the head, wet packs, sina- 
pisms on the chest and the calves of the legs, and perhaps an enema (to which 
vinegar may be added). These measures generally answer for mild cases. If the 
fits are very frequent and violent, we may allow even small children to inhale 
chloroform, often with great advantage. A dessertspoonful is to be poured upon 
a handkerchief and administered cautiously. 

Of course, we must also try to discover and remove the cause. The attacks 
due to overloading the stomach usually occur in not very young children, and are 
apt to be greatly benefited by a prompt emetic or purge. 

[A bath at a temperature of 90°-95°, while cool water is applied to the head, 
seems often to be of service ; if the child be exhausted by diarrhoea, the cold to the 
head should be omitted. In a teething child it can do no harm, and it sometimes 
has a very marked effect to lance the gums thoroughly. Enemas containing 
chloral with or without bromide of potash are more used in this country than is 
chloroform by inhalation. 

A drop of nitrite of amyl by inhalation is said by Eustace Smith to exert a con- 
trolling effect on the muscular movements.] 



CHOREA. 



739 



CHAPTER H. 

CHOREA. 

{Chorea Minor. St. Vitus' 's Dance.) 

JEtiology. — Centuries ago the name chorea (dance) was applied mainly to 
those strange states of " dancing mania " which were endemic in certain places, 
being due to excessive mental excitement and to the innate propensity to imita- 
tion. The specific for this condition was held to be a pilgrimage to some shrine 
of St. Vitus. At the present time, however, chorea is used to designate a perfectly 
definite disease, of which the characteristic symptom is the appearance of certain 
peculiar motor phenomena, due to irritation of the nervous centers. It is some- 
times called chorea minor, in contradistinction from what was formerly termed 
chorea major or magna. This latter is, however, not a genuine, independent dis- 
ease, but a manifestation of hysteria (q. v.), or apparently in many instances of 
epilepsy. 

Chorea proper is mainly a disease of children. It occurs most often between 
the fifth and fifteenth years, although it may be seen both earlier and later. 
There is a slightly greater liability to it in girls than in boys. Hereditary neuro- 
pathic tendencies are also a factor in its aetiology, but not a very important one. 

As to causation, in many cases nothing definite can be made out. Mental 
excitement, as from fright, seems in some few instances to favor the onset of the 
trouble. It is also certain that the imitative impulse will often lead to choreic 
movements in healthy children who come in contact with choreic patients, but it 
is doubtful whether this "imitative chorea" can be regarded as true chorea. 
There is a very interesting connection between chorea and acute articular rheu- 
matism. Although the statement of certain authors, that almost every case of 
acute articular rheumatism in children is followed by chorea, is far too strong, 
yet this sequence is comparatively frequent. Chorea is sometimes seen also in 
children who have a mild form of chronic rheumatism, or in such as have valvu- 
lar cardiac disease, whether preceded by articular rheumatism or not. Here 
chorea is seen as a sequel to an infectious disease ; perhaps this is a hint of the 
light in which we should view apparently idiopathic cases of chorea. 

Women are particularly liable to chorea during pregnancy. Chorea gravi- 
darum is most frequent in youthful primiparse. 

Clinical History. — Chorea usually begins gradually, and without any special 
prodromata. Sometimes, however, there are prodromal symptoms, chiefly a cer- 
tain mental depression and irritability, with indisposition to intellectual effort. 
There may be slight rheumatic pains or anorexia, and other evidences of con- 
stitutional disturbance. 

Ordinarily, the peculiar motor disturbances are the first thing to attract the 
attention of the patient or its parents. There are involuntary and irrepressible 
movements in the most diverse groups of muscles. Both single contractions and 
also complicated movements occur, independently of the will, and in all parts of 
the body, now in one place, now in another, sometimes in a single member, and 
sometimes in several at once. The movements may be made in rapid succession, 
or may be separated by long intervals of quiet. The facial muscles may be 
involved, causing an occasional wrinkling of the brow or distortion of the mouth. 
The eyes or the eyelids may also exhibit involuntary movements. The pupils 
are frequently dilated. If the patient is asked to protrude his tongue and keep 
it quiet, it will often be involuntarily withdrawn into the mouth or thrust to 
one side. The tongue may even be sufficiently affected to impair speech. The 



74:0 NEUEOSES WITHOUT KNOWN ANATOMICAL BASIS. 



laryngeal muscles have also been observed to make choreic movements. The arms 
are frequently the most affected of any part; they are twisted, flexed, elevated, 
put behind the back — in short, moved in every conceivable way. The trunk is 
generally but little disturbed in the milder cases, but in severe ones the whole 
body participates. The patient stands up, lies down again, turns upon his side, 
etc. The legs are seldom as much disturbed as the arms and face, but slight move- 
ments of the lower limbs are very frequent — the foot is thrust forward or extended, 
the knee is flexed, and so on. In general, it may be said to be characteristic of 
chorea that the abnormal motor irritation usually affects a considerable number 
of muscles simultaneously, thus exciting all sorts of combined movements ; and, 
secondly, that choreic movements, for the most part, are not short twitches, but 
take place in a manner decidedly similar to that of voluntary movements. 

The vigor of the movements varies greatly in different cases. At first they 
may be too slight for the unpracticed eye to catch. Many children in an incipient 
stage of chorea are unjustly punished at school because they write ill or do not 
sit quietly. Many cases are mild throughout, never having very severe disturb- 
ance. Others, though considerably annoyed, can nevertheless walk or stand 
alone. In the severest cases, however, the whole body is continually in active 
motion. The patient throws himself about in bed, and all the extremities exhibit 
constant violent and irregular movements. The ingestion of food is extremely 
difficult, sleep is disturbed, and the patient's flesh and strength are rapidly and 
greatly diminished. 

Further, each individual case presents variations in severity at different times. 
If the patient is left quietly to himself, the contractions are comparatively very 
slight. As soon as he is conscious of being watched, or as soon as any one speaks 
to him, his condition usually becomes much worse. During sleep the choreic 
movements cease altogether. 

In many cases all the voluntary muscles are involved ; but sometimes the dis- 
ease is limited to certain groups of muscles. Very frequently the disturbance is 
mainly unilateral (hemichorea) ; the opposite side of the body then exhibits few 
involuntary movements, or, it may be, none. As already stated, the face and 
upper extremities are often more affected than the trunk and lower limbs. 

These motor disturbances often constitute the sole or the predominant symp- 
tom of chorea. There is hardly ever muscular weakness or paralysis. It is 
remarkable how little feeling of fatigue there usually is, despite the incessant 
activity. In a few cases only, of genuine chorea, have we seen actual paresis, 
affecting, for instance, one arm, or in hemichorea the same half of the body. 
Sensation is unimpaired. The reflexes do not exhibit striking peculiarities. The 
tendon reflexes we have sometimes found to be noticeably diminished, although 
in other instances they were normal. There may be isolated spots in the spinal 
column tender on pressure ; but this is not at all constant. That chorea may be 
complicated by arthritis and valvular cardiac disease has already been stated. 
Some caution should be exercised in making a diagnosis of cardiac lesion here, for 
experience shows that choreic patients are apt to have functional murmurs, and 
slightly irregular cardiac action. The temperature is not elevated, in spite of the 
constant muscular contractions ; nor is the amount of urea excreted by the kid- 
neys increased. 

Slight mental disturbance is frequently observed. The patient is often rude, 
peevish, capricious, incapable of mental exertion, irritable, and inclined to tears ; 
but any great or permanent impairment of intellect is very exceptional indeed. 

The entire process generally occupies several months. In mild cases, however, 
recovery may ensue at the end of a few weeks, while, on the other hand, cases may 
last a year or even longer. Variations in the intensity of the chorea are often 



CHOREA. 



741 



witnessed. These are sometimes spontaneous, and sometimes are due to outward 
influences. Even when the disease is apparently extinguished, we must be pre- 
pared for a possible relapse. The disease may appear repeatedly in the course of 
a few years, in such a way that it is not easy to determine whether the different 
attacks are relapses or new illnesses. The protracted cases are, as a rule, compara- 
tively mild ; and many cases that begin with great violence end comparatively 
early. In adults, however, we have met with some rather severe cases which were 
very chronic, and seemed at last to become stationary. 

The termination of chorea, in the great majority of cases, is favorable. Now 
and then severe cases do occur, which end in death. In these the choreic move- 
ments are extremely violent. The patient is tossed about in his bed, and can eat 
little and sleep none. We have ourselves observed three such cases, in girls four- 
teen to seventeen years of age, and fatal within the first two or three weeks. Two 
died from general exhaustion and collapse, and the third from gangrene affecting 
numerous cutaneous traumatic lesions, which had occurred despite every possible 
precaution. 

Nature of the Disease. — All cases of genuine chorea thus far examined by 
pathologists have failed to furnish any lesions which can be regarded as essential. 
In the three cases above mentioned the autopsy revealed absolutely nothing 
abnormal in the central nervous system. We are at present, therefore, obliged to 
classify chorea as a " neurosis " — that is, as a disease that produces functional dis- 
turbances, for which latter there is no anatomical basis known to us. The symp- 
toms themselves show that the disorder must affect principally some motor region 
of the nervous system ; but just which motor region is involved can at present 
only be conjectured. It seems very probable, however, that the true seat of chorea 
is to be sought in the brain. In the first place, the frequent occurrence of hemi- 
chorea would indicate this; as would also the fact that slight mental anomalies 
are frequently combined with chorea; and, finally, " choreiform " movements may 
occur as the sole symptom of undoubted cerebral disease, as in post-hemiplegic 
hemichorea. We have, however, no hint as to whether the motor regions in- 
volved are those located in the cortex, or others. The surmise has quite often 
been expressed that chorea is due to embolism of a mild type; but, in our opinion, 
this view lacks proof entirely, and is even improbable. As already said, it may be 
that the connection existing between chorea and acute articular rheumatism will 
throw some light upon the nature of the former disease. 

[Money has produced choreic movements in dogs by the injection of starch 
into the carotids, thus causing embolism of minute cerebral vessels.] 

Diagnosis. — The diagnosis is almost always easy, and can often be made at a 
glance. The motor symptoms of athetosis, paralysis agitans, and of alcoholic, 
senile, saturnine, and mercurial tremor are so characteristic as to be readily dis- 
tinguished from the movements of chorea. It is not difficult to perceive the 
difference between genuine idiopathic chorea and the symptomatic choreiform 
movements occasioned by some other cerebral lesion. 

Prognosis. — As has been stated, the prognosis is almost invariably favorable, 
although the disease may prove very tedious. The possibility of relapses should 
be borne in mind. The prognosis is doubtful only in the worst cases of acute 
chorea, where there is great and rapid failure of the general health. 

Treatment. — Even in mild cases the patient must be kept from school and at 
home, in order to avoid all unnecessary excitement, from ridicule and the like. If 
the chorea be only moderately severe, it is not necessary that the child should be 
in bed; we may even allow moderate exercise in the open air. Where the 
motions are violent, we should seek to guard the patient from self -in jury by 
means of pillows and cushions. 



742 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



Among" the remedies recommended for chorea, the chief place is occupied by 
arsenic and potassic bromide. Arsenic in particular seems often to be of value. 
We give Fowler's solution in water ; beginning with five drops, two or three times 
a day, we gradually increase to eight or ten drops. In children under six, the 
dose should be made somewhat smaller. If the child be ansemic, iron may be 
given in addition ; or, if there be great restlessness and loss of sleep, narcotics 
may also be administered. Large doses of potassic bromide, a drachm (grm. 4) or 
more, daily, have often been decidedly useful in severe cases. Bromide should 
certainly be tried, if arsenic fails or is ill borne (causing abdominal pain, etc.). 
Numerous other drugs have been recommended: oxide of zinc, valerianate of 
zinc, nitrate of silver, and sulphate of copper. At present they are very rarely 
used. If the disease occurs as a sequel of articular rheumatism, we may try 
salicylic acid. Narcotics should be employed very cautiously in chorea. 
Although chloral has been recently recommended for grave cases, there are 
instances known where this remedy has been followed by unfortunate results.* 

Hydrotherapeutics of a mild kind do good, and can easily be carried out in 
most instances. Thus, we may use lukewarm baths, a wet pack, or gentle sponging 
with water at 72° -82° (18°-22° R.) to great advantage. 

Electricity may also be tried. A feeble current of galvanic electricity is applied 
to the head (in the region of the motor centers), or the spinal cord is galvanized. 
If there are points along the spinal column where pressure causes pain, it is said 
to be. an excellent plan to apply the anode to them; but the results of electrical 
treatment are seldom very brilliant. 

In the chorea of pregnancy, which sometimes is a very violent disease, the 
same remedies may be employed. If they do no good, artificial delivery may be 
required ; after which, as we have ourselves once observed, there may be a rapid 
abatement of all symptoms. 



CHAPTER III. 

PARALYSIS AGITANS. 

(Shaking Palsy. Parkinson's Disease.) 

iEtiology. — In 1817 Parkinson described for the first time a disease which he 
named the "shaking palsy." It is not of very frequent occurrence, and as yet lit- 
tle has been ascertained with regard to its aetiology. In most cases it develops 
very gradually, without any demonstrable cause. It almost always attacks elderly 
persons, being very rare before the thirty-fifth year. Sex does not seem to exert 
any great predisposing influence. Hereditary neuropathic tendencies can, indeed, 
be traced in some instances, but are certainly of less potency in paralysis agitans 
than, for instance, in epilepsy. Special exciting causes have sometimes been 
observed, like catching cold, violent emotional excitement, and traumatic influ- 
ences, such as injury to the nerves, burns, etc. Berger reports two cases, where 
the first symptoms appeared after an acute febrile disease (typhoid fever). 

Clinical History. — Paralysis agitans has two characteristic symptoms, viz., (1) 
peculiar evidences of motor irritation, evinced by tremor, and (2) a condition of 
stiffness and persistent shortening of certain muscles, consequent upon which is a 
series of peculiar motor phenomena. 

The trembling is generally the earliest symptom to attract the patient's atten- 

* [Da Costa states, that in a very severe case, when sleep and taking food were rendered almost 
impossible by the violence of the movements, hyoscy amine (gr. Y 100 [grm. 0-0006] three times a day) 
gave distinct relief. — Trans.] 



PARALYSIS AGTTANS. 



?43 



tion. It usually begins in the hands, especially in the right hand, and then 
gradually involves the arm and leg on the same side, next the other arm and 
leg, and finally, in well-marked cases, the entire body. The form of tremor is 
very characteristic. There are rapid, uniform, oscillatory movements of varying 
extent. The tremor is usually greatest in the hands and arms. At the same time 
the thumbs and half -flexed fingers exhibit a movement which suggests spinning 
or pill-rolling. The forearm is generally flexed and extended in rapid alternation, 
but it is always very difficult to determine just what muscles contract. With 
regard to the trunk, it is often a question whether its tremor is of independent 
origin, or due merely to the motion of the extremities. Charcot states that the 
head and the facial muscles are never implicated, but there is doubt about this 
point. We ourselves, as well as other observers, have repeatedly seen independent 
tremor of the head. As to the face, the muscles about the chin seem to suffer 
chiefly. 

The trembling of paralysis agitans is almost continuous. It may, indeed, cease 
for a moment in a limb, but only to recur immediately. The quieter the patient 
is, in mind and body, the less violent are the move- 
ments. If he is excited, or begins to speak, or is 
watched, the tremor at once becomes exaggerated, 
and may be violent enough to jar the whole body 
vehemently. Active motion does not intensify the 
tremor. On the contrary, it may often be observed 
that the trembling abates when the muscles undergo 
vigorous voluntary contraction, as when a weight is 
lifted, or the hand of another is firmly grasped. 

The second symptom is almost more characteristic 
than the first. It consists of a peculiar rigidity of 
the muscles. *We generally notice, even in the face, 
a peculiar tension of the muscles. This often pro- 
duces a stolidity of expression, so that the emotions 
are less clearly depicted than upon the countenance 
of a healthy person. The head gradually becomes 
more and more flexed. When the disease has lasted 
some years, the chin may even rest upon the sternum. 
The muscles of the trunk and extremities also stiffen 
gradually, and lead to peculiar and almost pathog- 
nomonic appearances. The body is bent over for- 
ward ; the arms cling to the trunk, and are flexed at 
the elbow- joint; the fingers are flexed, especially at 
the metacarpo - phalangeal joint ; the thumbs rest 
against the fingers, as if holding a pen, or else are 
flexed inward upon the palm ; and the legs are some- 
what bent at the knee. The accompanying picture 
(Fig. 102) is from the photograph of a patient who 
was for a long time under observation at the clinique 
in Leipsic, and gives a good representation of the 
characteristic posture. 

The stiffness of the muscles also operates to im- 
pair motion in various ways. In particular all move- 
ments of the trunk are greatly impeded. In advanced cases the patient can not 
get upon his feet, if he is lying in bed, without help. Inasmuch, however, as 
the muscular strength usually remains good {vide infra), he requires to exert 
but a slight traction upon some helping hand in order to attain an erect posture. 




Fig. 102.— Characteristic position 
of the body in paralysis agi- 
tans. 



744 NEUKOSES WITHOUT KNOWN ANATOMICAL BASIS. 



On the other hand, the patient is often utterly unable to turn in bed from one 
side to the other. In severe cases, therefore, it is often necessary to alter the 
patient's position several times in a night, especially as lying long in one atti- 
tude makes him feel very uneasy. If the patient is in a chair, he can not get up 
of himself, because it is impossible for him to bend his body forward in the 
necessary manner ; but, with just a little help, he can stand up, and is then able 
to walk alone or even to run. Then, since the flexion of the trunk forward brings 
the center of gravity forward also, and the trunk can not be sufficiently bent 
backward, he is apt to " get a-going," so that he can not stop until he brings up 
against a post or a wall. If such a patient, with a considerable degree of ante- 
flexion and rigidity of the trunk, is slightly pushed from behind, he will have to 
start into a run to avoid falling. This phenomenon is termed " propulsion." A 
push backward, which brings the center of gravity behind the point of support, 
is very likely to make such a patient fall, as he will seldom succeed in moving 
backward fast enough to recover his balance (retropulsion). Both propulsion and 
retropulsion are conceived by Charcot to be " forced movements " (see page 510) in 
the strict sense of the term. We are, however, convinced, as the result of numer- 
ous observations, that these phenomena can in every case be explained simply by 
the mechanical conditions arising from displacement of the center of gravity. 
Again, the reason why many patients are prone to keep their arms behind them 
as they walk is that such a position contributes slightly toward bringing the 
center of gravity farther backward. 

The movements of the extremities are less impaired than those of the trunk ; 
but they often betray a certain slowness and stiffness of motion. The strength of 
the muscles may be preserved for a long while, but often there is at last evident 
paresis. Even in the early stages of the disease the muscles may become easily 
fatigued. The impairment of facial expression has already been referred to. In 
many cases the muscles of the eye also seem to participate in the rigidity, making 
it difficult for the eye in reading to follow rapidly along each line, or to pass from 
the end of one line to the commencement of the next. 

The muscular rigidity is almost more characteristic of paralysis agitans than is 
the tremor. Indeed, there would seem to be cases, as we have ourselves observed, 
where, at least for a time, the posture of the patient is typical, and yet there is no 
trembling. Such cases might be called paralysis agitans sine agitatione. In 
uncomplicated cases all other nervous functions remain perfectly normal. Sensa- 
tion is never impaired. Sometimes some pain is felt at the commencement of the 
disease, particularly in the shoulders. There is no striking disturbance of reflex 
action nor of the bladder. In a few cases of paralysis agitans, cerebral and men- 
tal symptoms have been observed ; but they are so rare that it is impossible to 
say whether they belong to the disease or are merely accidental complications. It 
is also noteworthy that many patients complain of a subjective feeling of exces- 
sive warmth. The internal temperature is normal ; but it is said that the tem- 
perature of the surface of the body is frequently somewhat elevated. Sometimes 
there is a tendency to excessive perspiration. 

The disease runs a very chronic course, perhaps for twenty years or more. 
From the first, it keeps on slowly but gradually developing. The symptoms 
rarely exhibit marked alternations of mildness and severity, but for long periods 
the progress of the disease may be apparently arrested. Eecovery has never yet 
been observed. The final and fatal termination is not brought about by the dis- 
ease itself, but is due to some intercurrent affection or to general marasmus. The 
original of the above picture came to a pitiable end by tumbling face downward 
into a puddle of water. He could not get up, and was drowned. 

Nature of the Disease. — The true nature of the disease is unknown. Inasmuch 



ATHETOSIS. 



745 



as the disorder is purely a motor one, the corresponding lesions must be sought 
somewhere in the motor system. As yet, however, post-mortem examinations of 
the nervous system, even with the microscope, have revealed no definite changes. 
We must, therefore, confess that we have even had a doubt whether it is justifia- 
ble to claim that paralysis agitans is an affection of the nervous system at all, or 
whether it may not possibly be of purely muscular origin. Certainly it would 
not be impossible for abnormal processes in the muscles to excite the tremor and 
tonic contraction. But, as has been said, there is at present no ground for decid- 
ing this question; we would merely suggest it. 

Diagnosis. — Any typical case of paralysis agitans can be easily and certainly 
recognized. The important factors are the peculiar tremor, the characteristic car- 
riage, and the rigidity of the muscles of the trunk and extremities. It was for- 
merly a difficult matter to distinguish between paralysis agitans and multiple 
sclerosis ; but to-day the peculiarities of the two diseases are better known, and 
confusion is seldom possible. The character of the tremor varies in the two. In 
paralysis agitans it persists even when the patient is quiet, and it is decidedly oscil- 
latory. The motion in multiple sclerosis (q. v.) is almost always an intention 
tremor only ; and, what is of still greater importance in distinguishing between 
them, the general appearances of the two diseases are essentially unlike. 

Treatment. — As has already been implied above, we possess no means of con- 
trolling the disease. In most cases, therefore, the treatment is confined to general 
hygienic measures. Good may be done by lukewarm baths of considerable dura- 
tion, and by gentle massage of the muscles. Among internal remedies, some 
beneficial effects have been claimed for arsenic. Ergotine, potassic bromide, hyos- 
cyamine, and curare may also be tried. If electricity is to do any good at all, the 
case must be a recent one. It is said that in some instances stretching of the 
nerves has diminished the tremor considerably ; but our own observations would 
not lead us to recommend the procedure in this disease. 



CHAPTER IV. 
ATHETOSIS. 

In 1871 the American neurologist Hammond described under the name of athe- 
tosis (aOeros — without fixed position) a peculiar symptom of irritation of the motor 
centers, differing in a characteristic manner from all other forms of involuntary 
movements, including the epileptiform and choreic. The movements of athetosis 
(see page 509) are often very complicated and peculiar. The part affected by them 
is in continuous unrest. If the facial muscles (usually those of the lower divi- 
sion of the facial nerve) and the muscles of mastication are attacked, the face and 
mouth are constantly being twisted and distorted. If the tongue suffers, as in 
one case which we saw, speech is difficult and indistinct. If the muscles of the 
back of the neck are implicated, the head is usually drawn backward or to one 
side, and is turned and twisted in all sorts of ways. Most characteristic of all, 
however, are the movements exhibited by the hand and fingers when affected. 
The fingers are incessantly being separated, extended, flexed, and intertwined, 
assuming the oddest positions. The pictures given below may serve to illustrate 
this (vide Fig. 103). The character of the movements reveals that the interossei 
must be chiefly involved. It is a very frequent result of the unceasing stretching 
of the articular ligaments of the fingers that at last the articulations become 
relaxed to such a degree as to permit of hyperextension of the fingers, which it is 



746 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



impossible for a healthy person to imitate. The arms are generally less severely 
affected than the hands ; and in the lower limbs the trouble is not often so severe 

as in the upper. The 

^miirnflHIIIIfllli;. ^ oes ma y> however, ex- 
hibit motions analogous 
to those of the fingers. 

Although in general 
the movements are con- 
tinuous, their vigor fre- 
quently varies. Thus 
they almost always are 
aggravated if the patient 
becomes excited. Dur- 
ing sleep they generally 
cease, although in certain 
instances they have per- 
sisted even then, only be- 
ing diminished. When 
voluntary motions are 
being made, they ordi- 
narily grow feebler ; but 
they may, on the con- 
trary, become exagger- 
ated, taking the form of 
sympathetic movements. 

We must distinguish 
between genuine idio- 
pathic athetosis and a 
symptomatic form, which 
also occurs. 

Symptomatic atheto- 
sis is seen in various 
nervous diseases. The 
first observations report- 
ed by Hammond were, 
most of them, made in 
cases of epilepsy, or the 
severe psychoses, and the 
like. By far the most 
frequent source of the 
phenomenon, however, is 
hemiplegia, producing 
what is known as post- 
hemiplegic chorea, or 
better, post - hemiplegic 
hemiathetosis. This is, 
to be sure, a very rare se- 
quel to the ordinary hemi- 
plegia of elderly persons, 

Fig. 103.— Example of the position of the fingers in the movements of f°H° w ^ rather in 

athetosis (personal observation). f antile paralysis oi cere- 

bral origin {vide p. 704). 

Some traces of athetosis are seen in a majority of the cases of infantile hemiplegia. 





TETANY. 



Idiopathic athetosis is rare. Here the peculiar movements are the chief, if not 
the sole, symptom of disease. A few cases of this sort have been reported where 
the athetosis began without known cause, and usually was limited to some one 
region. It attacked elderly individuals who were previously healthy. Of especial 
importance is an apparently congenital form of athetosis, dating from the earliest 
infancy. Of this we have ourselves seen several instances, which closely resem- 
bled one another. The condition is a permanent one, not progressive, nor, on the 
other hand, capable of any great amelioration. The movements are almost always 
most pronounced in the face, head, and fingers. There are no other nervous dis- 
turbances, neither paralysis nor impairment of sensation. The intelligence of the 
patient may or may not be below par. 

Of the nature of athetosis, or the locality or nature of the irritation, we possess 
no information as yet. It is extremely probable that the lesion is in every case a 
cerebral one. Perhaps it is in the cortex. In symptomatic athetosis we find 
post mortem the changes caused by the original trouble. In idiopathic athetosis, 
no changes have thus far been reported. In a case of our own which came to 
autopsy, absolutely nothing abnormal was found in the brain. The patient was 
an elderly female, who displayed typical movements of the arm and hand. 

It is not yet known whether recovery is possible. A certain amount of improve- 
ment sometimes follows the administration of Fowler's solution, bromide of potas- 
sium, or galvanism. 

CHAPTER V. 

TETANY. 

{Intermittent Tetanus.) 

iEtiology. — Tetany, a name originating with Corvisart, is applied to a peculiar 
neurosis, characterized mainly by paroxysmal tonic convulsions in certain groups 
of muscles. The disease attacks by preference children and young adults between 
fifteen and thirty years of age. The physiological processes peculiar to the female 
sex seem to have an especial tendency to excite the disorder. It is comparatively 
so frequent in nursing women that Trousseau has called it " contracture des 
nourrices.''' 1 

Among exciting causes, catching cold deserves particular mention. Hence the 
earlier observers described the disease as " intermittent contracture of rheumatic 
origin." In other cases the disorder has appeared as a sequel to other acute dis- 
eases, like typhus or typhoid fever, small-pox, and intestinal troubles. A very 
remarkable fact was pointed out by N. Weiss — namely, that tetany is apt to fol- 
low operative extirpation of goitre. No explanation of this has yet been discov- 
ered. Reports from various quarters give color to the idea that tetany may 
sometimes be, to a certain extent, epidemic. It must be confessed, however, that 
it is somewhat doubtful whether the attacks referred to were genuine tetany. 
We are also inclined to believe that endemic influences may promote its occur- 
rence. At any rate, the published accounts would seem to indicate that tetany is 
much more frequent in Heidelberg (Erb, F. Schultze), Breslau (Berger), and 
Vienna (N. Weiss), than here in Leipsic, for instance, where it is one of the 
very rarest nervous diseases. 

Clinical History. — The paroxysm of tetany usually has certain prodromata, 
consisting of slight general discomfort and pain, and of a feeling of weakness and 
stiffness, most marked in the arms. These symptoms last some hours (at least) 
before the true convulsive stage begins. The upper extremities, and more par- 
ticularly the fingers, almost always suffer first ; and then, after the arms, the 



748 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



lower extremities become involved. The spasm usually affects the toes before it 
seizes upon the other parts of the leg. The symptoms are almost invariably 
bilateral and symmetrical. Exceptionally, the disturbance commences in a lower 
limb, or is confined to one side of the body. In most cases the flexor muscles are 
predominantly affected, giving rise to very characteristic postures. The fingers 
are in apposition with one another, and placed as if holding a pen, or, as Trous- 
seau says, as if the hand were about to be thrust into the vagina, during labor. 
The hands are flexed, the elbows are also slightly flexed, and the upper arm in 
severe cases is pressed against the chest. In the lower extremities, the toes are 
flexed, and the feet are in the posture of talipes equinus. The muscles of the 
thigh rarely suffer. The same is true of the trunk, face, and diaphragm. The 
main characters of a typical attack, such as has just been sketched, apply to all 
but a few cases. 

The intensity of the tonic spasm is very great. The affected muscles feel as 
hard as a board, and are usually rather sensitive to pressure. The attack some- 
times continues only a few minutes, but not infrequently it may occupy several 
hours or days. As a rule, there are no disturbances of sensation or other addi- 
tional nervous phenomena. There is no impairment of consciousness. In a few 
instances slight cedematous swelling has been observed, and also profuse perspira- 
tion. The temperature is normal or slightly elevated, but the pulse is often 
quite rapid. 

When the attack ceases, which it always does gradually, and never suddenly, 
the patient feels perfectly well, save for a slight pain and stiffness in the mus- 
cles. But even in the interval between the paroxysms there are usually some 
few objective symptoms, which have a most important bearing on the pathology 
of tetany. In the first place, the peripheral nerves are generally abnormally 
sensitive to electricity. The complete demonstration of this fact we owe to Erb. 
The weakest current will produce frequently violent contractions. In an analo- 
gous way, the nerves react to unusually slight mechanical stimulation. This is 
often peculiarly marked in the facial nerve, as Chvostek and N. Weiss have 
shown. Thus, if the face is vigorously stroked from above downward, almost all 
of the muscles contract energetically, one after the other. The direct mechanical 
excitability of the muscles, on the other hand, is not increased (F. Schultze). 

Another very characteristic symptom was discovered by Trousseau — u Trous- 
seau's sign." It is found in most cases, although not in all, and is this: a fresh 
paroxysm can at any time be artificially excited by pressure upon the larger 
arteries and nerves of the arm (particularly the median nerve and the brachial 
artery). It is not definitely known how compression accomplishes this. Berger 
found that mechanical or electrical irritation of certain painful points situated 
along the spinal column produces the same result. 

The frequency of the attacks varies greatly in individual cases. As a rule, 
there are several paroxysms daily ; but the intervals may last for days, or again 
may be almost inappreciable. The entire duration of the disease is generally sev- 
eral weeks. It is noteworthy that when the paroxysms grow less frequent and 
violent there is also a gradual diminution in the hyper sensitiveness of the nerves 
and in the reaction to Trousseau's test. As long as these symptoms persist, 
spontaneous attacks are also possible. 

The termination of tetany is almost always favorable. No essential anatomical 
lesions have yet been detected. The symptoms leave us in doubt whether the dis- 
ease affects the peripheral nerves or the nervous centers. 

Diagnosis. — The diagnosis is not difficult if we only consider carefully the 
symptoms presented, the nature of the paroxysms, and the other phenomena above 
enumerated. Similar conditions may result from ergotine-poisoning, or from cer- 



TETANUS. 



749 



tain occupations, as in " cobbler's cramp," but the differential diagnosis is usually 
easy. The peculiar tonic spasms of young children are not, in our opinion, to be 
regarded as tetany : they have already been described (vide page 543) under the 
name of arthrogryposis, and are characterized by persistent tonic contracture, not 
paroxysmal, and most pronounced in the distribution of the ulnar nerve on both 
sides ; and in them there is no abnormal sensitiveness of the nerves to mechanical 
stimuli. 

Treatment. — The main treatment, beside general hygienic measures, is elec- 
tricity. The stabile current is passed upward through the nerves affected; the 
galvanic current is also applied to the spinal cord, and the anode is applied to the 
various nerve-trunks, with the kathode on the sternum. This last procedure some- 
times dissipates a spasm actually present. Internal remedies, such as bromide of 
potassium, arsenic, and belladonna, rarely produce brilliant results. Berger was 
successful in some cases with subcutaneous injections of curare. Tepid baths, and 
cold sponging with friction cautiously employed, and applied especially to the 
back, often aid treatment materially. 



CHAPTER VI. 

TETANUS. 

(Lock-jaw.) 

iEtiology. — There are two chief exciting causes of this disease as are indicated 
by the names rheumatic tetanus and traumatic tetanus. The rheumatic variety 
results from catching cold, or getting a thorough wetting, or some similar mishap. 
The other occurs in persons who have some open wound, whether from injury or 
operation. There is no ground for establishing tetanus neonatorum as a third dis- 
tinct form. Cases to which this name has been applied are invariably connected 
with the falling off of the cord, and are therefore instances of traumatic tetanus. 
In a few instances it is impossible to discover what has been the immediate occa- 
sion of the disease ; such cases are classed as idiopathic tetanus. 

With us tetanus is a comparatively rare disease. In the tropics it is much more 
common. Negroes are well known to be peculiarly liable to it. Tetanus has been 
seen as an endemic and also as an epidemic. This has been most frequent in times 
of war, and is in part due to the unfavorable influence of certain external circum- 
stances, such as bad weather or bad hygienic surroundings. 

Clinical History. — In rheumatic tetanus the symptoms usually begin soon after 
exposure to the exciting cause. There may be, however, an interval, during which 
the patient feels perfectly well, or at most has only certain mild and indefinite 
premonitory symptoms, such as languor and headache. Similar prodromata may 
occur in the apparently idiopathic cases. 

Traumatic tetanus seldom begins immediately after the injury has been 
received. Several days or even weeks may intervene previous to the outbreak of 
the disease. Here, too, there may be mild prodromata for a brief period preceding 
the graver phenomena. The patient's wound presents no specific appearances. 
Tetanus may be associated with either slight or severe injuries, whether treated 
carelessly or kept aseptic. 

The symptoms of the disease proper are the same in both rheumatic and 
traumatic tetanus. They usually begin gradually. Ordinarily, the first thing 
noticed is a feeling of rigidity and tension in the muscles of the face, lower jaw, 
and nape of the neck. The stiffness spreads by degrees to the muscles of the back 



750 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



and abdomen. The disease is sometimes completely developed in a few hours, but 
sometimes not till after several days. 

The persistent tension of the facial muscles gives the countenance a strange 
immobility. The brow is usually wrinkled, and the corners of the mouth are 
often drawn back in a " sardonic grin." Most prominent of all is the tonic spasm 
of the masseters, or trismus. The teeth are so firmly pressed together that it 
finally becomes impossible to open the mouth more than one or two millimetres. 
The eyes are staring, the pupils usually contracted. The muscles at the back of 
the neck draw the head somewhat backward, and it is immovable. The spinal 
column is bent forward, so that the trunk is convex anteriorly, permitting the 
hand to be passed between it and the bed — opisthotonos. The epigastrium and the 
anterior part of the abdomen are flat. The abdominal muscles are as hard as a 
board. The lower limbs may be rigidly extended, but the arms generally can be 
quite freely moved. Convulsive dysphagia, as seen in hydrophobia (q. v.), may 
occur, but it is rare (vide infra). 

In many cases the continuous tonic spasm is occasionally interrupted by sudden 
and irregular paroxysms, during which all the affected muscles become still more 
tense. In severe cases this gives the whole body a violent shock, and makes the 
opisthotonos even more pronounced. In a very bad case the paroxysms are very 
frequent ; in a mild case they are rare or almost indistinguishable. Sometimes 
they are apparently spontaneous, and sometimes they are evidently of reflex ori- 
gin, being superinduced by external irritation. In severe cases the cause may be 
comparatively insignificant, such as a slight jar or noise. 

If there are other nervous derangements, little is known about them — partly, 
no doubt, because it is seldom possible to make an extended examination of the 
patient. Sensation is said to have been impaired in some instances ; but in others 
it is perfectly normal. The muscles affected by the spasms are usually the seat of 
severe pain. The cutaneous reflexes are almost always greatly exaggerated. In 
two cases which we saw very recently, the patellar reflex was much increased, 
and in one there was distinct ankle-clonus. Paralysis is extremely exceptional. 
There is often profuse perspiration. The intellect remains perfectly unclouded. 

There is a special form of tetanus which must be briefly mentioned. It was 
first described by E. Rose, and is called " hydrophobic tetanus," or " tetanus of the 
head." It occurs only in connection with injuries situated in the distribution of 
the cranial nerves — that is, in the face and head — and is characterized in most cases 
by violent spasm of the pharynx and oesophagus. This is in addition to the other 
ordinary phenomena of tetanus. The disease in many ways reminds one of 
hydrophobia. Another characteristic point is that in most cases there is facial 
paralysis on the injured side. 

Tetanus seldom gives rise to disturbances referable to the internal viscera. In 
one case, however, in the Leipsic hospital, croupous pneumonia and acute 
nephritis came on a few days before the end. Often there are dyspnoea and a 
most harassing sense of thoracic oppression — symptoms due mainly to the convul- 
sive rigidity of the muscles, by which the thorax is constantly maintained in the 
position it normally assumes during inspiration. Expectoration is impeded ; and ? 
finally, there may be such an accumulation of secretions in the mouth and air- 
passages as to cause a secondary diffuse bronchitis, or an inhalation pneumonia. 
Another occasional source of extreme dyspnoea is spasm of the glottis. 

The pulse often remains normal for a long while, but it is usually accelerated, 
not infrequently reaching 120 or 160 beats a minute in severe cases. Such a pulse 
is small, and may be somewhat irregular. The temperature is at first usually 
normal, or slightly elevated. Later it is almost sure to rise; and, as Wunderlich 
pointed out, it is often very high shortly before death — for instance, 107° to 111° 



TETANUS. 



751 



(42°-44° C). It is not rare for the temperature to keep on rising for a short time 
after death. No explanation of this terminal elevation of temperature has yet 
been furnished. It can not he the result of the increased production of heat 
occasioned by the muscular spasm, for in earlier stages the most violent convul- 
sions are unattended by any such change. Authorities are, therefore, inclined to 
assume that at the last there is a paralysis of the centers which regulate the 
warmth of the body, just as is seen in other severe nervous disorders, like menin- 
gitis, injury to the cervical portion of the cord, and uraemia. 

Interesting observations have been made with regard to tissue-metamorphosis 
during tetanus. The excretion of urea is not increased. This fact agrees well 
with Voit's view, that muscular activity has no connection with the breaking 
down of albuminoids. Senator failed to find any increase of kreatine and 
kreatinine in the urine. Probably the production of carbonic dioxide is abnor- 
mally large in tetanus. At least, physiological considerations would strongly 
indicate this, although it has not yet been actually demonstrated. Occasionally, 
traces of albumen and sugar have been detected in the urine. There is usually 
obstinate constipation, probably due to the persistent rigidity of the abdominal 
muscles; and, indeed, micturition is not a little impeded, from the same cause. 

General Course of the Disease. — It may be said that there are a severe and a 
mild form of the disease. What has been said above applies mainly to the severe 
form. In this, all the symptoms reach their extreme violence in a few days, the 
paroxysms occur in quick succession, and death usually takes place within a week 
or two. The fatal result is brought about by the suspension of respiration and by 
cardiac failure. Of course, the extreme difficulty of taking an adequate amount 
of food has an unfavorable influence. The bad cases seldom outlast the first 
week. If they do, there is some slight hope of recovery; the paroxysms may 
gradually become less frequent and less severe, until they finally cease altogether. 
The severe form, however, so rarely ends favorably that the prognosis is always 
very grave. The mild form, on the contrary, usually runs a much more favorable 
course. In it, all the symptoms are from the first much less severe. Often there is 
only more or less trismus, accompanied by no marked spasm in the muscles of the 
trunk, if any at all. There is little constitutional disturbance. The temperature is 
normal ; and the prognosis is rather favorable. The disease may sometimes drag 
on for some weeks, but it often ends in complete recovery. It must not be forgotten, 
however, that what at first seems a mild case may develop into the severe form. 

Nature of Tetanus. — The true character of the disease still remains a matter of 
hypothesis. The brain and spinal cord never show any lesions in tetanus. More 
than once lesions have been reported ; but the investigator has merely assigned 
undue importance to some non-essential change. A consideration of the facts 
learned from clinical observation would seem to us to suggest the idea 'that teta- 
nus is a specific infectious disease. We can not here give all the reasons for this 
view ; but it explains why tetanus is often endemic, why it follows external 
injuries (just as septicaemia does), and why there are in many cases premonitory 
constitutional symptoms. It also accounts for the lack of discoverable objective 
changes, despite the severity of the nervous phenomena, inasmuch as we may sup- 
pose that the infectious agent acts mainly in a toxic way, as, for instance, in 
hydrophobia. 

Diagnosis. — In most cases, tetanus can be easily recognized from the peculiar 
convulsions and the general aspect of the disease. It might be confounded with 
acute meningitis, for this may cause rigidity of the neck and back ; but here there 
are usually certain cerebral symptoms also present, like headache and impairment 
of consciousness ; and, on the other hand, in tetanus, trismus is an almost constant 
phenomenon, although exceptional in meningitis. Strychnine poisoning pro- 



752 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



duces convulsions similar to those of tetanus ; but they generally affect the 
extremities in a marked degree. Hydrophobia is distinguished from tetanus by 
the aetiology, the absence of trismus, the predominance of the pharyngeal convul- 
sions, and the greater distinctness of the individual paroxysms. 

Where trismus is the only symptom, we must guard against mistaking for 
tetanus the symptomatic rigidity of the jaws which occurs with severe sore throat, 
diseases of the teeth, or inflammation of the maxillary articulation. 

Treatment. — There is no specific method of treating tetanus. In accordance 
with the view above mentioned as to the nature of the disease, we have employed, 
in a few cases, large doses of salicylic acid. This seemed to work well in one 
case, but in others it did not. We must therefore rely mainly on symptomatic 
remedies, with the aim of preserving life until a spontaneous cure takes place. 
For this purpose, narcotics are apparently to be preferred ; and among them the 
best are opium in large doses and chloral, of which thirty grains (grm. 2) 
should be given two or three times a day, and the amount gradually increased. 
If deglutition be very difficult, the chloral may be given per anum. Bromide of 
potassium should also be mentioned (at least two and a half to four drachms, 
grm. 10-15, daily), and calabar-bean (a sixth of a grain of extract of physo- 
stigma, grm. 0*01, three to five times a day). The above remedies diminish the 
irritability of the nervous centers. In curare we possess a means of lowering the 
excitability of the terminations of the motor nerves in the muscles. It has there- 
fore been employed by many, but by few with success. It is difficult to say what 
the dose of curare is, inasmuch as the strength of different samples varies. The 
best way is to determine the strength of the solution to be employed by experi- 
menting on some animal. Usually a one-per-cent. solution of curare in water is 
employed, and an amount equal to one quarter of the contents of a Pravaz's 
syringe is injected, the dose being gradually and cautiously increased. [Such a 
syringe contains about thirteen minims (0*8 grm.).] 

It is very desirable to put the patient by himself in a darkened and quiet 
chamber. Nourishment should be liquid, and lukewarm stimulants, such as alco- 
hol and camphor, should be given from the first. Protracted warm baths may be 
given cautiously. We know from personal observation that such baths are very 
grateful to some patients. 

It need hardly be said that in traumatic tetanus the primary wound should 
receive careful attention. Still, when tetanus has once been developed, it is never 
cut short by excision of the wound, amputation, stretching of the nerves, or simi- 
lar procedures. The longer we keep the patient alive, the greater the hope of 
permanent recovery. 



CHAPTER VII. 

CONGENITAL MYOTONIA. 

(Thomsen'' s Disease.) 

In 1876, Thomsen, a Sleswick physician, described a peculiar disease which up 
to that time had escaped observation. He had had experience of it in himself and 
numerous members of his own family. Thomsen called it " tonic convulsions of 
the voluntary muscles," an appropriate but somewhat clumsy name, for which 
we suggested instead "congenital myotonia." Apparently the disease is very 
infrequent; but a considerable number of cases have already been reported in 
Germany, France, and Italy. 



CONGENITAL MYOTONIA. 



753 



The disease seems to be congenital ; at least, the symptoms invariably date 
from the earliest infancy. It is very often hereditary ; and males seem to suffer 
oftener, and also more severely, than do females. The essential symptom of 
myotonia is this : whenever any voluntary muscle has been inactive for a time 
and is then made to contract, it falls into a state of more or less persistent con- 
traction, a mild sort of tetanus, so that it can not be immediately relaxed. It is obvi- 
ous how this would interfere with any series of motions, and make voluntary 
movement difficult. The patient is not paralyzed at all, but he has a feeling of great 
resistance to be overcome in performing any act. Quick and accurate motions 
are often out of the question, so that, for instance, the patient can not perform 
military duty. It is noteworthy that the stiffness temporarily disappears after 
the patient has been moving his muscles for some time. On going up-stairs, the 
first steps are often very stiff and laborious, while succeeding ones grow easier 
and easier. Mental excitement invariably exerts a very unfavorable influence, 
exaggerating the stiffness of the muscles. 

Upon physical examination, the observer is usually struck by the extraordinary 
development of the muscles. The size of the extremities, in particular, almost 
deserves the term " genuine muscular hypertrophy," although the strength is not 
always proportionately great. It is a remarkable fact that, upon direct electrical 
irritation of the muscles, the contraction outlasts, in most cases, the passage of the 
current. This is also true, although less marked, when the electricity is applied 
to the motor nerves. Erb has also observed, during the stabile application of the 
galvanic current, wave-like contractions starting from the kathode and passing 
one after another over the muscles toward the anode. The direct mechanical 
excitability of the muscles is sometimes normal, but sometimes increased. The 
idio-muscular contractions {vide page 514) are especially apt to be increased. The 
reflexes, sensation, and, indeed, all other nervous phenomena, are normal. 

These facts render it very probable that the cause of the disease is to be sought 
in the muscle itself, and that myotonia is due to a congenital peculiarity of the 
muscular system. Erb reports that, upon microscopic examination of minute 
particles of muscular tissue which were excised, he found marked hypertrophy of 
individual muscular fibers, and an increase in the number of nuclei in the sar- 
colemma.* 

The disease persists through life. The patient gradually becomes accustomed 
to it, and learns to conceal his misfortune as much as possible. There may be no 
constitutional disturbance. Sometimes there is melancholia. Therapeutic efforts 
have not yet been attended with much success. We might try cold sponging, 
with friction, gentle massage, and methodical exercise of the muscles. 



* [In a recent treatise Erb admits only twenty-three typical cases known at present. His investi- 
gations show that on voluntary movement there are protracted contractions of the muscles lasting 
from five to thirty seconds ; these he terms myotonic disturbances of motion. Mechanical excita- 
bility of the nerves is perhaps diminished; faradic excitability of the nerves is normal, but a sudden 
increase of the current may excite protracted contraction ; galvanic excitability is nearly normal, but 
a succession of shocks may produce the tonic contraction. The mechanical excitability of the mus- 
cles is increased, a touch with the finger being enough to excite tonic contraction. Faradic excitability 
is very marked ; the muscles are quickly relaxed after weak currents, but a sudden increase produces 
protracted contractions. Galvanic excitability is increased quantitatively, anodic and kathodic closure 
contractions appearing with currents of one or two milliamperes ; qualitatively both poles react alike. 
The wave-like contractions mentioned above are very characteristic. Erb has given the name of 
myotonic reaction (MyE) to these electrical phenomena. Hereafter, he thinks, a tap with the percus- 
sion hammer and a few kathodioclosure contractions will suffice to establish the diagnosis. Beside 
the anatomical changes above mentioned, Erb also finds that the cross-section of the individual mus- 
cular fiber is rounded instead of polygonal, like the normal fiber, and that the interstitial tissue is 
increased. In one case he found a striking vacuolization of the individual fibers. — Tracts.] 
48 



754 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



CHAPTER VIII. 
CATALEPSY. 

Formerly catalepsy was regarded as a special form of disease, but at present 
the view is almost universally held that it is merely a symptom of several different 
diseases. As was mentioned on page 510, " cataleptic rigidity " is a term descrip- 
tive of that peculiar condition of the muscles in which the limbs maintain invol- 
untarily any position which the observer puts them into. If we change the posi- 
tion of the members which are cataleptic, the patient does not make the slightest 
effort to alter the posture in which we leave them, however strange and awkward, 
and apparently insupportable, it may be. The limbs may be moved in this way 
almost like wax, and have therefore been said to exhibit a " waxy flexibility." 

No real explanation of the cataleptic state has been given. We have not yet 
advanced beyond the study of the circumstances under which it appears, and of 
the associated phenomena. As has been said, the tonic muscular spasm of cata- 
lepsy is never very great, being little more than suffices to overcome gravity and 
maintain the limb in the posture given to it. This shows that there must, in every 
case, be a due proportion in the vigor of the contractions of antagonistic muscles ; 
and this relative force must vary with every change of position. How this con- 
tinuous and remarkable regulation of motor nervous energy takes place is an 
unanswered question. Perhaps reflex action has something to do with it. A 
further interesting point is, that changes of position induced by electrical stimu- 
lation of the nerves or muscles are not permanent ; when the stimulus ceases to 
act, the limb falls back into its old place. 

Catalepsy occurs oftenest as a symptom of hysteria. In this case it is usually 
associated with other disturbances, chief among which are impairment of con- 
sciousness and anaesthesia. The anaesthesia is especially marked in the muscles. 
For example, the patient will stand for an hour with arms extended, and yet 
experience not the slightest sensation of weariness. At last, however, the arms 
sink slowly down. Closely allied to hysterical catalepsy is hypnotic catalepsy, a 
condition which can be artificially produced by certain procedures (see the next 
chapter) in many hysterical subjects at will. Charcot has reported cases where 
the lethargy of hypnotism could invariably be transformed into catalepsy by open- 
ing the previously closed eyes. These cases also presented, in addition to the cata- 
lepsy, the strange phenomenon called " suggestion." If the patient were put into 
any posture associated with some definite mental conception (such, for example, as 
the attitude of prayer, or that assumed in terror, or to express detestation), then 
the corresponding thoughts would come into the mind, as a hallucination, but 
with all the vividness of reality. Ample proof of this was visible in the expres- 
sion of the face and in the whole bearing of the subject. An analogous fact has 
been observed by Duchenne, Lasegue, and ourselves — namely, that sometimes a 
hysterical person can be brought into the cataleptic state by artificial closure of 
the eyes (compare what is said in the next chapter about hysterical anaesthesia). 

Catalepsy is also seen in many psychoses, particularly in certain grave forms 
of melancholia, known as melancholia attonita and katatonia, and sometimes in 
progressive general paralysis. (For particulars see works on insanity.) The cata- 
leptic state may also develop in connection with grave organic cerebral disease, as 
in meningitis and apoplectic coma. It may finally be mentioned in passing that 
quite well marked catalepsy is sometimes observed in young children of one or two 
years when they are ill. Probably they fall into a sort of stupor ; or often it seems 
that they are rendered hypnotic, as it were, by the presence of strangers. 



HYSTERIA. 



755 



Catalepsy has been regarded as a special disease in those very rare cases where 
otherwise healthy persons are liable to " cataleptic fits." The condition comes on 
suddenly, unprovoked, and passes off spontaneously after a variable length of time. 
It is, however, very probable that these cases are either hysterical or epileptoid, 
and deserve to be classed with genuine epilepsy. 

Prognosis and Treatment. — Since catalepsy is a symptom of so many different 
diseases, it is impossible to make any general statements with regard to prognosis 
or therapeutics. The reader may gain some light from the remarks on the treat- 
ment of hysteria in the next chapter. 



CHAPTER IX. 
HYSTERIA. 

iEtiology and Definition. — It is impossible to give a definition of hysteria that 
shall be at once brief and accurate, for the aspects of the disease are so manifold 
that there is no one symptom which can be called pathognomonic or even uni- 
versally characteristic. From a clinical standpoint the following arguments may 
be adduced as justifying the claim of hysteria to be an independent disease distinct 
from others : 

1. All hysterical disturbances, no matter how severe the functional nervous 
derangement attributable to them, are without visible anatomical basis. The best 
proof of this is the fact that any case, however alarming, may recover completely 
in a very short time. 

2. The hysterical affection is almost invariably intimately associated with 
exciting causes of a psychical nature. Not only is its appearance and incipiency 
most closely linked with emotional excitement, but, later on, the mind is the 
main channel through which causes can operate to change the condition of the 
patient, whether favorably or unfavorably. 

3. It is, therefore, evident that the origin of all hysterical disturbances must be 
sought in the most central portions of the nervous system — those regions which 
are most directly concerned in the mental processes. Hysterical phenomena are, 
however, exhibited throughout the entire nervous system. The symptoms are 
often so manifold and complex that it is impossible to believe that the lesion has 
any one uniform anatomical location. Not all cases are so complicated, to be 
sure. Not infrequently the symptoms would strongly incline one to believe that 
an anatomical seat of the trouble might be inferred in that particular instance, 
according to the general rules for localization of cerebral lesions. Nor is it right 
to say that frequent and irregular changes in the nature and locality of the symp- 
toms are a universal characteristic of hysteria. On the contrary, not a few cases 
are marked by the great persistency and obstinacy of some one group of symp- 
toms; and the disease may exhibit an undeniable regularity, in its way, with 
regard to many phenomena. It must not be inferred that this is invariably true ; 
often the most diverse symptoms follow one another in quick succession. 

4. We have just indicated that hysteria may cause all sorts of functional 
derangements of the nervous system ; but yet there are certain definite symptoms 
which are to a considerable degree characteristic of the disease, and do not occur 
in the same way in other nervous affections. It is true that these symptoms are 
not present in all cases ; but if they are present, they make the diagnosis almost 
certain. Chief among them are certain convulsive attacks, and a peculiar kind of 
hemianesthesia. Very many regard a peculiar mental condition as character- 



756 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



istic. This last may be entirely wanting in hysteria ; and it may be one of the 
symptoms of other non-psychical diseases. 

With regard to aetiology, psychical causes, as has been said, are of first impor- 
tance. In numerous instances, hysteria comes on as an immediate sequel to violent 
emotional excitement or to a " psychical trauma," if we may use such an expres- 
sion. Hysterical convulsions or paralysis may be excited by great terror or vio- 
lent anger or any unusual agitation. Here the efficient cause is often hidden by 
some attendant circumstance. If, for example, a woman falls into the water or 
gets burned, or tumbles down stairs, and thereupon develops hysteria, the mistake 
is often made of ascribing the disease to catching cold, or to the injury received, 
although really it was the mental excitement which produced it. What is very 
remarkable in such cases is, that the special attendant circumstances at the time 
of the psychical disturbance often influence the localization of the hysterical phe- 
nomena : that part, to which attention was particularly directed at the time, not 
infrequently becomes, later on, the seat of the nervous disturbance. In hysterical 
joint-affections (page 498) the cause not infrequently proves to have been an 
injury to the particular joint now suffering from hysteria. A young girl, who was 
awakened at night by the smoke of her burning mattress and who had a severe 
laryngitis from inhaling the vapors, exhibited later an indubitably hysterical 
paralysis of the vocal cords. In the case of another girl, who in jumping from a 
carriage fell upon her side, we afterward saw hemianaesthesia of the same side. 
Many such instances could be cited. 

Certain hysterical cases, therefore, have for their obvious cause a single occa- 
sion of mental agitation; but, in many others, the disease is not thus abruptly 
excited. As in poisoning we can distinguish between the sudden action of a large 
dose and chronic cases, where minute amounts of poison are absorbed daily for a 
long period, so hysteria may come on, not only after a single violent shock, but 
also as the final consequence of psychical influences insignificant of themselves, 
but potent because of their frequent repetition or persistency. It is in cases of this 
sort that the causes do not become evident to the physician until he has gained the 
entire confidence of his patient ; for the root of the trouble is often entwined about 
the most private affairs. Anxiety, sorrow, disappointed expectations, abandoned 
hopes, and, in brief, everything which can depress and overwhelm the mind — 
these are factors which may at last excite the functional nervous derangements of 
hysteria. 

There are still other causes. The blow which brings a feeble body to the 
ground rebounds without effect from a massive frame. Exactly the same may 
be said of the " blows " to which the nervous system is subjected. Few entirely 
escape these influences, but there are some "strong natures" who resist the 
psychical assault without wavering, while others have a feebly resistant nerv- 
ous organization and are overpowered. We see, therefore, that the predisposition 
of different individuals to diseases of the nervous system varies. This fact is a 
very important one in the pathogenesis of all functional nervous disorders. In 
what this predisposition consists we do not know, being acquainted only with its 
results, and with some of its causes. 

In many cases this predisposition is hereditary. Hysteria is prominent among 
those neuroses which attack different members of a family — one suffering from 
one disease and another from another {vide page 729). It is also possible to 
acquire such a predisposition. At least, it may be developed and fostered, on the 
one hand, or, on the other, checked and repressed. In these directions physical as 
well as psychical factors are of importance. Anything which weakens the con- 
stitution, diminishes the resistant power of the nervous system. Among psychical 
influences, nothing favors the development of hysterical tendencies more efficiently 



HYSTERIA. 



757 



than does a bad education. Hysteria is often ascribable to an irritability and fee- 
bleness of the nervous system thus engendered. The whims of the child are not 
controlled, its will is not strengthened, nor its energy developed ; its imagination 
is unsuitably and excessively stimulated, or its intellectual powers are overtaxed 
and prematurely ripened. 

It is well known that hysteria occurs more frequently in the " feebler " female 
sex than among men; but it is by no means a rare thing for men to exhibit 
hysterical convulsions, paralysis, contracture, or other well-marked disturbances. 
Most cases occur between puberty and the end of middle life. It is not very rare 
to see pronounced hysteria in children, especially such as are not under eight or 
ten years old. And, indeed, the disease very frequently begins to be developed a 
year or two previous to puberty. Nationality and race also seem to exert some 
influence — for instance, the severer forms of hysteria are decidedly more frequent 
in France than in Germany ; and the Jewish race are particularly subject to the 
disease. 

One matter remains to be considered with regard to aetiology, to which a 
greatly exaggerated importance was formerly ascribed. It is the influence of dis- 
ease of the sexual organs. The very name " hysteria " (vo-repa = uterus) reveals 
what the old view was, namely, that hysteria invariably originated in disease of the 
female genitals. Not to speak of the fact that the disease occurs in men and chil- 
dren, an unprejudiced consideration of the matter will show that the above assump- 
tion is entirely groundless even in regard to women. A large number of hysterical 
women present no anomaly of their sexual organs ; and even if the latter are 
diseased, we are not justified in at once assuming that the hysteria is secondary to 
the sexual disorder. In these cases, also, we usually find, on careful inquiry, that 
psychical causes have been at work ; and these are incomparably more potent in 
exciting hysteria than is malposition of the uterus or constriction of the cervical 
canal. It is true, however, that disease of the genital organs may depress the 
spirits more than some other diseases would, and so indirectly promote hysterical 
disturbances. In the same indirect way, menstruation, pregnancy, and confine- 
ment exert an important influence upon the development and course of hysteria. 
Sexual excesses or total abstinence from sexual indulgence also produce their 
effects indirectly through the mind. 

Symptomatology. — 1. Mental and Physical Characteristics of Hysterical Indi- 
viduals. — Many hysterical patients betray in their whole mental and moral bear- 
ing certain peculiarities, which are sometimes so characteristic that the physician 
can form an opinion from the condition and behavior of his patient as to the 
nature of her disorder. Hysterical persons are irritable and emotional, easily 
depressed, sensitive, whimsical, and subject to violent extremes of feeling. They 
are inclined to exaggerate their sufferings, exact a great deal of attention, and are 
anxious to excite sympathy. They have little energy or force of will ; but they 
are sly and obstinate in carrying out any pet desire. Again, they can be very 
amiable and attractive, if they take the fancy. They are almost invariably clever. 
It is comparatively exceptional to see hysteria in dull and stupid persons. 

This brief sketch represents many cases, as we have said, but not all. Such 
patients very frequently present no very great disturbances, but complain merely 
of all sorts of general derangements, sometimes of one kind and sometimes of 
another, and yet are able to perform their daily duties tolerably well. A case 
of paralysis, contracture, or other important localized hysterical trouble may not 
present any marked mental peculiarities. Either there are none, or, if they exist, 
the patient conceals them from the physician. 

With regard to the general physical constitution of hysterical subjects, it has 
already been mentioned that any bodily weakness favors the development of the 



758 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



disease ; and yet hysteria is by no means confined to the ill-nourished, weakly, and 
anaemic. On the contrary, many patients seem to be in blooming health and well 
nourished. In a severe case of hysteria, however, the effects of the disease on 
general nutrition may be very distinct. Little food is ingested, sleep is disturbed, 
digestion is affected (vide infra), and the bodily health is gradually undermined. 

2. Hysterical Convulsions. — In bad cases of hysteria, convulsions frequently 
play an important part. Their diversity is great. Almost invariably their first 
onset can be directly referred to some unusual emotional excitement ; and even 
the later attacks are generally traceable to psychical causes. In a typical case the 
convulsions always involve the entire frame. They may exactly resemble an epi- 
leptic fit — "hystero-epilepsy." The similarity relates only to the character of the 
convulsive movements. The paroxysm of hysteria never induces complete loss 
of consciousness. Total insensibility shows genuine epilepsy ; so that, if it is pres- 
ent, and hysteria is known to exist, the case must be one of combined epilepsy and 
hysteria, which is undoubtedly possible. In most instances, however, the hyster- 
ical paroxysms, even in their worst forms, do not resemble those of epilepsy very 
closely, and a practiced eye can often distinguish the true hysterical character of 
the attack at the first glance. The convulsive movements of hysteria are usually 
much more extensive and complicated than of epilepsy. The arms and legs are 
thrashed violently about, the trunk is tossed to and fro, and sometimes performs 
complete rotation upon its own axis, or is bent into extreme opisthotonos. Not 
infrequently the arms make motions which are apparently thoroughly co-ordi- 
nated ; the patient strikes out with clinched fists, or tears out her own hair. The 
head may beat with great violence against the pillow. Twitching of the separate 
muscles of the face, as seen in epilepsy, is rare, although there may be marked 
trismus. The countenance is usually distorted, and it often exhibits an expression 
of fury, anguish, or the like. The intelligence is not unimpaired, but it is not 
entirely suspended. An important point is that there is no long period of uncon- 
sciousness after the convulsions have ceased, such as we expect in a severe epileptic 
attack. We shall revert below to certain special manifestations of disturbed intel- 
lect often occasioned by hysterical paroxysms. During the attack the pupils react 
to light normally. 

Another very frequent form of hysterical convulsions attacks the respiratory 
muscles. The paroxysm begins with a convulsive acceleration of respiration. 
The breathing becomes more and more rapid and hurried. Very often the whole 
body is at the same time rigidly extended, with trembling of the trunk and 
extremities. Respiration is sometimes accelerated to an almost incredible degree : 
there may be far more than a hundred respirations per minute ! 

A third variety of hysterical convulsion is distinguished by convulsive expres- 
sion of emotion. Thus there are hysterical crying-fits, laughing-fits, and scream- 
ing-fits, the characteristic symptom in each being indicated by its name. 

Sometimes the convulsions are confined to one group of muscles. We may 
have, for example, isolated spasm of the muscles of the neck, or of the respir- 
atory muscles, or of one arm or one leg. The laryngeal muscles may be affected 
(hysterical spasm of the glottis). The diaphragm is quite often involved, causing 
hysterical hiccough. The pharynx and oesophagus may likewise be attacked ; 
and it is to their spasmodic action that the production of the so-called globus 
hystericus is ascribed : the patient has a feeling as if a lump came up into her 
throat and then passed downward again. 

All the varieties of hysterical convulsions mentioned exhibit the greatest diver- 
sity in duration, violence, and frequency. Sometimes they last but a few minutes; 
again they persist, with brief interruptions, for days and weeks. Charcot was the 
first to observe that in many cases it is possible to excite the paroxysms artifi- 



HYSTERIA. 



759 



cially, by pressure upon the ovarian region, above Poupart's ligament. Charcot 
was, however, mistaken in his original belief that in this way the ovary itself was 
invariably compressed. This procedure does sometimes excite an attack, but not 
in all instances. Oftener (but not always) the attempt to cut short an attack by 
pressure upon this region will be successful. 

3. Hysterical Paralysis. — Hysterical paralysis also is frequently an immediate 
sequel to some violent mental excitement (for example, " paralysis from fright ") ; 
but it may come on gradually. Hysterical paralysis is indubitably of central 
origin. It is a paralysis of the will. The patient has lost the power to will a 
contraction of the affected muscles. One always has the feeling that the patient 
could move the paralyzed limb perfectly well, if she only desired to ; but she can 
not bring the will to bear on it, and this inability is the real trouble. 

The extremities are most frequently paralyzed, particularly the lower limbs ; 
but hemiplegia is not very rare. A very common manifestation is loss of the power 
to walk. The patient lies in bed or on a sofa, and sometimes while thus reclining 
she can flex and extend the legs very well ; but as soon as she is urged to stand up 
or walk, the knees double up, the patient begins to tremble, the respiration grows 
rapid and convulsive, and there is not the slightest effort made to move the legs. 
If only one leg is paralyzed, the gait is often very peculiar and characteristic. 
The sound limb makes long strides, while the paralyzed one is held perfectly rigid 
and often is dragged along with a loud shuffling sound. The arms are much less 
often affected. The facial muscles are hardly ever paralyzed. 

Hysterical paralysis of the vocal cords is seen very often. The voice is gener- 
ally lost suddenly, and the patient can talk only in a whisper — hysterical aphonia. 
On laryngoscopic examination, we are often struck, at the outset, by the anaes- 
thesia of the pharynx and its lack of reflex excitability. We find no trace of any 
anatomical lesion of the cords, but merely that they are paretic. The glottis can 
not be completely closed, and sometimes the vocal cords actually grow wider apart 
upon every effort at phonation. The patient then speaks exclusively in a whisper. 

Hysterical paralysis of the pharynx and oesophagus is much less frequent. 
If there is dysphagia, it is often not an easy matter to determine whether it is due 
to paralysis or to spasm. 

4. Hysterical Contractures. — Contracture may occur as an isolated phenome- 
non, or in combination with other symptoms, such as anaesthesia or paralysis. It 
is often obstinate and very annoying. The extremities suffer most frequently, 
although the trunk or the back of the neck may be affected. The arms, if affected, 
usually exhibit spasmodic flexion, and the hands are clinched convulsively. The 
legs are usually rigidly extended. It has already been mentioned (page 498) that 
contractures are often combined with hysterical "neuralgia of the joints." 

Sometimes contracture and paralysis are seen together. There may be para- 
plegia or hemiplegia. This condition sometimes follows directly upon an hyster- 
ical convulsive seizure. Anaesthesia produced by chloroform will immediately 
and completely relax any hysterical contracture. 

5. Hysterical Ancesthesia. — Anaesthesia is a very frequent symptom in hys- 
teria. Its completeness and extent vary greatly. We may find an almost uni- 
versal analgesia of the entire body. A needle may be thrust through a fold of 
skin without the slightest indication of suffering. Such analgesia explains most 
of those cases where hysterical patients inflict upon their own persons all sorts of 
injuries, in order to make themselves interesting. The mucous membranes are very 
frequently equally devoid of sensation. The laryngoscope, or the oesophageal 
bougie, fails to excite the usual reflex phenomena. 

The extent of surface affected with anaesthesia varies, as has already been 
remarked, in different cases. Sometimes the whole body is involved, sometimes 



760 NEUKOSES WITHOUT KNOWN ANATOMICAL BASIS. 



the anaesthesia is confined to separate small spots, immediately contiguous to 
which may exist pronounced hyperaesthesia (vide infra). Most characteristic of 
all is the phenomenon first accurately studied by Charcot, known as hysterical 
hemianaesthesia. 

Hysterical hemianaesthesia is one of the most common symptoms of profound 
hysteria. It must often be sought for, inasmuch as the patient herself frequently 
has no suspicion of its existence until her attention is called to it. It seems just 
as if one half of the body had been entirely lost to consciousness : the patient does 
not know whether it is or is not capable of feeling. 

In a typical and fully developed case, the hemiansesthesia does actually affect 
just one half of the body. There are rudimentary forms ; but in these complete 
ones, the boundary between the anaesthetic parts and the parts retaining normal 
sensitiveness accurately corresponds to the median line of the body. The skin on 
the affected side is entirely insensible to the prick of a needle or to heat. Often 
it seems somewhat blanched, and its blood-vessels seem to be constricted ; at least 
the skin very often bleeds surprisingly little if wounded. The mucous mem- 
branes upon the abnormal side are all equally anaesthetic, including the conjunc- 
tiva, that half of the buccal cavity, and of the tongue. The deeper parts, such as 
the muscles and joints, are also almost invariably anaesthetic. The patient can no 
longer feel in what position the limbs of the affected side are ; and, if they are 
moved passively, no sensation is communicated to her. The organs of special 
sense are usually involved. Hearing is impaired upon the affected side ; the cor- 
responding half of the tongue can not taste ; the corresponding nostril can not 
smell ; and sight upon that side is affected in a peculiar manner. There is no 
hemiopia, but a total amblyopia, or possibly amaurosis. Another characteristic is 
the narrowing of the field of vision and color blindness (achromatopsia). We are 
obliged to omit many interesting particulars, almost all of which have been dis- 
covered by Charcot and his pupils. It is the usual way in these cases for the per- 
ception of violet to be lost first, then of green, and then finally of blue and yellow. 

Sometimes this hemianaesthesia is the only manifestation of hysteria, but very 
often it is associated with paralysis or contracture. There is another remarkable 
phenomenon, which Duchenne was the first to describe under the name of " loss 
of muscular sense " (perte de la conscience musculaire), and which deserves brief 
mention here. The patient, whose arm, for example, is anaesthetic, can not move 
it if she closes her eyes, although with open eyes she can move it as well as ever. 
When the eyes are shut, the arm remains motionless in the position it has pre- 
viously occupied. If its position be altered by passive motion, the new posture is 
maintained with equal persistency. In other words, there is well-marked cata- 
lepsy (see the preceding chapter) if the eyes are closed. The same is true of the 
lower extremity. As yet, we are entirely unable to explain this symptom. 

Other peculiar symptoms will be mentioned further on, including metallo- 
scopic and allied phenomena, and the phenomena of transfer. 

6. Hyperesthesia and pain are also not infrequently observed in hysteria. 
These symptoms exhibit great variety. It has been already pointed out that 
marked hyperaesthesia is sometimes found close beside anaesthetic regions. In 
hemianaesthesia the patient occasionally complains of painful sensations refer- 
able to the affected side. Hysterical contractures are also often associated with 
violent pain. The hyperaesthesia may be so acute that the slightest touch makes 
the patient scream. We can not, however, be certain whether the pain is really 
so excruciating, or whether the patient exaggerates her suffering. 

Hysterical neuralgia is sometimes mentioned ; but, if there is a really typical 
neuralgia present, it is more natural to assume that there is a complication of 
hysteria with neuralgia. This is certainly not uncommon. Hysterical neuralgia 



HYSTERIA. 



761 



of the joints has a real existence, but differs in many respects from genuine 
neuralgia. 

Certain special painful sensations are quite characteristic of hysteria. First 
among these is pain localized at one particular point in the „head (so-called clavus 
hystericus), which is often paroxysmal and accompanied by general indisposition. 
Again, there is spinal irritation, producing marked tenderness of the spinal 
column on' pressure, either throughout its entire extent or at certain definite 
points. Another very remarkable symptom is that which Charcot termed 
"ovarie" or "ovarian hyperesthesia. " This consists of an often extraordinarily 
great sensitiveness to pressure in the ovarian region. It is not at all probable 
that the sensitiveness is in every case actually seated in the ovary itself. It is, 
however, certain that we quite often find tenderness in that neighborhood. As 
already mentioned, pressure in this locality will sometimes excite an hysterical 
convulsive seizure. Ovarie, like hysterical hemianaesthesia, is, on the whole, more 
frequent on the left side than on the right. 

Other portions of the body may be noticeably hyperaesthetic in hysteria, 
beside the ovarian region, such as the breasts, the sternum, and the epigastrium. 
And, in conclusion, it should be stated that sometimes there is hyperesthesia of 
the nerves of special sense, making the patient abnormally sensitive to light, or 
sound, or to certain odors and tastes. 

7. Symptoms referable to Certain Organs. — We have already spoken of nerv- 
ous dyspnoea, and of paralysis and spasm of the larynx and oesophagus. Certain 
derangements in other parts have still to be discussed, which are also to be classed 
as nervous. 

A not infrequent cardiac symptom is nervous palpitation, often accompanied 
by angina. Such attacks are particularly common after anger or other emotional 
excitement. It may be said here, in passing, that hysterical patients have been 
repeatedly observed to present more or less typical symptoms of exophthalmic 
goitre. This remark has been also made in another connection. Vaso-motor dis- 
turbance is very frequent. We have already spoken of spasmodic anaemia of the 
skin as a frequent accompaniment of hysterical anaesthesia. Abnormal degrees of 
anaemia or hyperaemia of the skin may also occur independently of disturbances 
of sensation ; the skin may be cool and pale, or hot and red. Probably similar 
conditions may arise in the viscera. Free haemorrhage from the internal organs 
appears to be of not infrequent occurrence in hysterical patients, and the attempt 
has been made to explain it as due to disturbance of the vaso-motor nerves. Hys- 
terical haematemesis " and " hysterical haemoptysis " may cause the inexperienced 
practitioner grave apprehensions with regard to the stomach or lungs. In such 
cases, however, the blood is usually peculiar; it is of watery consistence, and of a 
bright raspberry-red color. It is usually mixed with considerable mucus, in the 
shape of flecks and shreds. Almost invariably the amount is small, being rarely 
more than two or three ounces in twenty-four hours. In most cases its true source 
is not the stomach or the lungs, but the gums or the lining membrane of the 
mouth, or some similar tissue. Hysterical haemorrhage has also been observed 
from the genitals, and into the skin, producing "stigmata." 

The digestive disturbances which many patients have are mainly such as have 
already been discussed on page 375, under the head of " nervous affections of the 
stomach.' 1 Colicky pains, obstinate constipation, occasional diarrhoea, and similar 
symptoms, are by no means rare. Hysterical tympanites also deserves mention. 
It is due to the accumulation of a large amount of air and gas in the primae 
viae. This may be in part the result of a sort of paresis of the muscular coat of 
the stomach and intestines, but another frequent cause is the swallowing of large 
amounts of air. Perhaps the patient does this on purpose. The prominence and 



762 NEUEOSES WITHOUT KNOWN ANATOMICAL BASIS. 



tension of the abdominal walls may be so considerable as to simulate grave dis- 
eases, like peritonitis, or a tumor, or pregnancy. Doubts of this sort can always 
be dispelled by inducing anaesthesia with chloroform. It is possible to remove 
the gas completely in a short time by pressing upon the abdomen, or introducing 
a long tube through the rectum. 

Anomalies of the secretory and excretory organs have also been met with in 
hysteria. Many patients have a remarkably dry skin, while others sometimes 
perspire very freely. The secretion of saliva is subject to similar modifications. 
Very remarkable observations have been made in a few cases with regard to hys- 
terical ischuria; for days only a very small amount of urine has been passed, 
although there has been no retention. In one case of this sort, observed by Char- 
cot, there was violent vomiting at the same time ; and the vomitus contained a 
comparatively large amount of urea (vicarious excretion). Hysterical polyuria 
occurs more frequently than the ischuria. A large amount of very light-colored 
urine of low specific gravity is excreted. This polyuria is in many instances 
merely the result of excessive ingestion of liquids. Polydipsia (excessive thirst) is 
a very frequent symptom in hysteria, particularly at the close of a fit. 

Sometimes there are symptoms referable to the genital organs. It has been 
already pointed out that too much prominence was formerly given to the influence 
of sexual diseases in exciting hysteria. It is also true that nervous derangements 
of the genital organs may be among the symptoms of hysteria. In this way pain 
and hyperesthesia may be occasioned, and possibly many instances of dysmenor- 
rhcea and leucorrhcea have a similar origin. We can also readily understand 
that sexual relations often influence very excitable, hysterical individuals to no 
slight extent, as indeed is very frequently betrayed by the character of their hal- 
lucinations and their utterances when delirious. 

8. The " Grand " Paroxysms of Hysteria* — Nearly all the symptoms thus far 
enumerated belong to the comparatively mild manifestations of hysteria ; but in 
some cases, fortunately rare ones in Germany, there is a yet more complete sus- 
pension of all regulation of the psycho-motor and psycho-sensory processes. The 
symptoms of this " grande hysterie " have been most thoroughly studied by Char- 
cot, and by Bourneville and Regnard and P. Richer after him, most of the obser- 
vations being made at the Salpetriere, in Paris. We have space merely for the 
main points. 

The " grand paroxysms of hysteria " can almost always be divided into several 
stages. The first period is occupied with most violent epileptiform convulsions, 
during which the patient is apparently insensible. After these have lasted a few 
minutes the second period begins. In this there are " contortions, and movements 
which have a wide excursion"; or another name is " clownismus." The patient 
tosses about, kicks, crooks her whole body into an " arc of a circle," delivers blows 
with her arms, and screams. Gradually the second merges into the third period 
of statuesque postures and " attitudes of passion " (" attitudes passionelles "). The 
patient is wholly given up to some particular series of ideas ; she has hallucina-. 
tions, seems to be living over again some exciting experience of her previous life, 
her whole body, as well as her features, being expressive of passionate excitement, 
threats, defense, concupiscence, reproach, or scorn. The condition is usually fol- 
lowed by, or associated with, general delirium, hallucinations (particularly about 
animals), contractures, anaesthesia, and other hysterical symptoms. The other 
forms of the grand paroxysm are mainly combinations of the individual symptoms 
already sketched. In Charcot's cases the attacks could be interrupted at any time 
by pressing upon one ovarian region. 



* Genuine hysterical insanity is without our province. 



HYSTEEIA. 



763 



9. Hypnotic Phenomena. — The hysterical symptoms now to be discussed are 
marvelous and of great interest, although as yet obscure and almost mysteri- 
ous. These remarkable nervous conditions may be produced in many hysterical 
subjects by means of certain external influences, chief among which are a sud- 
den, brilliant light, the vibrations of a tuning-fork, or certain other rhythmical 
stimuli, and steady gazing. Eicher has described four main varieties of hyp- 
notism ; but they merge into one another in all sorts of ways. 1. There is the 
cataleptic condition, in which the limbs retain the postures they are given pas- 
sively (see preceding chapter). 2. The condition of " suggestion," when halluci- 
nations may be artificially produced. If the subject is put into an attitude express- 
ive of some definite action, all the ideas appropriate to that action are excited with 
the vividness of an hallucination. Examples of this are seen at public exhibitions, 
where grown men, under the influence of hypnotism, rock invisible infants, or 
eat raw potatoes as if they were delicious fruit. 3. Lethargy — that is, a condition 
of apparent unconsciousness, with closed eyes, completely relaxed muscles, and 
a remarkably increased irritability of the muscles and nerves. Merely a gentle 
pressure or a slight blow upon a nerve — for instance, the facial nerve — suffices to 
excite a tetanic and long-continued spasm of all the corresponding muscles. 4. 
Certain manipulations, such as rubbing the scalp, will transform the lethargic 
condition into that of hysterical somnambulism. The patient is half-conscious, 
but answers automatically any questions which are put to her, and does whatever 
she is bid. Sometimes the special senses exhibit abnormal acuteness. 

All the conditions enumerated may also attack hysterical persons in spontane- 
ous and isolated paroxysms. And, indeed, there is no hypnotic phenomenon 
which can be artificially produced in healthy persons but has its perfect analogue 
among the symptoms of hysteria, and is referable to the same main conditions. 

General Course of the Disease. — Our description of the symptomatology of hys- 
teria has been confined to the most important and frequent phenomena ; and yet 
even this meager outline shows what an infinite variety of shapes the disease 
assumes. 1. In one class of cases there are no severe symptoms whatever. The 
patient merely displays the general mental condition characteristic of hysteria : 
she is easily excited, prone to make much of her ills, has all sorts of symptoms, 
like pain, palpitation, dyspepsia, and dyspnoea, and these are aggravated by men- 
tal excitement, while at other times they may so nearly vanish that the patient 
does not appear to be ill. 2. A second class of cases has more severe disturbance, 
coming on after some unfavorable psychical influence. The patient may have 
displayed a general hysterical tendency previously, or may have seemed perfectly 
well. Here we may observe all the symptoms above enumerated and described. 
There may be paralysis, spasm, contracture, anaesthesia, or paresthesia. The indi- 
vidual symptoms may persist obstinately for weeks and months ; but again they 
may vanish on a sudden, or give place to other disturbances. Psychical influences 
are unmistakably potent, not merely in the incipient stage, but also in the further 
course of the disease. Any aggravation of the symptoms is usually referable to 
emotional excitement. This is particularly true of the hysterical convulsions. 
In many cases, almost every fresh paroxysm is due to anger, terror, or some simi- 
lar cause. 3. The third class comprises the most severe forms of hysteria, with 
those nervous disturbances briefly outlined above. They are as complicated as 
they are puzzling, and form manifold combinations with all the other hysterical 
phenomena, including anaesthesia, contracture, and paralysis. 

The entire duration of the disease varies greatly. The true root of all evil is 
the abnormal excitability of the nervous system, which always remains in 
unstable equilibrium ; and often it is not possible to cure this. If not, the trouble 
lasts almost indefinitely. New manifestations of the disease succeed to periods of 



764 NEUE03ES "WITHOUT KNOWN ANATOMICAL BASIS. 



apparently perfect health. Usually the symptoms do not abate till quite late in 
life. There are, however, many instances of complete and permanent relief. 
This favorable termination is more especially to be hoped for where the patient 
comes into suitable and appropriate conditions of life, having some regular occu- 
pation which is not exposed to all sorts of unfavorable psychical influences. Many 
cases of hysterical disturbance, in previously healthy children or young adults, 
and due to some distinct cause, terminate comparatively soon, and never recur. 
It is never possible, however, to be sure that there will be no relapse, inasmuch as 
a single appearance of hysteria shows unmistakably that the nervous system is 
abnormally vulnerable. 

Diagnosis. — An experienced physician is seldom greatly puzzled by hysterical 
affections. Although the disease may at first simulate some grave organic disor- 
der, a careful physical examination and continued observation will almost invari- 
ably disclose the true character of the case. In the first place, there are never 
any such symptoms as would absolutely prove the existence of some organic 
lesion. For example, we never find atrophy or loss of electrical reaction in con- 
nection with hysterical paralysis. Secondly, many symptoms are characteristic 
of hysteria and are never seen in any other disease. Such are numerous forms 
of convulsions, and hemianaesthesia with amblyopia of one eye. Above all, we 
should regard the whole psychical behavior of the patient, the influence exerted 
upon her by emotional disturbances, and the aetiology of the illness — for instance, 
if caused by some mental excitement or emotion. 

Treatment. — What has been said about the aetiology of hysteria at once sug- 
gests a possible method of prophylaxis. A watchful eye will often detect, even in 
childhood, the signs of abnormal nervous excitability, and in such a case the 
parent will make it his duty to impose a suitable physical and mental regimen, 
that graver disturbances may be averted. 

If hysteria is already developed, the first and most important treatment is 
mental. There could be no greater mistake than to deride the patient or treat 
her as a malingerer ; for hysteria is a disease, and its symptoms are just as inde- 
pendent of any conscious volition on the part of the patient as those of any other 
disease. It is, however, absolutely essential to carry out the moral training, 
which the physician must institute, with all the proper strictness and energy, 
because in this way alone can any good be accomplished. Sometimes this most 
important indication can be fulfilled only after the patient has been withdrawn 
from the over-anxious and over-assiduous parents or relatives, and like unfavor- 
able influences. In such cases, treatment in some institution will often be vastly 
better than the best care at home ; and our own experience leads us to recommend 
most urgently that the eventual necessity of removal to an asylum should be 
constantly borne in mind with regard to aggravated cases. Often the mere dread 
of removal to such a place has a favorable mental influence. 

Proper moral treatment achieves comparatively the best results where there is 
hysterical paralysis. When we are once certain that the paralysis is due to 
hysteria, the patient must be instructed how to regain by practice the lost power 
of the will over the paralyzed muscles. If the paralysis affects the lower extremi- 
ties, as it usually does, the patient must be set on her feet, regardless of all her 
opposition and complaints, and kindly but most firmly required to try to walk. 
Of course, at first she must be well supported. This exercise must be, methodically 
gone through with several times a day. Gradually the patient's gait becomes 
more and more secure. She regains confidence in her own ability, and, having 
once begun to improve, usually makes rapid progress toward complete recovery. 
Every experienced physician can recall numerous instances where hysterical 
paralysis which had lasted weeks and months was cured in a few days by 



HYSTEEIA. 



765 



this mode of treatment. Faradization of the muscles, cold sponging, with friction, 
and bathing, are excellent adjuvants ; and the disagreeable element in these pro- 
cedures of itself stimulates the patient to make every possible exertion to regain 
the use of her limbs, 

When there is hysterical paralysis of the vocal cords, a similar training will 
be found both practicable and efficient. Electricity is also of great value. It may 
be applied externally or within the larynx. Often the patient, terrified by the 
sudden pain it causes, recovers her voice at once. 

The treatment of hysterical contractures consists, first, in an effort to loosen up 
the contracture by massage and energetic passive motion. Faradism will be found 
of assistance here also. In order to maintain the ground thus gained, the patient 
must be induced to exercise the muscles regularly by making voluntary movements. 

For hysterical convulsions there is one sovereign remedy — cold water, either as 
a bath or a douche. This treatment is usually sufficiently disagreeable to enable 
the patient to summon up the necessary energy for controlling her muscles and 
terminating the convulsion. Dread of a repetition of the bath contributes greatly 
to the voluntary inhibition of any impending fresh attack ; but, if the attack is 
repeated, the bath must also be, immediately. As above mentioned, a paroxysm 
may often be cut short by pressure upon the ovarian region ; but the benefit is not 
a permanent one. The milder varieties of hysterical convulsion, such as hysterical 
hiccough or cough, are often controlled by a stern reproof. It is precisely in these 
cases that the moral effect of transfer to some institution frequently causes the 
abrupt disappearance of symptoms which have lasted for months. 

Hysterical anaesthesia is best treated with the faradic wire-brush. This vigor- 
ous irritation restores the anaesthetic i>arts to the domain of consciousness. It 
should be said, however, that these cases may prove obstinate or relapse. 

The most difficult of all hysterical cases to treat are those where the symptoms 
are not strongly pronounced, but where there is a general hysterical condition, 
expressing itself in a multitude of nervous derangements, like palpitation, dyspep- 
sia, and general debility, or in purely subjective symptoms, or in emotional 
tendencies. Such patients are often advanced in years, so that little is to be hoped 
for from moral training ; and then circumstances may be unfavorable without our 
being able to remedy the situation. Even here, however, the physician may 
greatly benefit the patient by means of psychical influences, if he once gains her 
complete confidence. It will also be found advantageous to employ such remedies 
as invigorate the nervous system (see the next chapter) ; electricity should be given, 
either in the form of general faradization or the faradic brush applied to the back 
and shoulders, or the galvanic current applied to the spinal column and the sym- 
pathetic nerve ; and of still greater importance is a methodical cold- water treat- 
merit, either by sponging, or bathing, or douches. Such patients are often vastly 
improved by sea-bathing in summer, or by going to the mountains. 

The numerous internal remedies for hysteria are also of more use in these 
general conditions than where there are marked nervous disturbances in special 
parts of the body. In the latter, internal remedies do good only indirectly and 
subjectively, and about in proportion to the confidence of the patient in the vir- 
tues of the medicine. This is the explanation of the frequent cases of rapid 
recovery after taking homoeopathic and "electro-homoeopathic" remedies, and 
those still more marvelous cures effected by means of holy water and relics. 

Among the " anti-hysteric " agents contained in our medical thesaurus, asafoeti- 
da, valerian, and castoreum are the most famous ; but probably few would at the 
present day claim that they possess any specific virtues. Perhaps the preparations 
of valerian are the most useful where there is hysterical excitement, as evinced by 
convulsions or palpitation. Bromide of potassium, arsenic, and other medicines 



766 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



which, ordinarily exert a favorable influence upon the nerves, seldom accomplish 
any permanent good in hysteria, although often prescribed. Narcotics do little 
good, and may do much harm. It is easy to develop the morphine-habit in such 
patients. 

If hysteria be complicated by some actual organic disease, the latter of course 
demands special treatment. Great benefit is hoped for by many from the cure of 
any uterine complaint which may be present. Cases are known where grave hys- 
terical disturbance has vanished upon dilatation of a constricted cervical canal or 
rectification of a displacement ; but there are numerous other instances on record 
where gynaecological treatment has proved entirely unavailing. It may also be 
questioned whether, in the successful cases, the main benefit was not due to sub- 
jective influences. Hegar has removed the ovaries in a few severe cases, but the 
operation is not yet fully established. At any rate, it is justifiable only when the 
ovaries are known to be in an abnormal condition. Friedreich claims to have had 
excellent results from energetic cauterization of the clitoris. We do not believe 
that in this he will have many imitators. 

Metallo-therapeutics. — We subjoin a few exceedingly interesting observations 
made upon hysterical subjects, although as yet they have not assumed practical 
importance : 

A French physician, named Burq, discovered years ago that by laying plates 
of metal upon a cutaneous surface affected by hysterical anaesthesia a remarkable 
result is sometimes produced. Almost at once sensation is restored to the imme- 
diate region, and often to a much larger area. Most of the cases have been those 
of hysterical hemianaesthesia. It is not every kind of metal which will prove 
effective, nor will the same kind affect all patients. It is said that iron is most 
frequently efficient ; but sometimes copper, zinc, or gold is required. The process 
of determining the metal essential to each individual case Burq called " metal- 
loscopy " ; and he stated that this metal would also have the same effect if given 
internally ! In 1876 a committee appointed by the Parisian Societe de Biologie 
tested these statements, at least with regard to the external application of metals 
— the idea of their internal administration having been pretty much abandoned — 
and confirmed them. Charcot also discovered many remarkable facts of a similar 
nature, which likewise soon received universal substantiatiou. The most remark- 
able of these phenomena is known as transfer. The return of sensation to the 
anaesthetic area, as a result of applying a metal plate, is accompanied by a simul- 
taneous development of anaesthesia upon the opposite, previously normal side, in 
an exactly corresponding place. Sometimes sensation oscillates from one side to 
the other and back again, so that now one half of the body and now the other is 
alternately sensitive or anaesthetic. If the metal be placed at the start upon the 
normal skin, that part becomes anaesthetic, while the corresponding part upon the 
opposite side of the body regains its former normal condition. 

It has also been discovered that other hysterical symptoms exhibit analogous 
phenomena. Transfer can sometimes be observed in hysterical amblyopia, achro- 
matopsia, deafness, loss of smell and taste, contractures, and paralysis. Such 
transfers may be induced by means of various means other than metal plates. 
These are classed as aesthesiogenous remedies, and include large magnets, feeble 
galvanic currents, and static electricity. Vibrating tuning-forks and sinapisms 
have also produced similar results. 

These remarkable statements, first made by such men as Charcot, Regnard, 
Vigouroux, Petit, and Dumontpallier, seemed at first incredible, but have never- 
theless been almost universally confirmed. As yet, it is impossible to explain 
them. Evidently these phenomena are connected with the deepest psycho-phys- 
ical processes. 



NEUEASTHENIA. 



767 



CHAPTEE X. 

NEURASTHENIA. 

{Nervous Debility.) 

When studying the disorders of the spinal cord, it will be remembered that we 
found one group of symptoms which did not rest upon any discoverable anatomical 
basis, but which were merely functional (vide page 570). In some part due to abnor- 
mal excitability of the nervous system, but mainly, however, the result of impaired 
vigor, this condition was denominated "nervous weakness." Perfectly analogous 
phenomena may originate in the brain, and are named cerebral neurasthenia, in 
contrast with spinal neurasthenia. In most instances we meet with both cerebral 
and spinal symptoms, and must therefore call the disease cerebro-spinal, or gen- 
eral, neurasthenia. 

The American neurologist Beard was the first to recognize the importance of 
this disease and to give it its present name. Beard was at first inclined to believe 
that neurasthenia was mainly an " American disease " ; but this is by no means 
the case, inasmuch as sufferers from neurasthenia form a very important contin- 
gent among the patients of G-erman specialists. Neurasthenia is certainly one of 
the most frequent and important nervous diseases, from a practical standpoint ; 
nor is its study by any means devoid of scientific interest. 

Causation. — A full list of the causes of neurasthenia would include almost all 
those influences which in any way act unfavorably upon the nervous system. 
Most of these have been enumerated on page 570. Where the disease is mainly 
of the cerebral form, excessive brain-work contributes very largely to its produc- 
tion, particularly when combined with certain kinds of excitement. The mer- 
chant is liable to it, whose bold ventures subject him to deep anxiety and eager 
hope; and the politician, who is incessantly agitated by party strifes; and like- 
wise the artist or scholar, whose ambition gives him no rest. In all these cases 
the nervous system finally becomes exhausted — that is, neurasthenia is established. 
Even here, however, neuropathic tendencies come into play, for some are crushed 
by a burden which others can bear. In very many instances this liability to the 
disease is inherited; in others it is acquired (vide page 756). 

As was mentioned under spinal neurasthenia, hypochondria frequently 
assumes an important role in these cases. It not only exaggerates the existing 
symptoms, but contributes others of its own. In this we find one essential differ- 
ence between neurasthenia and genuine hysteria. In the latter, however much 
complaint there may be, a genuine hypochondriacal tendency is extremely rare. 
Hypochondria becomes even the essential factor in those melancholy forms of 
neurasthenia which so often result from onanism or other sexual abuses. This 
same element is also probably the main one in the strikingly frequent cases of 
neurasthenia in physicians. 

The symptoms of spinal neurasthenia have been already briefly described, so 
that we may here confine our remarks chiefly to the still more important cerebral 
symptoms. Most frequent among these is a subjective sensation of pressure in 
the head. Patients give a very various description of this sensation. Essentially, 
however, it is a feeling of pressure and numbness, and makes the patient doubt 
whether he is in the full possession of his intellectual powers. The pressure is 
sometimes chiefly frontal and sometimes occipital ; it may rise to the height of 
actual pain, this being frequently associated with marked hypergesthesia of the 
scalp. 

Associated with this pressure there is, as we have just intimated, in many cases 



768 NEUEOSES WITHOUT KNOWN ANATOMICAL BASIS. 



a sense of incapacity for any methodical intellectual effort, an intellectual debil- 
ity often rendering the patient entirely incapable of performing the duties of his 
vocation. He can no longer write or read for any length of time, these pursuits 
being further interfered with, in some cases, by a feeling of weakness and pressure 
in the eyes themselves (neurasthenic asthenopia). A very important symptom is 
loss of sleep. This symptom is, in many cases, the most annoying of any, and 
makes the patient importunate for relief. There is almost sure to be depression of 
spirits ; the patient does not believe that he will ever recover, and gives voice to 
the most melancholy predictions. Beard has called attention to peculiar condi- 
tions of anxiety sometimes observed in neurasthenic patients. The sufferer dreads 
to go into society, or to mingle with a crowd, or to be subjected to any physical 
jar. Vertigo is also frequent, but is rarely very severe. 

The lack of intellectual energy is, in most cases of any severity, accompanied 
by decided bodily weakness. This, too, would often seem to be of cerebral origin, 
and consequent upon deficient innervation of the muscles by the nervous centers. 
The patient can not walk far without becoming weary, is incapable of any great 
manual effort, and in some cases feels so weak that he does not like to leave his 
chamber, and passes most of his time in bed or on the sofa. The various bodily 
functions may be interfered with. The appetite is diminished, the bowels consti- 
pated, the skin is dry, and the circulation feeble in the extremities, so that there is, 
in many cases, constant complaint of cold hands and feet. Sometimes the secre- 
tions are increased in amount rather than diminished. There is salivation or pro- 
fuse perspiration. There may also be palpitation of nervous origin. 

There are numerous other nervous phenomena occasioned by neurasthenia, 
which we need not here describe with great minuteness. Some of them are most 
marked in the " spinal form " of the disease; such are pain in the back, spinal irri- 
tation, paresthesia and pain in the extremities, and sexual derangements. Some- 
times, however, these symptoms appear to be rather of psychical — that is, of cere- 
bral — origin. Nervous dyspepsia is frequently conjoined with neurasthenia ; it has 
already been described on page 375. 

The general course of the disease is almost always chronic. In the milder 
cases there is little outward evidence of derangement; the patient endeavors to 
hide his troubles, as his indefinite symptoms seldom gain much sympathy, and are 
apparently contradicted by his well-nourished and healthy appearance. In the 
severe cases, however, the patient's vigor is so much impaired that the disease 
acquires a grave aspect even for others than the patient, and fills them, as well as 
him, with infinite anxiety. The course of the disease is apt to be varied by alter- 
nate improvement and relapse. 

Prognosis. — It is difficult to make a general statement as to the termination of 
cases of neurasthenia. The disease is never actually dangerous, nor does its exist- 
ence often prepare the way for more severe secondary nervous disease. And yet 
the nervous constitution of many neurasthenic patients is such that complete 
recovery can not be attained. There are, however, numerous cases, especially 
such as have resulted from a special exciting cause, which cause can be removed, 
where permanent and complete recovery ensues. In other cases the symptoms 
can be so far abated that the patient is practically well, although not entirely free 
from discomfort. 

Diagnosis. — Neurasthenia can usually be detected without difficulty, but the 
establishment of the diagnosis requires the exclusion of organic lesions of the 
nervous system. Every case, therefore, must be submitted to a thorough and 
careful examination. Grave cerebral diseases, such as incipient tumors or general 
paralysis, have been repeatedly mistaken for neurasthenia. One important point 
in diagnosis is the aetiology, including both the outward circumstances and the 



NEURASTHENIA. 



769 



presence or absence of a constitutional predisposition to nervous diseases. Hys- 
teria has certainly many points in common with neurasthenia, but it is essentially 
an entirely different disease. In neurasthenia we find none of those innumerable 
localized nervous disturbances which we saw in the preceding chapter to be so 
well marked in hysteria, nor do we ever observe in neurasthenia that rapid onset 
and sudden disappearance of the symptoms, nor their abrupt development as a 
consequence of some violent emotional excitement. A severe case of neurasthenia 
is decidedly the graver disease of the two, at least in this sense, that it represents 
a far more profound functional disturbance of the nervous system than does hys- 
teria. On the other hand, certain special symptoms, such as convulsions or paraly- 
sis, may be more severe in hysteria than in neurasthenia. 

Treatment. — As in hysteria, so also in neurasthenia, moral treatment is of 
prime importance ; but here it must be of a different kind than in hysterical cases. 
The neurasthenic requires sympathy. He must be repeatedly examined by the 
physician. Every fresh examination, at the end of which the physician is able to 
assure him of the absence of any serious objective change, has a most quieting and 
beneficial effect upon the patient. In so far as hypochondriasis is a prominent 
symptom, this moral influence may alone restore the patient to health. 

Where the neurasthenia rests on some other basis than mere hypochondriasis 
we must, in addition to moral treatment, employ remedies which have a tendency 
to invigorate the entire nervous system. In order to bring about any permanent 
improvement, the treatment must be methodical and long continued, so that the 
patient may remain under the personal influence of the physician for a consid- 
erable length of time. Moral training is always an important and, indeed, an 
essential part of the treatment of nervous debility. 

In any methodical course of treatment, regimen is of great importance. The 
rules laid down must be carefully adapted to the special circumstances of each 
individual. Severe mental labor must be forbidden, and mental excitement 
avoided. The diet depends upon the individual case. For a corpulent patient, 
treatment calculated to dimmish obesity will sometimes be followed by decided 
improvement in the general condition and in bodily vigor. In those frequent 
instances where the patient is pale and thin, and very likely oppressed by nervous 
dyspepsia (see page 375), we should, on the other hand, make vigorous efforts to 
improve nutrition.* Definite instructions must be given in order that the patient 
may ingest a proper amount of food. Milk, butter, fresh meat, eggs, and simple 
puddings are appropriate articles of diet. Often the weight and strength both 
improve rapidly. Any large amount of alcohol or of tobacco should be forbidden. 
Tea and coffee may be taken in moderation, if the patient is accustomed to their 
use. In regard to bodily exercise, we must again be guided by the condition of 
the individual. We would most earnestly warn the physician from the error, 
frequently committed, of driving weakly and debilitated persons to take long 
walks. For such, bodily rest is much more desirable ; and fresh air may be 
enjoyed at the same time, if the patient sits out-doors or drives. The sluggish 
and corpulent, on the other hand, often require an increased amount of exercise. 
It is a good plan in many instances to employ the Swedish movement cure, or 
similar gymnastic exercises. 

Less general remedies are electricity and hydropathic treatment. Electricity is 

Playfair, Weir Mitchell, and certain other neurologists, have built up a special "method" of 
treating neurasthenia and allied conditions of nervous exhaustion ; this consists in " overfeeding" the 
patient — that is, in introducing as large an amount of nourishment as possible into the system at the 
same time that complete bodily and mental rest is secured. Faradic electricity and massage are 
also daily employed. This mode of procedure is certainly excellent in many cases, but it must not be 
regarded as universally applicable. There are cases of neurasthenia for which it is not suitable. 
49 



770 NEUROSES WITHOUT KNOWN ANATOMICAL BASIS. 



warmly praised by many patients. The galvanic current is generally employed, 
and is applied either over the sympathetic nerve or along the spinal cord. Its use 
demands great caution. The current should not be too strong, and there should 
be no abrupt changes in it. Galvanism applied to the head is seldom well borne. 
Another very valuable mode of treatment was first practiced by Beard and Rock- 
well, and consists in general faradization. The patient is almost completely 
stripped, and places both feet upon a large, flat electrode, while the various parts of 
the body are stroked with another large sponge electrode ; in place of this second 
electrode the " electrical hand " of the physician may be employed. The physician 
takes the second electrode in his left hand and allows the current to pass through 
his own body. Various institutions have lately begun to employ electrical baths ; 
these also often seem to produce good results. In addition to peripheral galvani- 
zation and faradization of the nerves and muscles, it is also advantageous to 
employ the faradic wire-brush, particularly on the back of the neck, along the 
spinal column, and over the shoulders and thighs. 

The hydro-therapeutic treatment may be quite well carried out at the patient's 
home, but a severe case will be better off in some well-conducted institution. Cold 
sponging, douches, hip-baths, lukewarm baths (or swimming), are all employed. 
Douches must not be applied to the head. If there is sexual disturbance, hip- 
baths of cold water are advisable. They should not be taken at night. Douching 
of the genitals and loins is also excellent. Subsequently sea-bathing will prove 
extremely beneficial for many patients. We would recommend the sea-shore 
especially for emaciated and anaemic subjects, who are frequently greatly bene- 
fitted by the improved appetite and rest thus obtained. If the patient is well 
nourished, on the other hand, a journey on foot through the mountains, if made 
cautiously, may be very valuable. 

In neurasthenia, internal remedies should be given only as indicated by the 
symptoms. If there is anaemia, iron, quinine, or Fowler's solution is prescribed ; 
if there is dyspepsia, some stomachics, like dilute hydrochloric acid, pepsin, or 
some bitter. The constipation should be overcome mainly by diet. A valuable 
adjuvant is massage of the abdomen; and, indeed, massage is coming to be 
regarded as a valuable tonic for the whole system where there is nervous dis- 
turbance. It is especially appropriate where there are painful sensations in the 
nerves and muscles, and may here be combined with electricity. 

The treatment of the wakefulness which results from neurasthenia deserves a 
brief mention. In the first place, we would warn the physician against the abuse 
of chloral and morphine. The attempt should always first be made to secure sleep 
by a rational general treatment, or by some less injurious remedies. Often a 
warm bath for half an hour at bed-time soothes the patient and brings him sleep ; 
and in other cases a wet cloth laid upon the head or back of the neck produces the 
same favorable result. Patients often report that general faradization at bed- 
time is an excellent soporific. Sometimes a moderate dose of alcohol is efficient — 
for instance, a glass of beer or good wine taken before going to bed. If none of 
these means avail, our next resort should be the bromide of potassium. Very 
likely small doses of this have only a subjective eflPect, but there can be no doubt 
that a large dose, say about a drachm (grm. 3-5) in a glass of water, does have a 
direct tendency to produce sleep. We may also mention extract of cannabis 
indica ; the preparation known as cannabinum tannicum, five to ten grains (grm. 
0'2-0'5); paraldehyde, about a drachm (grm. 3-5) at night; and urethan, twenty 
to forty-five grains (grm. l'5-3) in water at bed-time. Paraldehyde has a very 
disagreeable taste. These various remedies seldom give great satisfaction ; and we 
must therefore rely mainly on general treatment. 



DISEASES OP THE KIDNEYS, THE PELVIS OF 
THE KIDNEY, AND THE BLADDER. 



SECTION I. 
Diseases of the Kidneys. 

CHAPTER I. 

GENERAL PRELIMINARY REMARKS UPON THE PATHOLOGY OP 

RENAL DISEASE. 

Although some knowledge of the occurrence and significance of renal affections 
had been acquired even by the older physicians, still the service of having pointed 
out the frequency of these diseases, and of having clearly recognized their most 
important anatomical forms and their chief clinical symptoms, belongs undoubt- 
edly to the English physician Eichard Bright, who was born in 1788 and died in 
1858, as physician in ordinary to Queen Victoria. Bright's first work on this sub- 
ject appeared hi the year 1827. In this he brought forward the special discovery 
that, in many cases of general dropsy, which are associated with the secretion of 
an albuminous urine, a primary affection of the kidneys must be regarded as the 
special cause of the disease. Since then, the disease described by him has been 
almost universally called "Bright's disease" (" Morbus Brightii"), a name still 
much employed, but in whose stead the anatomical terms would be more proper, 
since many forms were previously classed under it which, according to our more 
accurate present knowledge, must be separated. 

Bright's statements were either confirmed or expanded in subsequent times by 
many other observers. Christison, Osborne, and R. Willis in England, and Rayer 
and M. Solon in France, were the chief students of renal diseases. Frerichs pub- 
lished the first great work in Germany in the year 1851. His division of Bright's 
disease into three different " stages," based on Reinhardt's histological investiga- 
tions, was for a long time quite generally accepted, until gradually further clinical 
experience showed that it was untenable. A more accurate division of renal dis- 
eases was first opposed to it in England (Johnson, S. Wilks, and others), and then 
in Germany (Traube, Bartels). Under the incentive of these labors, especially the 
work of Bartels in 1871, renal pathology thus fell into a doubtful classification, 
with which the facts of experience could be harmonized only by force. Only of 
late years has a natural theory of renal diseases, derived from general pathological 
observations, at last become accepted — a theory which is based chiefly upon the 
anatomical work of Weigert, but which may also be brought into complete har- 
mony with the data of clinical observation. 

The chief reason why the kidneys are so often diseased, either alone or in con- 
junction with other organs, is to be found in the fact that the body must eliminate 



772 



DISEASES OF THE KIDNEYS. 



all forms of injurious matter, which circulate in the blood, in great part by the 
kidneys. Consequently the action of any injurious substance is often manifested 
chiefly in the kidneys, since they must, in a certain measure, be repaid for the serv- 
ice which they do for the rest of the body by their own disease. According to 
their nature and character, the injurious substances, which are here to be con- 
sidered, are divided chiefly into two great groups — the chemico-toxic and the 
organized infectious substances. In this way the kidneys may be involved sym- 
pathetically after the ingestion of many poisons, and also in the great majority of 
all the infectious diseases. In these cases, of course, as we shall see later, certain 
chemical and infectious poisons exert their action in a particularly frequent and 
in a particularly severe or definitely characterized fashion. Beside these forms of 
origin for many renal diseases, which are the chief ones to be considered, we must 
consider other causes of disease which are much rarer. One way in which the 
morbific agents may also enter is especially important — namely, from the lower 
urinary passages, the bladder, and pelvis of the kidney upward into the kidney. 
In this way those renal diseases arise which come on secondarily to cystitis, pyeli- 
tis, etc. Finally, of course, disturbances of circulation and mechanical traumatic 
injuries may also make themselves manifest in the kidneys. 

The clinical symptoms which are caused by the different forms of renal dis- 
ease, and which serve for its recognition, are referable only in very small part 
directly to the diseased organ itself. In renal diseases characteristic subjective local 
symptoms — like local pain — are but rare, and the anatomical position and the 
physiological conditions of the kidney make it almost impossible to discover any 
changes in their size, their physical consistency, etc., by a direct objective exam- 
ination. In the diagnosis of renal diseases we are therefore confined chiefly to 
the investigation of two groups of symptoms : in the first place, to the examination 
of the secretion from the kidneys, the urine, whose character, as we know by 
experience, may be materially altered when there is renal disease; and, in the 
second place, to the discovery of certain phenomena in other portions of the body, 
which are immediately dependent upon the renal affection. Since both the patho- 
logical changes in the urine, and the symptoms in other organs occurring in renal 
affections, have much in common in almost all the forms of renal disease, it is 
advisable first to describe the main features, at least, of the general symptomatology 
of renal diseases. We shall then be obliged, in the following special chapters, to 
mention only the precise circumstances of the occurrence and onset of each 
symptom ; the general significance of the symptoms being already known. 

1. Albuminuria. 

The most constant symptom, and one which in many cases first of all, and 
often even alone, renders the diagnosis of a renal affection possible with complete 
certainty, is albuminuria — that is, the appearance of albumen, and especially of 
serum albumen and serum globuline (paraglobuline), in the urine. From recent 
investigations (Leube, Fiirbringer, and others) we know that in some cases the 
urine may contain a very slight amount of albumen even in healthy persons, 
especially after physical exertion, in emotional disturbances, etc. These rare 
exceptions, however, do not invalidate the correctness of the assertion that when 
a definite amount of albumen is persistently eliminated by the urine it must be 
regarded as something pathological. 

The detection of albumen in the urine for clinical purposes, wherein no regard 
need be paid to the separation of serum albumen and serum globuline, is per- 
formed almost exclusively by means of the so-called heat test. If the urine is 
cloudy, it must be filtered before heating. The reaction of the urine must always 
be tested first. If it is acid, as it usually is, the urine is heated in a test-tube with- 



EEMAEKS UPON THE PATHOLOGY OF KENAL DISEASE. ?73 



out any further addition.* If the reaction of the urine is neutral or alkaline, 
we acidify it, before heating, with a few drops of acetic acid. If the urine contains 
albumen, a decided flocculent precipitate of coagulated albumen appears on heat- 
ing it. We can make a mistake only where there is an alkaline reaction in the 
urine, which sometimes happens in neutral or very faintly acid urine, owing to 
the escape of carbonic acid during the heating, and the consequent precipitate of 
phosphates, especially of calcic phosphate. In order not to mistake such a pre- 
cipitate of phosphates for a precipitate of albumen, it is necessary, after the urine 
has been heated for a short time, to add to the precipitate, if present, nitric acid (an 
excess does no harm). A precipitate of phosphates is dissolved at once, but a 
precipitate of albumen usually becomes thicker and more compact. We can 
measure the amount of albumen contained in the urine approximately by the 
height of the settled precipitate on the bottom of the test-tube. We often speak of 
"one half or one fourth of the volume being albumen," but we can not state 
any definite relation between this estimate of the volume and the precise amount 
of albumen. 

If we have found out that the urine certainly contains albumen, we must then 
decide whether we have really a true renal albuminuria — that is, whether a urine 
already albuminous is secreted in the kidneys, or whether the albumen is not 
mixed with a perfectly normal or at least non-albuminous urine later, in the kid- 
neys themselves or in the urinary passages, the pelvis of the kidney, or the bladder 
(spurious, accidental albuminuria). Such a spurious albuminuria occurs when 
the urine is contaminated with blood (as in haemorrhages from the kidneys, the 
pelvis of the kidney, the bladder, or the urethra), or with pus (in pyelitis, cystitis, 
etc.). In these cases, of course, the albumen contained in the serum of the blood 
or pus is found in the urine. Spurious albuminuria is usually easily recognized, 
since the presence of pus or blood in the urine, which is shown by the appear- 
ance of the urine or upon microscopic examination (red blood-corpuscles, pus-cor- 
puscles), points with immediate certainty to the origin of the albuminuria. Beside 
that, the amount of albumen in these cases is usually but slight, and corresponds 
to the amount of pus or blood in the urine. A disproportion in this respect must 
excite the suspicion whether, beside the spurious albuminuria, there is not perhaps 
at the same time an affection of the kidneys causing a true renal albuminuria. 
The determination of this point is not always perfectly easy, but we can usually 
come to a decision by finding abnormal morphological constituents of the urine, 
the so-called urinary casts {vide infra), which give indubitable evidence of the 
existence of a disease of the kidneys. 

What general pathological significance has the true renal albuminuria, and 
what are the causes of its origin ? According to our present theories, the answer 
to these questions is simply this: Almost every pure albuminuria is a direct 
sign of an abnormal perviousness of the walls of the glomeruli ; and the patho- 
logical changes, which the glomeruli undergo in the different diseases of the 
kidney, have as their immediate result this abnormal perviousness, and the conse- 
quent transudation of albumen into the urine. The fact that the easily filtrated 
serum albumen of the blood, as well as the water, does not pass through the 
vascular loops of the glomeruli, even under normal conditions, is due entirely to 
the circumstance that the capillaries of the Malpighian bodies are not inserted 
bare into the beginning of the uriniferous tubules, but that they are covered with 



* The heat-test becomes absolutely certain, but it is rather more elaborate, if we first add to the 
urine a few drops of acetic acid and about one sixth of its volume of a concentrated solution of common 
salt or Glauber's salt, and then heat it. We omit mentioning the other tests for albumen with nitric 
acid, with acetic acid and ferrocyanide of potassium, with metaphosphoric acid, etc. 



774 



DISEASES OF THE KIDNEYS. 



epithelium. This epithelium of the glomeruli has the task and the power of pro- 
viding for the retention of the albumen in the blood. If it suffer a pathological 
change in any way, it loses this power, aud then the albumen passes into the urine 
(Heidenhain). The simplest experimental proof of this theory is furnished by the 
albuminuria which appears whenever the supply of arterial blood to the kidney is 
checked by a temporary constriction of the renal artery. The epithelium of the 
glomeruli thereby suffers a visible microscopic change, as its nuclei are found con- 
siderably swollen. If the kidneys in this condition are removed as rapidly as 
possible and boiled, according to Posner's suggestion, we can discover under the 
microscope in the capsules of the glomeruli the albumen that is thus coagulated 
(Ribbert) — the most certain sign that the passage of the albumen from the blood- 
vessels into the urinary passages has in fact taken place in the glomeruli. 

Almost all cases of albuminuria may readily be referred to analogous disturb- 
ances of nutrition in the epithelium of the glomeruli, whether they be excited by 
anomalies of the circulation, like arterial anaemia or venous stasis, by toxic or 
infectious influences which have reached the glomeruli, or by any other circum- 
stances. In ^hese cases the changes in the glomeruli need not always be of a 
very severe or irreparable nature ; for we often see a slight albuminuria appear 
under the most different conditions, and rapidly pass off again. This is the so- 
called "transitory albuminuria,'' which is seen, for example, in various febrile 
affections, after slight intoxications, after epileptic attacks, or in other severe 
nervous conditions, in lead-colic, etc. We will show later, in the separate 
chapters, how the anatomical changes which are found in severe renal diseases 
explain the occurrence of albuminuria. 

The other factors, which have also been made answerable for the origin of 
albuminuria, are without doubt quite subordinate to the changes in the epithe- 
lium of the glomeruli, and at most they can affect the amount of albumen 
eliminated. The changes in the composition of the blood, on which formerly 
great stress was laid, especially the hydremia and hypalbuminosis (the diminished 
amount of albumen) of the blood, have probably only an indirect significance, 
since the nutrition of the walls of the glomeruli suffers in such a faulty consist- 
ency of the blood, and this circumstance again is the special cause of the elimina- 
tion of the albumen. 

The significance of the blood-pressure for the occurrence of albuminuria was 
also formerly very much overrated. According to the older hypothesis, it was 
believed that, in an increase of the blood-pressure, the molecules of albumen in the 
blood could be pressed through the filter formed by the membrane of the glome- 
ruli. This hypothesis, which was not based upon experiments, has been dis- 
proved, especially by the experiments of Runeberg ; these experiments showed 
that, in the nitration of solutions of albumen through animal membranes, a rise 
in the filtration pressure was followed by a decrease, and a fall in the pressure 
by an increase of the per cent, of albumen in the filtrate. Runeberg attempted 
to refer the origin of albuminuria in many cases directly to a diminution of the 
blood-pressure in the renal vessels ; but the attempt, on the ground of these results, 
is not sufficiently justified. A diminution of the blood-pressure hardly ever is 
itself followed by albuminuria, and the clinical facts which may be brought to 
support the above hypothesis may all be explained by the change in the character 
of the walls of the glomeruli, which is always present at the same time with the 
decreased pressure. 

Although in the preceding paragraphs only the Malpighian bodies have been 
regarded as the spot where the transudation of the albumen of the blood into the 
urine takes place, we must also note that, under some circumstances, we may 
admit the possibility of a passage of albumen directly into the tubules from the 



EEMAEKS UPON THE PATHOLOGY OF EENAL DISEASE. 775 



capillaries that encircle the uriniferous tubules; but we must also necessarily 
assume in such cases that there is a disturbance of nutrition in the membranse 
proprise, or at least in the epithelium of the uriniferous tubules. Such an 
assumption seems to explain the albuminuria, according- to Senator's experiments, 
in venous stasis in the kidneys, although in these cases the epithelium of the 
glomeruli also suffers soon, and then becomes pervious to albumen. 

Finally, we may briefly mention that in some cases other soluble albuminous 
substances are also found in the urine in renal diseases as well as serum albumen 
and globuline, especially paralbumen, hemialbumose, etc., but the presence of 
these substances has not yet attained any practical diagnostic significance. 

2. Casts and other Abnormal Morphological Constituents op the Urine 

in Eenal Disease. 

Beside albuminuria, certain peculiar morphological constituents of the urine, 
visible under the microscope, are of especial importance for the diagnosis of renal 
affections — the urinary casts, whose significance was first correctly recognized by 
Henle in 1842. These are cylindrical bodies, whose breadth corresponds to the 
width of the uriniferous tubule, and whose length only exceptionally reaches a 
millimetre, and which must be regarded in their chemical nature as consisting 
mainly of a coagulated albuminous substance. To the latter circumstance we 
owe their old name of "fibrine casts," or "fibrous casts," a name which can 




Fig. 104.— Different forms of casts, a. Hyaline cast with occasional granules, b. Hyaline cast with fat- 
drops and granular cells, c. Hyaline cast with red blood-corpuscles attached, d. Hyaline cast with 
white blood-corpuscles attached, e. Epithelial cast. /. Waxy cast. g. Oast with a large number of 
fat-drops. 

no longer be used with propriety, since the coagulated albuminous substance of 
most casts is, at any rate, not identical with fibrine. 

Since the precise conditions of the occurrence, and the character of the renal 
casts in the different diseases of the kidneys, will be spoken of later, we need dis- 
cuss here only the general properties, the origin, and the significance of casts (see 
Fig. 104). 

1. Hyaline Casts. — The hyaline casts are the commonest and most important 
form of casts, and, to a certain extent, are the ground-form for different 
varieties. They are perfectly homogeneous, clear as glass, colorless, soft, and 
flexible. We find them either wide or narrow, sometimes broken off short, some- 
times quite long, usually straight, but in many cases partly curved. They are 
easily stained with carmine or gentian-violet. On heating the urine, they are dis- 
solved, but they are quite resistant to acids. 



776 



DISEASES OF THE KIDNEYS. 



The hyaline casts are very often covered to a greater or less extent with all sorts 
of deposits, which are usually affixed to the soft substance of the cast in the kidney 
itself, but which may often be attached to it later. These deposits may consist, 
first, of red blood-corpuscles. This condition is important, because it points with 
certainty to the existence of haemorrhages in the kidneys themselves. Second, of 
white blood-corpuscles. These are often considerably swollen, so that we must 
guard against mistaking them for epithelium. Third, of renal epithelium, which 
may be recognized by its size, its more angular shape, and its nuclei. Of course, 
we often find the epithelium cloudy and granular, or shriveled and atrophied. 
Fourth, of fatty granular globules — that is, both fatty degenerated epithelium 
and also white blood-corpuscles which are filled with fat-drops from the fatty 
degenerated cells. Fifth, of little granular masses whose nature can not always 
be easily recognized. They are either coagulated granules of albumen, or fat- 
drops,* or urates, or bacteria, or, finally, granules of hasmatoidine, which have 
come from the destruction of red blood-corpuscles, and are usually easily recog- 
nized by their dark, brownish-yellow color. Sixth, we rarely find in the casts 
drops like myeline, as to whose precise significance nothing is known. 

2. The so-called granular casts are in most cases nothing but hyaline casts 
which are completely covered with the above-mentioned granular masses, but 
sometimes the coagulated masses of albumen or the granules of haematoidin may 
themselves assume cylindrical forms. 

3. The pure blood-casts are not very common. They consist of coagulated 
blood, and form casts of the uriniferous tubules into which the haemorrhage has 
taken place. 

4. The epithelial casts are composed exclusively of renal epithelium, although 
probably a hyaline cast often affords a basis for the epithelium to cling to. 
The epithelial casts are usually easily recognized, and always point to a marked 
desquamation of epithelium in the diseased kidney. We must guard against 
mistaking renal epithelium for swollen white blood-corpuscles, as we have 
already said. On the epithelial casts the single epithelial cells may also present 
different changes, such as granular opacity, fatty degeneration, or atrophy. 

5. The so-called waxy casts are almost always quite broad, uniformly yellowish, 
opaque casts, which proceed, perhaps, from a metamorphosis of the albumen of 
the hyaline casts. Their special diagnostic significance is unknown. At all 
events, they are not by any means found chiefly in the amyloid kidney, but they 
are found most commonly, comparatively, in acute and subacute nephritis. 

Nothing definite can at present be stated as to the mode of origin of hyaline 
casts ; the origin of the blood and epithelial casts is self-evident. Hyaline casts 
are most probably formed from the coagulated albumen eliminated from the kid- 
neys, since the formation of casts is almost always coincident with albuminuria. 
We can not state definitely how far destroyed white corpuscles or degenerated 
renal epithelium participate in the formation of casts. 

The clinical diagnostic significance of renal casts is very great. They are, in 
the first place, always a sure sign of the existence of some renal disease, since in 
normal urine casts are not found at all, or, at most, they are exceptional and are 
present in small numbers. The consideration of the special forms of casts, and of 
the deposit upon them, is also of great diagnostic importance, although from it we 
can never decide immediately upon the general form of the renal disease, but we 
can recognize with certainty the type of special pathological processes in the kid- 
neys. The blood-casts and the red blood-corpuscles sticking to the cylinders point 
to the occurrence of renal haemorrhages ; the epithelial casts to a desquamation 



* It is doubtful whether the hyaline casts themselves may in part undergo fatty degeneration. 



KEMAEKS UPON THE PATHOLOGY OF EENAL DISEASE. 777 



of the epithelium in the kidneys ; the white blood-corpuscles to an emigration 
of the colorless cells from the vessels ; the fatty granular cells and the fat-drops 
to the presence of processes of fatty degeneration in the kidneys. 

We have already learned to recognize in a great measure in the preceding, as 
occasional deposits on the casts, the other morphological constituents found, 
beside the casts, in the sediment of the urine in renal disease. Briefly recapitu- 
lated, they are as follows : 

1. Red blood-corpuscles. A large amount of blood in the urine (hsematuria) is 
almost always to be recognized by its blood-red color. The presence of blood may 
be made out with certainty by the microscope, or by Heller's blood-test. The lat- 
ter is performed by heating the urine in a test-tube with sodic or potassic hydrate. 
The blood-corpuscles are thus dissolved, and the haematine is precipitated with the 
phosphates, giving to the precipitate of the latter a very characteristic blood-red 
color. Finally, of course, the spectroscope may serve for the detection of hsema- 
turia. Hemoglobinuria will be described in a special chapter later. 

2. White blood-corpuscles. Only when they are also attached to the casts can 
we assume with certainty that these come from the kidneys, and not from the 
lower portions of the urinary tract. 

3. Renal epithelium. 

4. Fat-drops and fatty granular cells. 

5. Uric-acid crystals, urates and calcic oxalate, bacteria, etc. 

3. The Dropsy op Renal Disease. 

Although the changes in the urine must be alone decisive in the diagnosis 
of any renal disease, there are yet certain other symptoms which are also due 
immediately to the renal affection, and which may first direct our suspicions to 
the existence of a disease of the kidneys, and consequently lead to a careful exami- 
nation of the urine. Among these symptoms the dropsy of renal disease is one of 
the commonest and most important. This may, indeed, quite frequently be en- 
tirely absent, both in acute and chronic nephritis, and in other diseases of the kid- 
neys ; but in many cases it is decidedly prominent in the whole clinical picture. 

If we ask what is the reason of the frequent occurrence of dropsy in renal dis- 
ease, the answer at first does not seem difficult. Since the main function of the 
kidneys is to excrete water from the body, and since, as we shall see later, in many 
cases the diseased kidney can no longer fulfill this task, or it can fulfill it only to 
a slight degree, we are not, in fact, very much out of the way in considering the 
retention of water in the body as the main cause of the consequent oedema. Clin- 
ical observation seems in general to agree completely with this assumption. The 
oedema in renal disease seldom appears until the daily amount of urine has been 
below the normal for some time, while, on the other hand, in those cases where 
the amount of urine passed is normal, or even abnormally great, in spite of the 
existing renal disease, the oedema is usually wholly absent. In individual cases, 
too, we very often see a decrease of the oedema associated with an increase in the 
amount of urine, and an increase of the oedema associated with a corresponding 
diminution in the excretion of urine. The pathological process accordingly seems 
to consist of an accumulation in the body of the water which can not be excreted 
from it, and which transudes from the vessels and thus gives rise to the develop- 
ment of oedema. 

On more careful consideration, however, there are some objections to this 
theory, which is apparently so simple. In the first place, it might be supposed that, 
when there is a retention of water, the body must get rid of the surplus water by 
employing to a greater degree the other channels of elimination which are at its 
service — the skin and the intestines. Since we can never determine accurately 



778 



DISEASES OF THE KIDNEYS. 



the time when the water first begins to be retained in the body, the clinical experi- 
ence just mentioned may also be thus interpreted, that the lessened excretion of 
urine is not the cause of the oedema, but that, on the contrary, the appearance of 
oedema is rather the cause of the diminished elimination of water by the kidneys. 
For many cases this objection seems somewhat artificial, because the anatomical 
changes in the kidneys must often, without doubt, have a direct influence upon 
the secretion of urine ; but, still, this can not be entirely and conclusively demon- 
strated. The results of Cohnheim's and Lichtheim's experiments also are not in 
harmony with the above theory of the origin of oedema. By injecting a large 
amount of a half-a-per-cent. solution of common salt into the vascular system of 
an animal we can so greatly overload its blood with water as to produce an arti- 
ficial " hydrsemic plethora," and nevertheless there is not the slightest oedema, not 
even when the animal's renal arteries are tied. In conclusion, we must also state 
that cases have been seen repeatedly where a complete anuria has existed for sev- 
eral days, as a result of the plugging or compression of the ureters, and where 
there was nevertheless not a trace of oedema. 

There seems to be, then, another factor beside the retention of water in the 
body which plays a part in the origin of oedema; but it is not easy to decide 
what it is. Cohnheim lays the greatest stress upon a change in the walls of 
the vessels, by which they become abnormally pervious and permit the water 
accumulated in the blood to pass out into the tissues. This hypothesis seems j)lau- 
sible, especially with reference to the dropsy ir» scarlatinal nephritis, and in the 
cases that arise after the skin has been thoroughly chilled ; but we must also admit 
that in many cases such a vascular change has not been certainly discovered. 

The discussion so far relates mainly to the origin of the dropsy in the acute 
and subacute forms of nephritis. In chronic nephritis the oedema, without doubt, 
often arises in quite another fashion, especially as a result of the disturbance of 
compensation in the final paralysis of the hypertrophied left ventricle {vide infra). 
This oedema is then a true general oedema of stasis, and may be regarded as analo- 
gous to the oedema in uncompensated heart disease. 

The special peculiarities in regard to the appearance of oedema in the different 
diseases of the kidney will be described later. The first signs of the development 
of dropsy are generally noticed in the skin, usually in the face, and especially in 
the eyelids. The ankles and legs also swell, then the scrotum, the dependent parts 
of the trunk, etc. In all severe cases the whole subcutaneous cellular tissue 
finally takes part in the dropsy, so that the whole body is swollen to the utmost 
degree. We almost always find at the same time an effusion into the cavities of 
the body, hydrothorax, ascites, and finally even hydropericardium. In some cases 
the dropsy of the serous cavities may attain even a high degree without there being 
very much anasarca — that is, general oedema of the skin. More rarely we see 
cedematous swelling in the mucous membranes, especially in the conjunctivas, the 
soft palate, and the arytaeno-epiglottic ligaments (oedema of the glottis). Among 
the cedemas of internal organs, oedema of the lungs has a great practical signifi- 
cance. The questions as to the occurrence and significance of oedema of the brain 
will be spoken of below (see uraemia). 

In its chemical composition, the dropsical fluid corresponds to a very thin 
blood-serum. The amount of water is usually 97 to 98 per cent., the amount 
of salts one to one and a half per cent. The amount of albumen is usually very 
slight. Urea has been repeatedly found in it. 

4. Uremia. 

If the diseased kidneys can no longer perform their secretory functions in a 
satisfactory way, not only does the elimination of water from the body thereby 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE. Y79 



suffer, but the soluble constituents of the urine, the salts, the urea, and the other 
final products of tissue metamorphosis may also be retained in the blood and accu- 
mulate there. Hence we often find the blood, in patients with renal disease, not 
only more watery than under normal conditions, so that the specific gravity of 
the serum may fall from 1030 to 1020, or even lower, but, in almost all cases where 
there is a diminished excretion of urine, it is also richer in urea, as many experi- 
ments have shown, and, under corresponding- conditions, it is probably also fre- 
quently richer in the other constituents of the urine. 

This accumulation of the urinary constituents in the blood, and further, per- 
haps, in the tissues themselves, is the cause of a class of symptoms which are often 
seen in diseases of the kidneys, and which are termed uraemic symptoms or 
uraemia. It is probable that the retention of urea plays the main part here, but 
it is also probable that the retention of other constituents of the urine, perhaps 
the potassium salts chiefly, is likewise not without significance. Many experi- 
ments have shown that, by extirpating the kidneys or by tying the ureters in 
animals, we can provoke a symptom-complex, characterized by vomiting, con- 
vulsions, and coma, which corresponds almost perfectly to the uraemia of renal 
disease. That large amounts of urea injected into the blood of healthy animals 
usually have no injurious results is explained simply by the fact that, in this case, 
the urea is very rapidly and completely eliminated again by the kidneys. If, 
when feeding an animal with large amounts of urea, we hinder its elimination, as 
Voit has shown, by withholding water at the same time, ursemic symptoms also 
appear. 

Clinical experience in most cases also agrees perfectly with the theory that 
uraemia is caused by a retention of urinary constituents in the body. In most 
cases the uraemic symptoms appear only when the daily amount of urine has pre- 
viously fallen to a very low figure, or when the secretion of urine has wholly 
ceased for several days. That in these cases not only the elimination of water, 
but also the elimination of an amount of urea corresponding to the food taken, 
and also the elimination of the other urinary constituents, is very much dimin- 
ished, is shown by the experiments in regard to this point made by Fleischer and 
others. Furthermore, a great increase of the amount of urea in the blood in 
uraemic patients has been found in many if not in all cases. 

Of course there can be no question that some clinical facts can not be brought 
into exact harmony with what has been previously said. If cases are repeatedly 
reported in which no uraemic symptoms have appeared in spite of anuria for 
several days, it does not prove too much, since we can never make an exact esti- 
mate of the matter accumulated m the blood which ought to have been eliminated ; 
for the organism can certainly get rid of the final products of tissue metamor- 
phosis in other ways than through the kidneys— for instance, through the skin 
or the intestines — and we must also bear in mind that different individuals show 
a great variation in tolerating the action of any poison in the body. It is harder, 
however, to explain those cases which are sometimes seen, where uraemic symp- 
toms suddenly appear in patients with renal disease without being preceded by 
any noticeable diminution of the secretion of urine. In these cases we must 
assume that, in spite of the abundant elimination of water — that is, in spite of a 
normal amount of urine— there is a retention of the solid constituents. Such 
cases, however, should always make us consider whether, in renal disease, other 
circumstances than the retention of urinary constituents may not give rise to the 
development of severe nervous symptoms. In some such cases the appearance of 
uraemia coincides with the disappearance of the previously existing oedema. It has 
therefore been conjectured that, in such cases, the blood all at once becomes rich 
in urea from the rapid absorption of the oedema fluid which contains urea, and 



780 



DISEASES OF THE KIDNEYS. 



that therefore uraemic symptoms now arise, in spite of the abundant elimination 
of urine which at once sets in. This hypothesis does not seem to us very prob- 
able, since, as was said above, very large amounts of urea may be injected into the 
blood of animals with healthy kidneys, without the appearance of uraemia. In 
the cases above mentioned we must therefore still further suppose that nothing 
but the water is rapidly passed off again by the kidueys, while the solid constitu- 
ents remain. 

Among the other theories of uraemia which have therefore been advanced 
to explain the apparent contradictions in the clinical observations mentioned, 
Traube's theory must be mentioned especially ; according to this an acute oedema 
of the brain is the cause of the uraemic symptoms. There is no doubt that this 
theory does not apply to many cases of uraemia ; but, on the other hand, we can 
not claim that it never finds an application. It seems to us that, in general, the 
possibility of actual anatomical changes in the brain in renal disease has not yet 
been sufficiently considered as a cause of severe nervous symptoms, since the fre- 
quent occurrence of special changes in the retina, which also consists of nervous 
elements, is closely connected with such a theory. In most cases of uraemia we 
can, however, hold to the original explanation, according to which these symptoms 
owe their origin to the retention of the urinary constituents in the blood ; but we 
can not exclude the possibility that, under some circumstances, severe nervous 
symptoms may arise from other causes in patients with renal disease, which of 
course do not deserve the name of " uraemia," although clinically they may greatly 
resemble it. 

Finally, we may mention here the theory advanced by Frerichs in the year 
1851, which at first found much favor, but which at present is almost universally 
abandoned. According to this, the urea retained in the blood was not in itself 
the cause of the uraemic symptoms, but it was changed into carbonate of ammo- 
nia by the action of a ferment in the blood, and from this the severe nervous 
symptoms arose. This theory is untenable, because carbonate of ammonia is 
scarcely ever found in the blood of uraemic patients. It is much more probably 
formed first in the stomach and intestinal canal of uraenric patients from the urea 
there excreted {vide infra), as Claude Bernard, Treitz, Voit, and others have 
shown. 

In regard to the clinical symptoms of uraemia in the individual case, they show 
all possible transitions from the mildest symptoms, which are only intimated, up 
to the severest nervous symptoms, which may be the immediate cause of death. 
The severe forms of uraemia may sometimes come on quite suddenly, while in 
other cases they may be preceded for a long time by milder uraemic symptoms, 
which are then termed prodromata. The severest symptoms may not appear at 
all, and the milder symptoms may exist alone for a longer or shorter time. This 
latter condition is called chronic uraemia. 

The milder uraenric symptoms, which are observed either alone or as precursors 
of severe uraemia, consist of headache, somnolence, and mental stupor, of a pecul- 
iar uneasiness, or of a feeling of anxiety and constraint (sometimes associated 
with hurried respiration), and very often of nausea and repeated vomiting; and, 
finally, not infrequently, of various symptoms of motor irritation, of slight 
twitchings or temporary tonic rigidity of the face or the extremities, etc. 

The most characteristic symptom of severe uraemia is the uraemic convulsion, 
or the so-called uraemic eclampsia. It corresponds almost exactly in its details to 
the pure epileptiform attack ; it usually begins with a short tonic stage, in which 
the whole body is generally in a position of extension in opisthotonos, and then 
follow vigorous clonic contractions in the face and extremities. The face becomes 
cyanotic, a bloody froth comes from the mouth, the pupils are usually dilated and 



EEMAKKS UPON THE PATHOLOGY OF KENAL DISEASE. 781 



almost without reaction, the respiration is accelerated (but at times it is intermit- 
ting from spasm of the respiratory muscles), the pulse is small and accelerated, 
and can scarcely be felt in the radial artery, and the temperature is sometimes 
raised. There is only rarely a single attack. The attacks are much oftener 
repeated after longer or shorter intervals, so that there may even be twenty or 
more in the twenty-four hours, during the whole of which time a complete loss of 
consciousness persists. Severe and fully developed epileptiform attacks often 
alternate with slighter convulsions. 

Some other ursemic symptoms beside the convulsions have already been briefly 
mentioned, but they merit a somewhat fuller description. 

The ursemic amaurosis occasionally seen is especially interesting. It is usually 
left after recovery from the convulsions. Only rarely does it precede them or 
appear without them. It always develops quite rapidly, so that the first disturb- 
ance of vision soon passes into complete blindness. The reaction of the pupils to 
light is almost always retained, and the ophthalmoscope shows a perfectly normal 
retinal image. From this we can scarcely doubt that genuine ursemic amaurosis 
is of purely central origin ; it is probably due to a disturbance in the cortex of the 
occipital lobe. Its prognosis is on the whole favorable, since the disturbance of 
vision usually disappears completely in a day or two, though sometimes not until 
after a longer time. Anomalies are only rarely seen in the region of the other 
nerves of special sense, the most frequent, comparatively, being a difficulty in 
hearing, or even complete deafness. 

Other motor disturbances, except twitchings and convulsions, are rare. Only 
in a few cases have hemiplegic or monoplegic paralyses, contractures, etc., been 
observed. Mental symptoms are more common. Delirium, and maniacal, or 
sometimes melancholic, states sometimes follow ursemic coma. 

Those ursemic symptoms have also a great interest which are to be regarded 
as a sort of self-help on the part of the organism, since they often lead to a vica- 
rious elimination of urea. The first of these is ursemic vomiting, which is a 
frequent and often an extremely obstinate symptom both in acute and chronic 
ursemia. In many cases it is of central origin, and is to be regarded as analogous 
to the vomiting so frequent in different forms of cerebral disease ; but it is often 
produced by the irritation which the gastric mucous membrane suffers from the 
urea eliminated, or rather from the carbonate of ammonia arising from it. The 
latter is always first formed from the urea in the stomach itself, and we find in 
the vomitus of ursemic patients either the still undecomposed urea or the carbon- 
ate of ammonia in considerable quantities. Sometimes there is quite a violent 
hiccough beside the vomiting. 

Ursemic diarrhoea has the same significance as ursemic vomiting. It is usually 
provoked by the carbonate of ammonia arising from the urea in the intestines. 
The latter often causes quite a severe catarrhal, and even at times a diphtheritic, 
inflammation of the intestinal mucous membrane. 

Another way in which the organism sometimes tries to get rid of the amount 
of urea accumulated in it is by the sweat-glands. Schottin first described the 
remarkable discovery of a coating of urea on the skin in the ursemia of cholera, 
an observation which since then has been repeatedly confirmed in other cases of 
ursemia. This coating is most frequently seen on the face, especially on the sides 
of the nose, to which little faintly lustrous scales are seen sticking after the 
evaporation of a clammy sweat. Chemical examination shows that these scales 
are urea. The excretion of urea is much more rare in other parts of the skin, but 
perhaps the occasional severe ursemic itching of the skin is due to an irritation 
of the cutaneous nerves by some of the constituents of the urine that are 
excreted. 



782 



DISEASES OF THE KIDNEYS. 



Other organs beside the skin and the digestive tract are but rarely to be 
considered as a means of the vicarious elimination of urea, but Fleischer was 
once able to discover considerable amounts of urea in the sputum of a uraemic 
patient. 

In conclusion, we must describe the condition of the pulse, of the temperature, 
and of the respiration in uraemia. The pulse is often very slow before the appear- 
ance of severe symptoms, sometimes 48 or 40 ; but it is almost always tense and 
hard. In chronic uraemia, also, a moderate slowness of the pulse is not infre- 
quent. When uraemic convulsions appear, however, the pulse usually becomes 
small and very frequent, especially in cases that terminate unfavorably. The 
temperature bat rarely remains unchanged in severe uraemia. If there are con- 
vulsions, it usually rises several degrees, in severe cases even to 106° or 108° (41°- 
42° C). We have seen these high temperatures, especially as a terminal rise with 
an unfavorable issue, although there may sometimes be an improvement even in 
such cases. On the other hand, there are also great declines in temperature, down 
to 93° or 91° (34°-33° C), most frequently again as a terminal temperature of col- 
lapse, in cases which end in deep coma without marked symptoms of motor irrita- 
tion. We might also mention the " urseinic chills " which we have seen several 
times — that is, a chill coming on suddenly along with other uraeruic symptoms, 
with a great increase of temperature, and followed by a rapid fall in the tempera- 
ture. The respiration in uraemic patients is sometimes very much accelerated, and 
is especially deep, a symptom which recalls the peculiar breathing in diabetic 
coma (vide infra). Certain severe attacks of dyspnoea in patients with renal dis- 
ease have been described as " uraemic dyspnoea " or " uraemic asthma " ; but it is 
not always easy to decide whether this is really a uraemic nervous symptom in 
these cases, since similar conditions of sudden dyspnoea may depend upon insuffi- 
ciency of the left ventricle or upon inflammatory affections of the lungs. 

In regard to the general course of uraemia, we have already spoken of the 
different ways in which it occurs, either coming on quite suddenly or announcing- 
itself by different prodromata. In most cases the special exciting cause of uraemia 
is to be found in a failure of the renal activity caused by the anatomical lesion of 
the kidneys, either because the glomeruli are unable to perform their functions 
owing to the disease, or because the uriniferous tubules are considerably plugged 
by casts, or from similar reasons. In the more chronic forms of nephritis with 
cardiac hypertrophy (vide infra), the activity of the heart sometimes plays a very 
considerable part in the occurrence of uraemia, since, when insufficiency of the left 
ventricle sets in, the insufficiency of course leads to a fall in the arterial pressure 
and to a consequent diminution in the excretion of urine. 

In regard to the duration of uraemic symptoms and to the different forms and 
ways in which the various uraemic symptoms may be combined in the clinical 
picture, we can give only a few general statements. The division of uraemia into 
an acute and a chronic form, already mentioned, is generally very useful practi- 
cally. In the acute form we usually have the severe uraemic symptoms, especially 
uraemic convulsions and uraemic coma. This condition usually lasts some days, 
while chronic uraemia, in which the milder cerebral symptoms — uraemic vomiting, 
difficulty in breathing, etc. — are most prominent, may last as many weeks. 

The termination of uraemia is always doubtful in every severe case, but it is by 
no means always unfavorable. Even after coma lasting for several days, with 
very severe and often-repeated convulsions, the uraemic symptoms may wholly 
disappear, while, on the other hand, of course, uraemia is by no means a rare cause 
of death in the most diverse forms of acute and chronic renal disease. In judging 
of the individual case, the most stress is to be laid on the condition of the pulse, 
the respiration, and the temperature ; we must also consider, of course, the char- 



REMARKS UPON THE PATHOLOGY OF RENAL DISEASE. 783 



acter of the urinary secretion, and especially the other morbid symptoms dependent 
upon the primary disease. 

5. The Changes in the Circulatory Apparatus in Renal Disease. 

Although it had not escaped Bright's observation that changes in the heart are 
also present in diseases of the kidney, this condition was first generally known 
when Traube, in 1856, in a treatise which has become famous, discovered that a 
change in the heart was very common in certain renal affections, and thus gave 
the chief impulse to the numerous clinical and experimental investigations that 
have been made since then as to the connection between cardiac and renal 
disease. 

This connection, generally considered, may be accounted for in three ways : 
First, the heart disease may, without doubt, be the primary disease, and only 
secondarily lead to a disease of the kidneys, as a result of disturbances of circula- 
tion. In this way develop the kidney of passive congestion {vide infra and page 
280) and the embolic processes in the kidney. 

Secondly, heart disease and renal affections may also develop independently of 
each other, as a result of an injurious influence that affects both organs at the same 
time. Thus, for example, a general arterio-sclerosis leads to cardiac hypertrophy 
or to myocarditis, and also to a granular kidney {vide infra), as a result of an 
implication of the renal vessels. Certain other injurious influences, such as toxic 
and constitutional influences, alcohol, syphilis, or improper living, may also cause a 
disease of the heart and the kidneys at the same time. Later on, if both affections 
have developed, their influence upon each other is often, of course, considerable, 
a circumstance which may render our judgment as to the condition decidedly 
difficult. 

In the third place, finally — and this is the point with which we are here chiefly 
concerned — the renal affection may be the primary disease, and is itself the cause 
of a change in the heart, and especially of a secondary hypertrophy of the left 
ventricle. At present there can no longer be any doubt of the fact of this depend- 
ence. We also know now that the secondary development of cardiac hypertro- 
phy is not confined to one form of chronic nephritis, the so-called contracted 
kidney, as was at first believed, but that it is almost as constant in many other 
forms of nephritis. Opinions are at present still much divided as to the precise 
nature of this connection, and as to the causal factors which act here, as the fol- 
lowing account will show. 

The theory which Traube himself advanced for t,he explanation of the cardiac 
hypertrophy in nephritis was that, in the first place, less water is withdrawn 
from the blood in nephritis for the formation of the renal secretion, and that, in 
the second place, the flow of arterial blood into the venous system is hindered 
by the changes in the kidneys. Both circumstances must raise the pressure in 
the arterial system, and therefore gradually lead to cardiac hypertrophy. Thus 
formulated, Traube's theory can not be maintained. The first statement especially 
is untenable, because, in many cases of chronic contraction of the kidney with 
co-existing cardiac hypertrophy, there is never a diminution of the elimination of 
water by the kidneys, and, besides, this can never of itself cause an increase of the 
arterial pressure. The greatest stress, however, has lately been laid by Cohnheim 
on the second factor in Traube's theory, on the disturbance of circulation in the 
kidney, although he modifies the form of Traube's statement. Cohnheim shows 
that the hindrance to the circulation in the kidneys, which develops chiefly from 
disease of the glomeruli, must be followed by an increase of arterial pressure, 
because the flow of arterial blood to the kidneys is not lessened in nephritis. 
Abnormal resistance to the circulation forms behind the little renal arteries into 



DISEASES OF THE KIDNEYS. 



which an abundance of blood pours, and this may cause an increase of the general 
arterial pressure. 

This theory, however, is opposed by the fact that even complete ligature of 
both renal arteries does not raise the arterial pressure, because the blood at once 
escapes into other vascular regions which dilate. The place where the contraction 
of the caliber of the renal artery occurs, whether in the main trunk or in the ter- 
minal branches, can make no difference, because by it only the length of the 
impeded, or rather, to a certain degree, of the stagnant blood-column, is altered, 
which is without influence on the general blood-pressure. 

Beside Traube's and Cohnheim's "mechanical theory," the "chemical theory" 
of cardiac hypertrophy, which was advanced in a partial form by Bright, has 
lately found many advocates (Senator and others). According to this, the reten- 
tion of urinary constituents, especially urea, in the blood causes the increase of 
arterial pressure. Of course the quantitative changes to be considered here are 
comparatively very slight, even if we admit the retention of urinary constituents 
in all forms of renal disease which lead to cardiac hypertrophy, but the possibility 
of the final effect of such slight but permanent influences can not be questioned. 

We can not at present give a definite decision as to the cause of cardiac hyper- 
trophy in diseases of the kidneys. Experiments, to provoke hypertrophy of the 
left ventricle in animals by artificial disturbances of the circulation in the kid- 
neys, by feeding with urea, etc., have given scarcely any absolute and positive 
results, so that it seems needless to go into them more fully in this place. It may, 
however, be assumed as certain that the cause of the increased arterial pressure is 
to be found in the renal affection itself, and that the hypertrophy of the left ven- 
tricle appears only as a result of the permanent increase of pressure. Correspond- 
ing to this increase of pressure, the increased tension of the arterial system is often 
found clinically very early, while the signs of the consecutive hypertrophy of the 
left ventricle gradually develop later. In the following chapters we will discuss 
the great compensatory significance belonging to cardiac hypertrophy in renal 
disease, and how the condition of the heart finally occuj)ies almost entirely the 
center of the whole morbid picture. 

The relation between certain diseases of the vessels and diseases of the kidneys 
will be spoken of in the chapter on contracted kidney. 



CHAPTER II. 

ACUTE NEPHRITIS. 

(Acute Brighfs Disease.) 

-ZEtiology. — Acute nephritis, like most of the other forms of nephritis, is not 
a disease whose aetiology is uniform. The same anatomical change, which we 
term " nephritis," and which is attended by about the same morbid phenomena, 
may be excited by influences of very different kinds. Almost all these influences 
have one thing in common, namely that, as we have stated in the preceding chap- 
ter, they reach the kidneys by way of the circulation, and are here in part 
eliminated, and thus exert their specific injurious action upon the parenchyma of 
the kidneys — but they differ considerably from one another in their precise chemi- 
cal or biological nature. Since the pathological change in the kidneys depends 
upon the amount of the noxious material, upon the intensity of its action and the 
duration of its influence, we see that the cases of nephritis that arise in this way 
must present a perfectly continuous series from the mildest to the severest, from 



ACUTE NEPHKITIS. 



785 



those that pass off rapidly to those that last perhaps for years and years. The 
history of renal pathology teaches us in the plainest way that all attempts to 
divide the forms of nephritis into different clinical and pathological " varieties " 
can not be strictly carried out. The more scientific experience increases, the more 
numerous must be the forms established, and still we only too frequently have to 
assume all sorts of " transitional forms " merely to bring the reality into harmony 
with the scheme. It, therefore, corresponds merely to our practical needs if we 
take certain types from this whole list and divide nephritis into various groups ; 
for, from the nature of the case, there can be no question of a sharp separation of 
the various forms. 

We accordingly call those inflammatory renal affections acute nephritis which 
arise comparatively rapidly from any of the injurious influences soon to be enu- 
merated, and which terminate, after a few days or a few weeks, either fatally or 
with recovery. Acute nephritis, on the one hand, follows immediately, without 
any fixed boundary, the mildest morbid changes in the kidney, which are usually 
not termed actual nephritis, but simple " parenchymatous degeneration " ; while 
on the other hand it shows a continuous transition to those forms which last for 
several weeks or months, or longer, and hence are called subacute or subchronic 
nephritis. 

Among the causes of acute nephritis we must mention first a large group which 
consist of infectious influences (acute infectious nephritis). In these cases the 
nephritis usually develops as a secondary complicating disease upon an already 
existing primary infectious disease, and may be regarded in most cases as a special 
" localization " of the specific morbid poison present in the body. There is scarcely 
a single infectious disease in which there may not be occasionally a renal affection 
as a complication. We observe these affections in our experience much more fre- 
quently in certain infectious diseases than in others, so that we may rightly assume 
that certain infectious substances have a special injurious relation to the kidneys. 
Since we have already dwelt upon the occurrence, the frequency, and certain 
peculiarities of secondary nephritis in the description of the different infectious 
diseases, a brief recapitulation of the facts which have already been, for the most 
part, described will suffice here. 

The infectious disease which most frequently gives rise to an acute nephritis 
is scarlet fever. As has been shown previously (see page 39), the renal affection 
appears but rarely at the beginning of the disease, and then in a very mild form, 
while the special severe scarlatinous nephritis usually attains its development 
only toward the end of the third week of the disease. In measles secondary 
nephritis is very much rarer than in scarlet fever; in rotheln it is only of very 
exceptional occurrence. It is commoner again in small-pox, especially in the 
severe hemorrhagic forms. In varicella, renal affections are very rare, but they 
have been occasionally observed. They are always of but slight intensity. In 
typhoid fever a slight albuminuria is very common, but genuine acute nephritis 
is quite rare. There are some cases, however, where a nephritis appears very 
early, and where the other typhoid symptoms are so crowded into the background 
by it that it is decidedly more difficult to make the diagnosis of typhoid ; this is 
called the " renal form of typhoid fever." In typhus and recurrent fevers severe 
cases of nephritis are not especially common, but they are seen more frequently 
than in typhoid fever. 

The nephritis that often comes on in cholera is of great practical importance. 
This is seen in the earlier stages, and is especially one of the most frequent causes 
of the so-called cholera typhoid (see page 77). Of course it may appear question- 
able whether the renal affection here is always of an inflammatory infectious 
nature, or develops only in consequence of the disturbance of circulation. 
50 



786 



DISEASES OF THE KIDNEYS. 



Nephritis develops quite frequently in the course of diphtheria, especially in 
severe cases of this disease ; but the renal affection only rarely reaches a high 
degree. We sometimes see, however, very severe forms of nephritis in the so-called 
septic diseases (septic nephritis, see page 101), in acute ulcerative endocarditis and 
endocarditis verrucosa, and allied affections, such as puerperal fever, septic wounds, 
etc. Among other acute diseases which, in comparatively rare cases, may be 
accompanied by nephritis, we may mention croupous pneumonia, epidemic men- 
ingitis, certain forms of sore throat, certain acute intestinal affections, acute articu- 
lar rheumatism, and tetanus. 

Finally, acute nephritis may also develop in the course of chronic infectious 
diseases, especially tuberculosis and syphilis. We have ourselves repeatedly seen 
a mild or even a severe acute nephritis come on in the secondary stage of the latter 
disease. A genuine acute nephritis may also arise in the course of pulmonary 
tuberculosis, but for the present we can not decide whether this is directly con- 
nected with the tuberculosis or arises in consequence of the absorption of septic 
substances from the contents of the cavities. 

Beside the infectious forms of nephritis just described, there is a second great 
group, which may be classed under the general heading of toxic nephritis. In 
these cases we are dealing with the deleterious action of chemical substances 
which are removed from the body by the kidneys. It is wholly impossible to 
enumerate all the substances which have this injurious effect; we will there- 
fore confine ourselves to mentioning those of the greatest practical importance. 
Among the poisons proper we may mention the mineral acids, sulphuric, hydro- 
chloric, and nitric acids, oxalic acid, phosphorus, arsenic, lead, and chromate of 
potassium. Among remedies used internally, which may excite nephritis when 
given in too great doses, we may mention cantharides, squills, balsam of copaiba, 
turpeutine, salicylic acid, and chlorate of potassium. It is also very important to 
know that many remedies applied to the external skin are absorbed by the skin, 
and in this way may reach the kidneys and excite severe changes there. Among 
these are cantharidal plaster, preparations of tar, petroleum, styrax, naphthol, 
and pyrogallic acid. We must mention, in addition to these, the renal affection 
which may arise from the too abundant use of carbolic acid or iodoform to the 
surface of open wounds. Under s<Jme circumstances renal affections may even 
arise in individual cases from taking excessive amounts of certain foods and drinks, 
like spices, alcohol, or very acid foods. 

In the forms of acute nephritis which can not be immediately referred to 
infectious or toxic influences, and whose number is comparatively small, we can 
sometimes find no definite cause at all. We then speak of a primary idiopathic 
acute nephritis. We are indeed justified in thinking of causes of origin here 
similar to those in the cases previously described, but causes which at present 
escape direct detection. In other cases an acute nephritis immediately follows 
exposure to severe cold or wetting of the skin. We can not doubt the possibility 
of such a connection after quite numerous and indubitable clinical experiences, 
although the exact conditions to be considered here are still almost wholly 
unknown. We usually take refuge in a rather non-committal reference to the 
"well-known connection between the activity of the skin and of the kidneys." 
The experiments on this point have also confirmed the fact itself, but have fur- 
nished no precise explanation of its cause. 

We have still to mention the nephritis of pregnancy {nephritis gravidarum) 
as a special form of acute nephritis. This usually comes on in the last months of 
pregnancy in women previously perfectly healthy, and is decidedly more frequent 
in primiparae than in the course of later pregnancies. The precise causes of the 
nephritis of pregnancy are still very obscure. Some authors lay the blame on the 



» 



ACUTE NEPHRITIS. 



787 



pressure of the pregnant uterus on the renal vessels, others on its pressure upon 
the ureters, etc. (compare the text-books on obstetrics). 

Finally, we must mention that an acute nephritis may ensue on a chronic 
nephritis that has existed for a long time, perhaps without symptoms (acute recur- 
rent nephritis of Wagner). 

Pathological Anatomy. — The anatomical changes, which are excited in the 
kidneys by the causes mentioned in what has gone before, show a continuous series 
from the mildest to the severest degrees, according to the intensity of the injurious 
action. The mildest changes, which, as we have said, are not called actual " inflam- 
mation," but usually simple parenchymatous degeneration, affect exclusively the 
parenchyma of the kidney — that is, the epithelium — while the interstitial tissue, 
the connective tissue, and the vessels remain perfectly normal. This fact is espe- 
cially important since it implies that, in almost all the injurious influences 
acting on the kidneys, the specific renal parenchyma itself is diseased first and 
before any other. On macroscopic examination, the kidneys may show scarcely 
any plainly perceptible changes, but it sometimes strikes the practiced eye that 
the kidneys are a little enlarged, that the cortex on section shows either a more 
reddish - gray, dimmed coloring (cloudy swelling), or a more grayish - white, 
yellowish hue (fatty degeneration). The microscopic examination gives more 
accurate information as to the degree and the extent of the disease. We distin- 
guish different conditions according to the form of change in the epithelium, of 
which the three following are most important : 1. Cloudy Swelling : It is most 
easily made out in the epithelium of the cortical tubules, but it may also be seen 
in the epithelium of the glomeruli. The cells swell, their contents become uni- 
formly granular and cloudy, the nuclei swell, and finally disappear. Such 
changes are often found in acute infectious diseases, like typhoid, small-pox, and 
diphtheria. 2. Fatty Degeneration : This may proceed from the cloudy swelling, 
or may develop independently. Many fat-drops appear both in the cells of the 
uriniferous tubules and also in the epithelium of the glomeruli, and they may 
finally lead to the disintegration of the cells. Simple fatty degeneration of the 
kidneys is sometimes found in acute infectious diseases, after certain poisons, 
like phosphorus, and finally in anaemic conditions. 3. Necrosis of the Renal 
Epithelium : The nuclei of the cells disappear, and the cells are changed to clear 
homogeneous flakes, while in some cases they are greatly swollen ("dropsical 
degeneration " of Nauwerck-Ziegler). Genuine epithelial necrosis is found in the 
kidneys, chiefly after the action of toxic substances — like cantharides, the chromic 
and chloric salts, etc.— but sometimes also in infectious diseases. Combinations 
of simple necrosis with granular cloudiness and fatty degeneration are not infre- 
quent. Both the last-named states may undergo resolution if they have not 
reached a high degree. Otherwise all the degenerations mentioned lead to the 
destruction and disintegration of the cells ; nevertheless, a complete restoration is 
possible, from the regeneration of new epithelial cells from epithelium that is still 
present. 

We term those changes in the kidneys genuine acute nephritis, in which not 
only the renal parenchyma proper, the epithelium, but also the interstitial tissue, 
especially the vessels, is affected ; so that we can make out the exudative changes 
characteristic of all inflammatory processes — the escape of fluid and cells from the 
vessels. In these cases the different histological processes may be combined in 
the most varied ways, so that the anatomical picture presents quite great variations, 
although it is almost always principally concerned with the same processes. 

If we begin with the histological lesion in acute nephritis, in order to learn to 
recognize at once the essential changes, we have first precisely the same processes 
of degeneration in the epithelium which have been already described, but they are 



788 



DISEASES OF THE KIDNEYS. 



usually present here in a more marked degree. In some cases the simple ne- 
crotic processes predominate; in others, the fatty degeneration. We often find 
degenerated cells, and not infrequently a more or less marked desquamation of 
epithelium. We see besides the special inflammatory changes. We find a fluid 
inflammatory exudation, rich in fibrine, and therefore soon coagulating in the inter- 
stitial connective tissue, which is dilated and swollen by it — inflammatory oedema. 
The same exudation is also found in the uriniferous tubules, and, by the proper 
methods, by alcohol or by boiling the fresh kidney, the albuminous effusion can 
be made out both in the capsules of the glomeruli and in the uriniferous tubules. 
The interpretation of the exudation is, of course, made very difficult, or often 
wholly impossible, by the presence of albuminous urine in the uriniferous tubules. 
The second characteristic of inflammation, the " cellular exudation " — that is, the 
emigration of white blood-corpuscles — is also present. In the interstitial tissue we 
find accumulations of round cells, usually distributed in foci, and white blood- 
corpuscles in greater or less numbers also enter the interior of the uriniferous 
tubules. We often find many hyaline casts in the lumen of the straight tubules 
or of Henle's loops, whose origin is, in all probability, connected with the albu- 
minous exudation and the emigrated white blood-corpuscles (see page 776). The 
vessels themselves are often hyperaemic and dilated, but in some cases they 
are compressed by the interstitial inflammatory oedema. It is of special signifi- 
cance that in very many cases there are haemorrhages, either into the interstitial 
tissue or into the interior of the uriniferous tubules, or even into Malpighi's 
capsules. 

All the changes described are not always found uniformly distributed over the 
whole kidney. Some parts are often much diseased, others but slightly, while 
others still are nearly, if not quite, intact. We may accordingly speak in indi- 
vidual cases of a diffuse or of a localized nephritis, although there are no strict 
limits here. 

If the histological processes have been made clear, the understanding of the 
macroscopic appearance of the inflamed kidney is very simple. We can under- 
stand that either this or that "form" of acute nephritis must be present accord- 
ing to the predominance of this or that histological process. If an abundant 
interstitial exudation is present, the kidney is much enlarged ; if this exudation 
is slight, the kidney varies but little, or not at all, from its normal size, not- 
withstanding any other severe changes. In the first case it usually feels soft, 
from inflammatory oedema; in the second case, it is comparatively firm. If 
there is a marked hyperaemia of the kidney, it appears much reddened; if the 
kidney is anaemic, it is paler ; and if an extensive fatty degeneration is also pres- 
ent, it is yellowish- white or yellow. If haemorrhages are present, they can easily 
be recognized with the naked eye on the outer surface beneath the capsule as dark- 
red points that can not be wiped away. We speak then of an " acute haemorrhagic 
nephritis. " On section, the medullary substance is more or less dilated, its normal 
striated appearance is almost always obliterated, and its color shows the same 
variations as the outer surface of the kidney. Since, as we have said, the nephritic 
changes often show not a uniform, but a nodular arrangement, we can understand 
that the kidneys sometimes have quite a mottled appearance, since hyperaemic or 
haemorrhagic red spots alternate with the lighter anaemic and the yellow fatty- 
degenerated parts. 

There are, accordingly, cases of nephritis which show almost nothing abnormal 
to the naked eye, while, on the other hand, there are haemorrhagic and non- 
haemorrhagic forms, appearing pale, yellow, red, or variegated, none of which 
can in the essential features be separated from one another, but which are com- 
bined with one another in all conceivable ways. The forms of nephritis that 



ACUTE NEPHRITIS. 



789 



differ in aetiology have, to a certain degree, definite and characteristic anatomical 
types, but strict rules can not be laid down in regard to this. 

In addition, quite a characteristic anatomical form of acute nephritis deserves a 
brief mention, in which the changes are almost exclusively limited to the glo- 
meruli, and which are therefore called glomerulo-nephritis (Klebs, Friedlander, 
Ribbert). In the purest cases of this form, as it is seen especially in scarlet fever 
and also in other infectious diseases, we find degeneration and abundant des- 
quamation of the epithelium only in the glomeruli of the kidneys ; and we usually 
find, besides, a marked disease of the vessel-walls, which swell and acquire a homo- 
geneous hyaline appearance. The glomerulo-nephritis can not in its essentials be 
perfectly definitely separated from the other forms of acute nephritis, since in 
these, under some circumstances, the glomeruli may first be chiefly affected ; but, 
as it seems, this need not happen in all cases by any means. 

Clinical History. — The most essential symptom of acute nephritis is the abnor- 
mal character of the urine. In most of the milder, and even in many of the 
severer cases of nephritis, the change in the urine is the sole objective clinical 
symptom which renders the diagnosis possible. The physician must, therefore, 
make it his practice to submit the urine to repeated examinations in every case of 
disease where there is any possibility of the presence of a nephritis. 

The simple parenchymatous degenerations of the kidneys, cloudy swelling, 
fatty degeneration, etc., which we will first briefly touch upon, may probably 
sometimes exist without being followed by any discoverable change in the urine ; 
but they often lead to a slight albuminuria, which is easily explained from the 
change in the epithelium of the glomeruli. If, then, the urine contains a slight 
amount of albumen (which usually soon passes off) in the course of any febrile 
infectious disease or other affection (the so-called febrile albuminuria, etc.), we are 
justified in assuming some of these mild conditions of degeneration in the kidneys. 
Usually the urine shows no other peculiarities, but sometimes we find in the 
sediment a few hyaline casts, a few white blood-corpuscles, etc. As we have 
repeatedly stated, these conditions pass into nephritis proper without any sharp 
limitations. 

Character of the Urine in Acute Nephritis.— In almost every severe 
nephritis the amount of urine for the twenty-four hours is more or less dimin- 
ished. This is either caused directly by the lessened elimination of water by the 
kidneys, or by the plugging of many uriniferous tubules by casts, desquamated 
epithelium, etc. The amount evacuated daily is often only fifteen or twenty 
ounces (400-700 c. c), but it sometimes falls to a much lower figure, two or three 
ounces (100-50 c. c), and there may finally be even complete anuria. In general, 
though not without exceptions, the diminution of the amount of urine runs 
parallel to the severity of the anatomical changes in the kidney. Improvement 
in the disease is very often first seen in an increase of the amount of urine. 
If there was a previous oedema, and this is absorbed, the daily amount of urine 
often rises during convalescence to a very considerable quantity, eighty to a hun- 
dred ounces (2500-3000 c. c). 

The specific gravity of the urine is at first usually increased, since the urine is 
poor in water, but comparatively rich in solid constituents, especially in albumen 
(vide infra). Of course there are great differences here, and a urine secreted in 
an abnormally small amount may show a specific gravity of only 1010 or 1015, 
while, on the other hand, urines with a specific gravity of 1020 to 1030, or even 
more, have been observed. If during convalescence a very abundant, watery 
urine is passed, it of course usually has a low specific gravity, 1005 to 1008. 

In many cases, but of course not in all, we may suspect the abnormal character 
of the urine from its appearance. This depends chiefly upon an admixture of 



790 



DISEASES OF THE KIDNEYS. 



abnormal morphological constituents. If these are present in large numbers, as is 
usually the case, the freshly passed urine is cloudy, and deposits a more or less 
abundant floccular sediment. The appearance of the urine is most altered if 
blood be mixed with it (hsemorrhagic urine). According to the amount of blood, 
the urine is a light or dark red, or even a dark black-red, and often has a greenish 
reflection when the light falls on it. 

The microscopic examination of the sediment gives more accurate information 
upon the different morphological constituents. We can not, of course, enumerate 
all the possibilities that may exist in these cases (see page 775 et seq.). It is 
generally the case that in most of the severe forms of acute nephritis the urine 
contains many casts of all sorts, usually hyaline, but sometimes partly fatty or 
waxy, and very often covered with red or white blood-corpuscles, epithelium, 
detritus, etc. The different cases are often characterized by a striking predomi- 
nance of some one constituent — epithelium, white blood-corpuscles, or red blood- 
corpuscles — but no special rules in regard to this can be given. We have spoken 
previously (page 776) of the special conclusions we can draw from the different 
objects found in the sediment. We can accordingly distinguish an acute hsernor- 
rhagic, or non-haemorrhagic, an acute desquamative, and a fatty degenerative 
nephritis, but we must always bear in mind that all these forms pass into one 
another without sharp boundaries. 

The cheinical examination of the urine gives, as the most important and con- 
stant result, usually a considerable amount of albumen. Since the reaction of the 
urine is almost invariably acid, the albumen is immediately precipitated on heating 
the urine, and sinks to the bottom of the test-tube, where it usually takes up about 
one half or three fourths of the volume of urine used for the heat-test. More 
accurate quantitative determinations of albumen give most frequently in acute 
nephritis an amount of albumen of from three tenths to one per cent. ; higher 
percentages are rare. The daily total amount of albumen eliminated amounts to 
about one or two drachms (5-8 grammes), Or sometimes more, but the daily loss 
of albumen from the body hardly ever exceeds the amount of five drachms (20 
grammes). The variation in the amount of elimination of albumen in different 
cases is quite noticeable. 

The examination of the other solid constituents, which is not generally em- 
ployed in practice, usually gives a diminished secretion of urea, phosphoric acid, 
etc., corresponding to the diminution in the whole amount of urine. 

The other Symptoms of Acute Nephritis.— Local symptoms in the kidneys 
themselves are only rarely present. There is, of course, a certain tenderness in 
the region of the kidneys, which, however, is too ambiguous to have a great symp- 
tomatic importance. It is more frequently the case that the abnormally concen- 
trated urine causes the patient to micturate more frequently than usual, and that 
micturition itself is associated with a disagreeable burning — a sort of vesical tenes- 
mus. 

The subsequent symptoms of acute nephritis, which appear in the rest of the 
body, and among which dropsy takes the first place, are far more important than 
the local symptoms. Although oedema may be entirely absent in acute nephritis, 
it is present in most severe cases, and often is predominant in the clinical picture. 
We must always be prepared for its appearance, es£>ecially when the amount of 
urine shows a considerable diminution. 

The oedema is usually discovered first in the face, which has a bloated, and 
often a pale and somewhat shiny appearance. The eyelids are usually most 
swollen at first. Beside the face, the ankles, the legs, the scrotum, and the depend- 
ent parts of the trunk may be the chief seat of the cedema, the severity and extent 
of which may of course vary greatly in different cases. If a high degree of gen- 



ACUTE NEPHEITIS. 



791 



eral dropsy develops, tliis is a source of great distress to the patient. The move- 
ments of the hody are much restrained, and all changes of position are difficult, 
associated with great exertion, and painful. In the severest degrees of dropsy 
small fissures may form here and there in the excessively tense skin, from which 
the dropsical fluid oozes. Such little wounds are sometimes the starting-point for 
disagreeable erysipelatous inflammations, etc. 

If great oedema of the skin is present, we usually find at the same time a more 
or less marked dropsy of the serous cavities. It is often hard, however, to make 
out ascites or hydrothorax on physical examination, owing to the oedema of the 
skin that is present. The symptoms mentioned acquire their chief clinical signifi- 
cance from the difficulty of respiration necessarily associated with them, since the 
diaphragm is pressed upward by ascites, and the lungs are compressed by hydro- 
thorax. If a hydrothorax is more marked on the left, or especially if hydroperi- 
cardium sets in, the activity of the heart is materially impaired. 

A marked oedema of the mucous membranes develops but rarely; in a few 
cases we have seen oedema of the conjunctivae, oedema of the soft palate, and 
oedema of the glottis. Of the oedemas of internal organs, oedema of the brain has 
already been mentioned as a possible cause of severe nervous uraemic symptoms. 
CEclema of the lungs, which often comes on toward the end of the disease, when 
it terminates unfavorably, is usually not to be regarded as a part of the general 
oedema, but as a result of the final cardiac weakness. 

In regard to the other symptoms in the different organs, the symptoms on the 
part of the circulatory apparatus must first be mentioned. The pulse is often 
abnormally tense, hard, and full (see page 784). In the beginning of the disease 
it is often somewhat slow ; later it is usually accelerated. A beginning cardiac 
hypertrophy can often be made out post mortem, and sometimes clinically, in 
cases which have lasted a somewhat longer time, two to four weeks. It seems 
to develop most rapidly in children who were previously well and strong. We 
pay especial regard to the condition of the apex-beat, and to the accentuation of 
the aortic second sound. The occasional nose-bleeds are probably connected with 
the increased arterial tension. Pericarditis is seen as a very rare complication — 
a complication which is connected with the general fact that in all forms of 
nephritis the different internal organs, especially the serous membranes, have a 
tendency to inflammation. Whether this circumstance is connected with the 
retention of urinary constituents, as has been repeatedly imagined, can not at 
present be decided with certainty. 

Of the symptoms in the respiratory apparatus, we have mentioned above the 
dyspnoea consequent upon the dropsical symptoms. In severe cases the lungs 
themselves are often drawn into sympathy, since a diffuse bronchitis or a peculiar 
form of pneumonia develops in them, which latter stands midway between a 
catarrhal and a croupous inflammation. It exhibits, to a certain degree, a form 
of stiff inflammatory oedema, and occurs in just the same way in the chronic 
forms of nephritis as in acute nephritis. When it involves both lungs to a great 
extent, it may be the immediate cause of death. The development of a pure gen- 
eral pulmonary oedema is almost always a sign of beginning weakness of the left 
ventricle, as we have said above. 

Vomiting is the most important symptom in the digestive apparatus. If it 
appears in a marked degree, it may almost always be considered as a uraemic 
symptom, and then is often the precursor of severe nervous symptoms. The appe- 
tite is almost always diminished in acute nephritis; the bowels are usually consti- 
pated, but there may be quite severe diarrhoea (see page 781). We may mention 
peritonitis, which is sometimes purulent, as a very rare complication {vide supra). 

The temperature is markedly influenced by acute nephritis only in those cases 



792 



DISEASES OF THE KIDNEYS. 



where the disease develops in previously healthy persons, or at least in those free 
from fever. Then we see quite frequently a moderate fever, with an irregular 
rise of temperature of about 100° to 102° (38°-39° C). It is quite rare that an appa- 
rently primary acute nephritis begins suddenly with a chill and high fever, 104° 
(40° C.). The condition of the temperature on the onset of uraeniic symptoms has 
already been described (page 782). 

The state of the general nutrition suffers in quite a noticeable degree in most 
of the severe cases of acute nephritis. The emaciation is often concealed by the 
oedema ; but the anaemia is the more prominent, and often lends to the bloated face 
a peculiar pallid aspect. 

Uraemic symptoms may come on at any time in the course of acute nephritis. 
We are often prepared for the onset of uraemia by a previous marked decrease in 
the secretion of urine, or by the well-known prodromal symptoms, but in other 
cases it begins very suddenly with severe symptoms of eclampsia. In regard to 
all further details we may refer to what was said on page 780 et seq. 

The Course and Different Forms of Acute Nephritis.— The whole clin- 
ical picture of acute nephritis depends very materially upon the form of its 
development. If an acute nephritis comes on in the course of a severe infectious 
general disease, as in the course of a septic affection, of ulcerative endocarditis, or 
of severe typhoid, the changes in the mine are often the sole factor pointing to 
the occurrence of the complication. The type of the severe febrile general disease 
is in no way materially modified by the added renal affection ; oedema and uraemic 
symptoms do not usually appear, often because the primary disease soon ends in 
death. 

Also when nephritis comes on in previously healthy persons or in chronic 
invalids, the tuberculous, etc., in many cases the changes in the mine are the 
chief symptom, while the other general and secondary symptoms are scarcely evi- 
dent at all, or at least only in a very slight degree. Such mild cases are associated 
only with more or less general dullness and loss of appetite. CEdema is entirely 
absent, or present only to a very slight degree. Of course such cases demand 
great caution, since even in them we may have a sudden outbreak of severe 
uraemic symptoms. 

The fully developed type of severe acute nephritis is seen especially in scar- 
latinous nephritis (q. v.), which comes on in children who are fully convalescent 
or apparently wholly well ; it is also seen in many cases of apparently idiopathic 
nephritis, or nephritis coming on after exposure to cold, etc. In these cases there 
is often the development of a general dropsy, secondary pulmonary affections, 
uraaniic symptoms, the symptoms mentioned in the circulatory apparatus, etc. In 
these cases, too, the examination of the urine affords the only certain means of 
judging accurately of the condition, but the other morbid symptoms which appear 
early — oedema, anaemia, and vomiting — may direct our suspicions to the develop- 
ing renal affection. 

Scarcely any more general statements can be made as to the whole course and 
the duration of acute nephritis, since the variations in this respect are too great. 
To describe here in particular all the different forms of nephritis according to the 
aetiological conditions in question would lead us too far. We will therefore refer 
to the description of the different primary diseases in which the characteristic 
marks of any renal complication are always stated. The primary nephritis from 
exposure to cold and the nephritis of pregnancy still demand a few remarks. 

The nephritis from exposure TO cold — primary idiopathic nephritis — usually 
comes on quite speedily after the exciting cause. The first symptoms of the dis- 
ease are sometimes insignificant, but at other times they are quite severe — chills, 
fever, renal pain, etc. Sometimes other " rheumatic symptoms," like angina or 



ACUTE NEPHEITIS. 



793 



articular pains, are also present. The further course may be mild or severe. In 
the former case the oedema that has appeared is but slight, the changes in the 
urine (albuminuria, haematuria, etc.), do not attain a very high degree, and after 
a few weeks complete recovery ensues. In other cases, however, the type of a 
severe, acute, and very often hemorrhagic nephritis develops, with great general 
dropsy, uraemia, etc., which in three or four weeks, or sooner, may lead to death ; 
but improvement may follow in spite of the severest symptoms. Then the amount 
of urine gradually increases, and the abnormal constituents of the urine, the 
oedema, and the other morbid symptoms, gradually disappear. Of course, it is 
often a long time before complete recovery ensues, since, even when the patient 
feels perfectly well subjectively, the urine may still sometimes contain some albu- 
men, a few casts, or a few red blood-corpuscles. We must also bear in mind the 
possibility of a transition from acute to chronic nephritis. 

The nephritis of pregnancy usually begins gradually. Frequent micturition 
and oedema of the lower extremities make their appearance, and beside these there 
are often nausea and even vomiting. If we examine the urine, we usually 
find it quite rich in albumen, but comparatively poor in corporeal elements. The 
slight sediment consists of hyaline casts, a few white blood-corpuscles, and some 
epithelium. Only rarely does the urine assume a haemorrhagic character. 

The condition described almost always lasts to the end of pregnancy. In the 
cases that proceed favorably a very rapid recovery often follows after the birth 
of the child ; but the onset of eclampsia gravidarum is to be dreaded as a not 
infrequent and a dangerous complication. This is to be regarded as entirely anal- 
ogous to uraemia. It begins after mild prodromal symptoms, or even quite sud- 
denly, with violent general convulsions, during which the child is usually born. 
A more or less persistent coma follows the convulsions. The convulsions may be 
very frequently repeated. Death ensues in about one third of the cases ; the other 
cases usually recover, only rarely passing into chronic nephritis. The prognosis 
is still more unfavorable for the child than for the mother, inasmuch as the child 
dies in nearly one half of the cases. 

The anatomical changes in the nephritis of pregnancy are hardly ever very 
striking to the eye. The kidneys are usually pale and but little enlarged. Under 
the microscope we usually find a slight interstitial oedema and degenerative 
changes in the epithelium. Only rarely are more marked nephritic appearances 
present. 

Diagnosis. — Acute nephritis can be overlooked only when the examination of 
the urine is neglected or can not be carried out. The latter sometimes happens, 
for example, when the patient does not come under observation until after the 
onset of severe uraemic symptoms. Otherwise, however, the changes in the urine 
always furnish evidence enough to recognize the existence of the affection of the 
kidneys. We can, of course, decide that the nephritis is acute only by considera- 
tion of the history, the aetiological conditions, and the whole course of the dis- 
ease. We must also bear in mind the possibility that there may be an acute exa- 
cerbation in a chronic nephritis that has already existed for a long time, and has 
been perhaps without symptoms — acute recurrent haemorrhagic nephritis. 

Prognosis. — The prognosis of acute nephritis depends in many cases not only 
upon the renal affection, but also upon the underlying primary disease. We can 
not here describe in detail the numerous conditions that must be considered, but 
they are to be found in the appropriate chapters. 

Many cases of primary nephritis from toxic action, or exposure to cold, and 
also many cases of secondary nephritis after scarlet fever, in pneumonia, typhoid 
fever, or syphilis, during pregnancy, etc., recover perfectly in a short time or 
after several weeks, according to the severity of the individual case. On the 



794 



DISEASES OF THE KIDNEYS. 



other hand, however, it must be said that every nephritis must be judged with 
great caution, partly because it may be the starting-point of a subsequent chronic 
renal disease, and partly because dangerous sequelae may sometimes develop in 
cases that at first are apparently mild. The dangers of acute nephritis are 
chiefly, first, the appearance of severe general dropsy, especially in the internal 
cavities of the body. Of the forms of dropsy hydrothorax is the most dangerous, 
as it may produce suffocation by compression of the lungs. Second, uraemia, espe- 
cially in its severe convulsive forms, with high temperature and finally cardiac 
paralysis. Third, the inflammation of internal organs, among which secondary 
pneumonia, in particular, is a frequent cause of death, while secondary peri- 
carditis and peritonitis, as we have said, are seen in but very few cases. We must 
bear in mind, however, that in individuals otherwise healthy the severe sequelae 
just mentioned may also be recovered from. The most extreme dropsy may be 
re-absorbed, and we sometimes see recovery, especially in children, after the 
severest uraemic symptoms. 

Treatment. — Since we may omit the description of the treatment of any pri- 
mary disease, we have here to speak only of those remedies which the physician 
has at his command against the nephritis itself and its sequelae. 

Although it seems alluring to try to exert a favorable influence upon the 
nephritic process by drugs which, like the injurious substances, also reach the 
kidneys directly, we can not report any definite practical results from such treat- 
ment. The remedies employed with this object in view — tannin in one- to five- 
grain powders (grm. 0 05-0*2) several times a day, and the drugs containing 
tannin, like uva ursi, in a decoction of 10 to 150, and also nitric acid, tartar emetic, 
etc. — prove, on sober observation, to be almost wholly useless. We may, there- 
fore, try them only when there are no more pressing indications to be fulfilled. 
Fuchsine, which has of late been often praised, is also not to be recommended. 

We expect as little result at present from " external antiphlogosis " as from the 
internal remedies mentioned — that is, from local blood-letting, applications of ice 
to the region of the kidneys, etc. Only in the rare cases where severe pain in the 
region of the kidneys comes on at the beginning of nephritis, in an otherwise 
robust individual, are we at present justified in trying leeches or a few dry cups. 
The warm baths, to be described more fully below, have perhaps an immediately 
favorable action on the process in the kidneys, since they produce a hyperaemia 
of the skin, and thus lessen the flow of blood to the kidneys. 

Although we must accordingly admit that there is scarcely any remedy at our 
service which has a direct therapeutic influence upon the diseased kidneys, the 
treatment of nephritis may nevertheless produce very significant results, since 
both a number of hygienic measures and the fulfillment of certain symptomatic 
indications are of the greatest importance. 

Among the general hygienic measures we must mention first strict confine- 
ment to bed. In the severe cases its necessity is self-evident ; but, even in the 
milder cases, which run their course without any severe subjective symptoms, 
constant rest in bed is necessary throughout. In this way we not only avoid the 
unfavorable action of cold upon the external skin, but the activity of the skin, 
which must act vicariously for the kidneys, is also excited by the uniform warmth 
of the bed, while any useless muscular exertion, which would tax the heart's capa- 
city for work, is also avoided by staying in bed. In general it is advisable to cover 
the patient quite warmly, so as to keep him in a constant slight perspiration. 

The regulation of the diet is very important. All those foods and drinks which 
may irritate the kidneys are to be strictly avoided, especially spices, very sour 
substances, strong tea and coffee, or alcoholic drinks. Milk has for a long time 
proved itself to be by far the most suitable and best food. This has won for itself 



ACUTE NEPHEITIS. 



795 



the reputation of a remedy in renal disease, and the best results have often been 
seen from a methodical "milk-cure" — that is, from feeding the patient almost 
exclusively with milk. The great aversion of some patients toward milk, how- 
ever, is sometimes an obstacle to its use. We may often be aided, then, by mak- 
ing the milk more acceptable to the patient by the addition of a little coffee, salt, 
a little cognac, or soda-water. Among other foods to be recommended are 
buttermilk, milk-gruel with rice or groats, and flour-gruel. We should be very 
cautious about giving meat as long as there are severe symptoms. We may allow 
meat-broths, with eggs, sooner. For drinks, beside milk, we may give water and 
lemonade, which latter is especially suitable. Of alcoholic beverages, a little 
weak red wine is usually the only thing to be permitted. Stronger wines are 
given only when there is cardiac weakness, and then they are of doubtful benefit. 

The chief object in the symptomatic treatment consists in preventing the inju- 
rious results of the defective elimination of the water and the solid constituents 
of the urine by the kidneys, or in removing these results if they have already 
occurred. This purpose can be attained only by exciting, as far as possible, the 
activity of other organs which in this respect may act vicariously for the kidneys. 
The skin deserves the first attention here, through which, by means of the sweat- 
glands, large amounts of water, and also, to a certain extent, the solid constituents 
of the urine, which have been retained, may be eliminated. The diaphoretic treat- 
ment of renal diseases has, therefore, been generally in vogue for a long time. If 
the patient's general condition permits, we always begin with it as early as possi- 
ble, even before there have been any signs of oedema, uraemic symptoms, etc. Hot 
baths from 95° to 105° (36°-40° C.) are best. The patient stays about half an hour 
or an hour in the bath, is then rapidly dried somewhat, wrapped up in bed in a 
previously warmed sheet, and then is well covered up to the neck with blankets. 
In order to make the procedure somewhat easier for the patient, it is a good plan 
to cover the forehead with a cold compress, always to wipe the sweat carefully 
from the face, and frequently to give him a little swallow of fresh cold water. 
The production of sweat is, of course, better excited during the pack if the patient 
takes some hot drink, hot milk with soda-water, or hot elder-tea. It sometimes 
seems to aid diaphoresis if an internal diaphoretic be given at the same time, the 
best being five to ten grains of Dover's powder (grm. 0'3-0 - 5), or three or four 
drachms (grm. 10-15) of liquor ammonii acetatis {spiritus Mindereri) in a cup of 
elder-tea. We have also found a good rubbing of the whole body with dilute 
warm French brandy of service before the pack. The pack may last two or three 
hours. 

In this way we succeed in many cases in causing a considerable production of 
sweat, so that the patient loses several pounds in weight at each pack, and an 
existing dropsy may sometimes be made to disappear completely in a compara- 
tively short time. On the other hand, however, we can not deny that it is very 
hard sometimes to make patients sweat, even when there is oedema of the skin, 
and also that many patients do not bear hot baths and packs at all. The latter is 
especially true if the patient has dyspnoea, and if signs of cardiac weakness have 
already set in. Then we have to be very cautious about using sweating as a 
remedy. Sometimes we can bathe the patient, but we have to omit the pack, 
while in other cases he can take the hot pack in bed ; but we must avoid carry- 
ing him to the bath and back. We also have to get along with hot wet packs, if 
baths can not be used for extrinsic reasons. 

Beside hot baths and packs, one diaphoretic remedy is to be especially consid- 
ered in renal disease, and that is the hydrochlorate of pilocarpine, derived from the 
jaborandi-leaves. We use it best in the form of a subcutaneous injection, of one 
sixth to a third of a grain in one dose (grm. 0 '01-0 "02) ; but it may also be given 



796 



DISEASES OF THE KIDNEYS. 



internally in the form of pills, in like doses. Its action consists in the production 
of a copious sweat, and also usually of a very considerable now of saliva, which is 
often very disagreeable to the patient. In general, we prefer the baths to pilo- 
carpine, and we try the latter only when the baths are contra-indicated or do not 
exert any satisfactory action. The diaphoretic action of pilocarpine, moreover, is 
often decidedly less in dropsical patients with kidney disease than in other cases. 

Next to the skin, the intestinal mucous membrane is the organ from which we 
may soonest expect to produce a vicarious elimination of water, and also of urea, 
for the kidneys. It is sometimes, therefore, of distinct service to prescribe drastic 
cathartics in nephritis with a diminished secretion of urine, especially if there is 
a tendency to constipation beside the dropsy, dyspnoea, etc. The drastic cathartics 
chiefly used are infusion of senna, decoction of colocynth, 3 or 6 to 150, gamboge 
in two-grain powders (grm. 0"1), etc. 

Finally, it may be asked whether we should not excite the secretory function 
of the kidneys themselves by the exhibition of diuretics. The objection is, how- 
ever, that all diuretic remedies irritate the kidneys, increase the flow of blood to 
them, and therefore can act only injuriously upon the nephritis. We must, there- 
fore, be very cautious in using diuretics. Only the milder remedies, especially 
acetate of potassium, may sometimes be used with advantage, especially in the 
less acute cases or during the period of convalescence. The diuretic action of digi- 
talis, which is very important under some circumstances, will be mentioned later. 

The therapeutic measures so far spoken of correspond to the task of prevent- 
ing as far as possible the retention of urinary constituents in the body. They 
are also very much employed when the signs of this retention have already 
appeared. The dropsy especially can be successfully treated only by methodical 
sweatings, with the aid, eventually, of drastic and diuretic remedies. When urae- 
mia is threatening, and often even when it has broken out, we may try to produce 
an elimination of the injurious products of tissue metamorphosis from the body in 
the well-known ways above described, by sweating or drastic purgatives. Beside 
this, the uraemic symptoms, however, often demand a special symptomatic treat- 
ment. If very violent and frequent uraemic convulsions appear, we consider it 
advisable to try to suppress the attacks by chloroforming' the patient. At any rate, 
it seems to us to be better to use chloroform in uraemia than to give narcotics 
internally, because with this we can watch the action of the remedy better, espe- 
cially the condition of the pulse and respiration. Chloroform is also generally used 
by the obstetricians as the main remedy in the eclampsia of pregnancy. If the 
attacks are not very frequent, but if there is marked somnolence or coma, tepid 
baths with cold shower-baths are often employed with distinct advantage. Cool 
baths are also serviceable where there is a great increase of the temperature. If we 
are treating a robust individual with a full pulse, and during severe uraemia there 
is a decided redness or cyanosis of the face, venesection may be indicated. This 
sometimes has a striking and instant effect, as has lately been confirmed by 
various observers. Great attention is to be paid to the condition of the heart. As 
soon as the pulse becomes small and weak, energetic stimulants, like subcutaneous 
injections of camphor, must be used. If the signs of cardiac weakness appear 
before the beginning of severe uraeraic symptoms, digitalis must be used in infusion 
or powder. Through its action in raising the blood-pressure — it being advisable 
under some circumstances to combine with it acetate of potassium — a greater 
diuresis sometimes comes on, and with it a disappearance of the danger from 
uraemia. The tinctura nervina Bestuschefni [nearly equivalent to the tincture of 
the chloride of iron, U. S. P.] may also be sometimes used to advantage in urae- 
mia. We are not apt to interfere with uraemic vomiting or uraemic diarrhoea, 
because these symptoms, as we have said, are to be regarded as a form of self-help 



SUBCHEONIC AND CHEONIC FOEMS OF NEPHRITIS. 797 



by the organism. Only when these symptoms are very distressing do we give 
cracked ice, morphine, opium, etc. If the vomitus contains ammonia, it is a good 
plan to give ten or fifteen drops of dilute hydrochloric acid in water several times 
a day. 

[A method of treatment of ursemic convulsions, whether post partum or con- 
nected in no way with parturition, which gives excellent and prompt results, is the 
administration of pilocarpine hypodermically — grain £, and repeat in twenty 
minutes — followed by the hot-air bath, to maintain the action of the skin after 
it has once been started. 

Pilocarpine sometimes acts as a decided cardiac dej)ressant, so one must be 
ready to administer stimulants — brandy or ether — under the skin if, as is apt to be 
the case, there is doubt as to the readiness with which they will be absorbed from 
the stomach or rectum.] 

In severe cases, the patient's dyspnoea often demands urgent relief. If this be 
caused, or at least increased, by hydrothorax, and we do not succeed in removing 
the hydrothorax in any other way, it is necessary to evacuate it by puncture. In 
acute nephritis, indeed, we may hope by this means sometimes to preserve the 
patient's life until improvement sets in. Great ascites must also sometimes be 
punctured. Against u renal pneumonia" our remedies are powerless. Tepid 
baths and shower-baths sometimes procure relief . In " uraemic asthma," morphine 
injections may act beneficially. If pulmonary oedema ensues, the heart again is 
chiefly to be considered. We may try, besides, large mustard plasters, baths, and 
acetate of lead. 

We accordingly see that many remedies are at our service in the treatment of 
nephritis, the choice of which in the individual case must be committed to the 
personal judgment of the physician. In the main, we should always begin with 
the necessary hygienic measures, and, if possible, with a methodical diaphoretic 
treatment, and govern ourselves otherwise by any symptomatic indications. 
After recovery has set in, great caution is still necessary for a long time. The 
patient must guard against physical over-exertion, errors in diet, and exposure 
to cold. Preparations of iron are to be prescribed when there is a subsequent 
anaemia. 

In regard to the influence of the onset of an acute nephritis on the treatment 
of the primary disease, we may yet mention that cold baths are in general not to 
be freely used, as in typhoid fever with nephritis, but they are not absolutely 
contra-indicated if they are otherwise urgently desirable. We may mention besides 
that certain internal remedies, especially salicylic acid, must be used only with 
great caution when there is nephritis. In the eclampsia of lying-in women the 
induction of premature labor is only rarely indicated, since the child is usually 
born during the paroxysms without interference. 



CHAPTEE III. 

THE SUBOHRONIO AND CHRONIC FORMS OF NEPHRITIS, WITH THE 
EXCEPTION OF THE GENUINE CONTRACTED KIDNEY. 

(" Second Stage of BrigMs Disease.'''' Chronic Parenchymatous Nephritis, Chronic Hoemorrhagic 
Nephritis, Large White Kidney, Secondary Contracted Kidney.) 

iEtiology. — While the acute nephritis described in the preceding chapter runs 
its course in several days or weeks, and only rarely extends over some months, 
we will now speak of inflammatory degenerative affections of the kidneys which 



798 



DISEASES OF THE KIDNEYS. 



last at least several months, and often go on for a year or two. The term " sub- 
acute " or " subchronic " is chosen for the cases that last a comparatively short 
time. As we must once more repeat, there is no sharp limit in this respect. 

In regard to the aetiology of these forms of nephritis, they do arise from an 
acute nephritis, but this is quite rare. Formerly such an origin was erroneously 
regarded as the rule, and this is the reason why the changes in the kidney in these 
cases were described as the "second stage of Bright's disease" (Frerichs). The 
English clinical observers Wilks and Johnson, whom Bartels followed in Ger- 
many, first pointed out the fact that in most cases the disease shows a chronic 
character from the start, and that we can only exceptionally, as after scarlet fever, 
recognize an acute " first stage." The name " chronic parenchymatous nephritis," 
since frequently used, is chosen entirely from practical reasons, inasmuch as it 
briefly states the distinction from the genuine contracted kidney ; but it is incor- 
rect in principle, as will be shown from the description of the anatomical condi- 
tions later. 

If we look for the serological conditions in cases that have a chronic course 
from the beginning, we can often discover nothing definite at all. The disease 
seems to have developed " of itself " in previously healthy persons. Most probably 
we have here some toxic or infectious agency that acts on the kidneys, whose 
detection, however, is at present impossible. In malarial regions the malarial 
poison may often lead to chronic nephritis. It is also attributed to syphilis and 
tuberculosis, but the cases met with are usually combinations of these diseases with 
amyloid kidney {vide infra). Frequent exposures to wet and cold, damp dwell- 
ings, etc., seem sometimes to be of more material significance, but it is, of course, 
hard to form a definite opinion on this point. 

Persons in middle life are most frequently aff ected by the disease, and men 
more often than women. In children and old people the disease is quite rare. 

Pathological Anatomy. — There is no essential distinction between the ana- 
tomical lesions of the kidney in acute and in chronic nephritis. The changes that 
are seen in both are essentially the same, only they develop and extend more 
slowly in the chronic forms ; and they also, during their longer duration, lead to 
certain sequelae in the kidney, which can not develop at all in acute nephritis, 
owing in part to the lack of time. Even in chronic nephritis the individual cases 
differ from one another in many respects. First this and then that histological 
process is especially prominent, and thus lends certain peculiarities to the macro- 
scopic appearance of the kidneys. Certain sequelae — like contractions — have 
also developed but little in many cases that soon end fatally, but they develop 
far more in other cases of longer duration. Hence it happens that we can quite 
well regard certain anatomical forms that are more frequently observed as types, 
although we must never lose from sight the principle, to be firmly held, of the 
pathological unity of all these forms and types. Then we shall not lose the clew 
to the understanding of the morbid process if the individual case does not always 
harmonize with the scheme of the text-books. 

We distinguish the three following chief anatomical types of subchronic and 
chronic nephritis : 

1. Chronic Hemorrhagic Nephritis in the form of the Large Eed or Varie- 
gated Kidney. — The kidney is at least of normal size, and often a little or a good 
deal enlarged. It feels firmer than normal ; its capsule is often adherent to the 
surface in some places. The surface looks either uniformly a more gray red or 
more mottled, while dark-red spots alternate with lighter gray or even yellow 
spots. The red spots on the surface can not be wholly wiped off, and thus prove 
to be haemorrhages. The gray or yellow parts correspond to the anaemic and fatty 
degenerated portions. On section, the cortical substance is usually broader, its 



SUBCHRONIC AND CHRONIC FORMS OF NEPHRITIS. 799 



normal boundary is obliterated, and its color is a uniform gray red, or also mottled 
and striated. 

Under the microscope we find in part the same changes as in acute nephritis — 
parenchymatous and fatty degeneration of the epithelium, casts or haemorrhages 
in the uriniferous tubules, inflammatory oedema or granular infiltration of the in- 
terstitial tissue, the capsules of the glomeruli sometimes thickened, the epithelium 
of the glomeruli sometimes proliferated or desquamated, etc. The special char- 
acteristic of this chronic form, in contrast with acute nephritis, is that in many 
places a complete destruction of the uriniferous tubules has occurred, and that 
a genuine interstitial connective tissue, richer or already poorer in cells, has taken 
their place. In this lies the anatomical evidence of the longer duration of the dis- 
ease, since the two processes — both the complete atrophy of the epithelium, and 
especially the secondary proliferation of connective tissue — of course need a certain 
time for their development. The atrophy and the proliferation of connective tissue 
usually predominate in some parts, while in others nothing but fresher inflam- 
matory and degenerative changes are perceived. 

2. The Inflammatory Fatty Kidney, or the Large White Kidney (yellow 
would be more proper). — In this form of chronic nephritis the kidney is usually 
enlarged, or at least of normal size. Its outer surface is smooth and of a yellow 
or an alternating yellow and gray-yellow color throughout. The broader cortical 
substance shows a yellow and usually somewhat mottled appearance, while the 
pyramids almost always appear considerably reddened. Haemorrhages are also 
almost always present in this form, usually, of course, in smaller numbers than 
in the variegated kidney, but they are sometimes quite abundant, as in the haem- 
orrhagic fatty kidney. 

The microscope shows the great affinity between this form of nephritis and the 
preceding. We have almost precisely the same changes, and we always have 
especially a partial destruction of renal tissue with a subsequent increase of inter- 
stitial connective tissue. The macroscopic appearance of the kidney is due to the 
fact that it is anaemic, and that the fatty degeneration preponderates in the epithe- 
lium. It is worthy of note that in these kidneys marked changes in the glome- 
ruli are usually present. 

3. The Secondary Contracted Kidney.— While in the two forms of nephritis 
thus far described the outer surface of the kidney is still smooth, and the kidney, 
on the whole, is somewhat enlarged, we have to do here with kidneys of about 
normal size, on whose surface there are granulations, which as yet are slight, but 
which still are already plain. This granulation signifies nothing more than that 
the destruction of the renal tissue has here advanced farther, and that the newly 
formed connective tissue has in part undergone cicatricial contraction. These 
kidneys, therefore, represent a later stage of the two forms first-named. They 
usually come under observation when the nephritis has lasted about a year and a 
half or two years, or even somewhat longer. The first beginnings of granulation 
may, of course, show themselves earlier, while, on the other hand, when the 
process lasts a longer time, a completely contracted kidney may develop. 

The color of these kidneys is usually reddish or mottled, the red spots corre- 
sponding to the sunken atrophic parts, and the gray or yellowish spots to the ele- 
vated parts. Yellow kidneys, however, may also show at times decided granu- 
lations. Microscopically, we find already marked atrophy of the renal paren- 
chyma, with a corresponding increase of the interstitial connective tissue. 

Formerly these kidneys were called the " transition between the second and 
third stages of Bright's disease." As follows from the above, they are to be 
regarded only as a more advanced form of chronic nephritis. Since the kidneys, 
in spite of their granulation, have on the whole a normal size, we can decide from 



800 



DISEASES OF THE KIDNEYS. 



this, and from the clinical course, that they were usually, though of course not 
always, previously enlarged. Therefore the name of " secondary contracted kid- 
ney " is quite suitable, in opposition to the genuine contracted kidney, which 
represents a much more chronic form of renal atrophy. 

Of other pathological lesions, apart from the changes in the kidney, we will 
mention here only the hypertrophy of the left ventricle, which is found with few 
exceptions {vide infra) in all the above-mentioned forms of nephritis. The 
chronic parenchymatous nephritis without cardiac hypertrophy, alleged by 
Bartels in his time, does not exist. Such cases were probably confused with amy- 
loid kidneys. 

Clinical History. — Only in the comparatively rare cases when the renal affec- 
tion begins acutely, do the symptoms of chronic nephritis follow immediately on 
the first acute stage. In most cases, however, the disease develops slowly and 
gradually from the start, as we have said, like most of the other chronic organic 
diseases, so that it is usually impossible to determine accurately the moment 
when the disease begins. 

The first signs of the disease consist of certain general symptoms, pallor, 
dullness, loss of appetite, nausea and headache, and later of oedema. The latter 
is often the first symptom which sends the patient to the physician, since in 
the beginning he often pays little attention to the symptoms first named. The 
oedema usually appears first in the ankles and legs, more rarely at an early period 
in the face. It often disappears at first after a night's rest, but always develops 
afresh during the day, gradually increasing in intensity. The patient himself 
now sometimes notices a change in the urine, either an abnormal color or cloudi- 
ness or a diminished amount. The accurate examination of the urine by the 
physician first establishes the diagnosis with certainty. 

In regard to the more special symptomatology of chronic nephritis, we meet 
exactly the same symptoms as have been described in the preceding chapter on 
acute nephritis. The characteristic distinction is based merely upon the whole 
course of the affection and the order of development of the different symptoms, 
and not by the symptoms themselves. 

The urine almost always is diminished. Of course the figures vary quite 
considerably both in different cases and at different times in the same case. The 
small amount of urine, ten to twenty-five ounces (300-700 c.c.) a day, is almost 
always an unfavorable sign, while a free diuresis signifies an improvement of 
the condition, an absorption of the dropsy, and finally a passage of the renal 
affection into a still more chronic condition, the secondary contracted kidney 
(vide infra). Under such circumstances the amount of urine may even be in_ 
creased above the normal, to fifty or sixty ounces (1500 or 2000 c. c.) or more. 

The specific gravity of the urine is often increased to about 1015-1025, corre- 
sponding to the amount of albumen and of other solid constituents. It is of 
course correspondingly lower when there is a more abundant elimination of 
water by the kidneys. 

The amount of albumen in the urine is quite marked in all severe cases, being 
one third to three fourths of its volume. It amounts to about l'5-3 per cent, by 
weight, so that the patient's daily loss of albumen may reach half an ounce to an 
ounce (15-30 grammes). 

The examination of the sediment, which is usually abundant, is of the greatest 
importance for the accurate determination of the form of the anatomical changes 
in the kidneys. Above all, the question arises as to the presence or absence of blood 
in the urine. Every abundant haematuria may be recognized by the naked eye 
from the color of the urine. The detection of smaller amounts of blood can be 
made only by the aid of the microscope. It goes without saying that the amount 



SUBCHRONIC AND CHRONIC FORMS OF NEPHRITIS. 801 



of blood in the urine varies quite considerably in the different cases, and in the 
same case the urine often contains much more blood during certain periods in 
the course of the disease than at other times. The portions of urine passed at 
different times taken separately often show quite marked variation in this 
respect ; the day's urine especially usually contains more blood than the night's. 
From the detection of renal haemorrhages, of course in connection with other 
symptoms, we can always make with certainty the diagnosis of a "chronic 
haemorrhagic " nephritis. 

In most cases casts are quite abundant in the sediment of the urine, but of 
course their amount and variety undergo quite great variations in different cases 
and at different times in the same case. They are the direct sign of the presence 
of an inflammatory exudative process in the kidneys, although the deposits on the 
casts are more important for the diagnosis of the special form of renal disease 
than are the casts themselves. Those formed constituents of the sediment are most 
characteristic in this respect which point directly to the processes of fatty degen- 
eration in the kidneys : the fatty granules and fatty granular cells, free or 
attached to the casts. The number of these elements is especially great in the 
chronic inflammatory fatty kidney, the " large white kidney." The usually clear, 
non-haemorrhagic urine may in some cases have even a fatty lustrous surface. 
Renal epithelium is, on the whole, more rarely present in the sediment in chronic 
nephritis than in acute, but it occurs at times in some cases. 

Of the other symptoms, the one that usually most strikes the eye is dropsy. It 
usually comes on, as we have said, in the beginning of the disease, and slowly or 
rapidly reaches a great extent and intensity. A medium or even a high degree of 
general dropsy may often persist almost unchanged for months. In other cases 
it shows either spontaneous variations or variations influenced by treatment ; it 
decreases for a time only to increase anew. The severer and more acute the 
case, the greater in general is the dropsy. In the more chronic cases, in sec- 
ondary contracted kidney, its intensity may be slight for a time or even perma- 
nently. The dropsy may even be absent in some cases, as we learn especially 
from the observations reported by Wagner under the name of " chronic haemor- 
rhagic Bright's disease without oedema." In regard to the different localizations 
of the dropsy, and to dropsy of the internal cavities, hydrothorax, ascites, and 
hydropericardium, and their results, the same holds true as was described in the 
account of acute nephritis. 

Of the internal organs, the condition of the heart lays claim to the most inter- 
est. In all cases of chronic nephritis, in which we do not have to do with espe- 
cially weak and run-down patients, who can not save the necessary nutritive 
material for the formation of a cardiac hypertrophy, we find a pronounced and 
often a very marked hypertrophy of the left ventricle, either with or without a 
co-existing dilatation of its cavity. A chronic nephritis without cardiac hyper- 
trophy, which was put forward by Bartels and others as the type of " chronic 
parenchymatous nephritis," does not exist, as we have said, except under the 
above-mentioned conditions. The detection of cardiac hypertrophy during the 
patient's life is sometimes difficult, especially when there is general dropsy, but 

t the diagnosis can usually be correctly made with proper attention to the abnor- 
mally tense radial pulse, the accentuated, valvular aortic second sound, and the dis- 
placement outward of the apex-beat, or at least its increased strength. We often 
find in the cadaver, and can sometimes make out during life, a hypertrophy of 
the right ventricle. This is usually a sign of a disturbance of compensation — that 

. is, the paralyzed left ventricle can no longer send forward in a sufficient manner 
all the blood coming from the pulmonary veins, so that there ensues a stasis in 
the pulmonary circulation, and a consequent hypertrophy of the right ventricle. 
51 



802 



DISEASES OF THE KIDNEYS. 



A second important sequel of chronic nephritis consists of the changes in the 
retina — albuminuric retinitis. Although very rare in acute nephritis, these changes 
are present in by far the greater majority of the cases of this class. Sometimes 
the patient's subjective visual disturbance (dinmess of vision, defects in the field 
of vision), point to a disease of the retina, but the existence of disease can be estab- 
lished with certainty only by ophthalmoscopic examination. In these cases we 
find two changes, in varying numbers and combinations : first, retinal haemor- 
rhages ; and, second, white spots and streaks, especially in the vicinity of the optic 
nerves. The origin of the spots, which may appear and disappear again, is not 
yet entirely clear. At any rate, there are cncumscribed fatty degenerations of 
the special retinal elements. • The degree of amblyopia depends, of course, chiefly 
upon the localization of the changes, whether in the macula lutea, or other parts. 

We can say little in regard to the other symptoms, since they agree essentially 
with those of acute nephritis. The general anaemia is very pronounced in many 
cases, but it is less marked in the very chronic forms. The cerebral symptoms, 
especially the headache and the mild vertigo, may depend in part upon the cere- 
bral anaemia ; otherwise, they are a uraemic symptom {vide infra). Cerebral 
haemorrhages have been observed in a veiy few cases. Haemorrhages on the 
inner surface of the dura mater are more frequent, but they are usually without 
clinical significance. The mouth, larynx, and pharynx usually show nothing 
particular, except accidentally complicating inflammations. We must, however, 
remember the occasional occurrence of a very distressing or even dangerous 
oedema of the soft palate, or of the arytaeno-epiglottic ligaments — oedema of the 
glottis. Similar forms of bronchitis and pneumonia, as in acute nephritis, are 
found in the bronchi and lungs. Bronchitis and chronic oedema of the lungs also 
make their appearance in the more advanced stages of the disease as a result of 
cardiac insufficiency. Finally, we must remember the hindrance to respiration 
from hydrothorax, and also from uraemic dyspnoea. The changes in the heart 
have already been spoken of. Complicating inflammations, such as endocarditis 
or pericarditis, are very rare. 

Loss of appetite is a very common symptom on the part of the stomach. Very 
persistent vomiting is usually to be regarded as a chronic uraemic symptom. The 
bowels, as a rule, are constipated, but there may also be severe diarrhoea, as in 
acute nephritis. In severe cases, esx^ecially in the last stages of the disease, ulcer- 
ative and dysenteric processes have repeatedly been observed in the large intestine 
and the ileum. Peritonitis may occur, but it is at all events extremely rare. The 
liver and spleen usually show no peculiarities. 

Uraemic symptoms, both of the milder chronic variety and also in their severest 
acute form, may come on at any time, although they do not by any means 
attain their full development in all cases, and are somewhat rarer than in genuine 
contracted kidney. 

The temperature remains normal, as a rule, as long as it is not influenced by 
complicating inflammations, or by the appearance of uraemia. 

Course, Duration, and Termination of Chronic Nephritis.— In general, the whole 
course of chronic nephritis presents quite a great uniformity. The different symp- 
toms may show certain variations within long periods, but the patient often pre- 
sents almost the same appearance day after day for months. The duration of the 
disease shows all the transitions from three to six months, in the subacute cases, to 
two or three years, or even more, in the very chronic cases. The cases of long 
duration are almost all cases of secondary contracted kidney. They sometimes 
show in then clinical relations the transition from the enlarged to the granular 
kidney, since the picture in many of its details is more like that in the genuine 
contracted kidney : the oedema decreases, disappears completely, or, at least, con- 



SUBCHEONIC AND CHEONIC FOEMS OF NEPHEITIS. 803 



tinues in a lesser degree ; the amount of urine becomes more abundant, and the 
specific gravity and the amount of albumen become correspondingly less. The 
condition thus lasts for a long time until it grows worse again, through uraemia, 
or disturbance of the compensation in the heart. 

The final termination of chronic nephritis is in most cases unfavorable. In the 
severe forms death ensues in from three months to a year, either in consequence 
of general dropsy or from uraemia, from complicating inflammations, etc. The 
conditions when the nephritis goes on to secondary contraction are comparatively 
more favorable, inasmuch as the patient may then find himself in a tolerable con- 
dition for a time at least. Complete recoveries doubtless occur in chronic nephri- 
tis, but they are rare. An apparent recovery may be simulated by the appearance 
of secondary contraction. Even after signal improvement, however, relapses are 
always to be feared. There are even genuine acute attacks in the course of chronic 
nephritis. 

Diagnosis. — On careful examination of the urine in all suspicious cases of 
oedema, anaemia, etc., the diagnosis of chronic nephritis can always be correctly 
made. In regard to the more exact distinction of the different anatomical forms, 
we will here give a brief schematic glance at the most important conditions : 

Chronic Hcemorrhagic Nephritis (large variegated or mottled kidney). — Dura- 
tion from six to eighteen months. Urine often haemorrhagic ; usually quite rich 
in red blood-corpuscles and casts. CEdema. Cardiac hypertrophy. Eetinal changes. 
Quite frequently uraemia. 

Inflammatory Fatty Kidney (large white kidney). — Duration also six to eighteen 
months, but usually somewhat shorter than in the preceding form. Urine not at 
all, or only slightly, haemorrhagic. Frequently many white blood-corpuscles, and 
especially signs of fatty degeneration in the kidneys, fatty granular cells, fat-drops 
in the urine, etc. Significant amount of albumen in the urine. Marked oedema. 
Cardiac hypertrophy. Very often retinal changes. Death by uraemia frequent. 

Secondary Contracted Kidney. — Longer duration of the disease, from a year and 
a half to three years. At first the symptoms of the preceding forms ; later, urine 
more abundant, less oedema, etc. Death from an increase of the dropsical symp- 
toms due to cardiac insufficiency, uraemia, etc. 

Treatment. — The treatment of chronic nephritis corresponds in all its details 
so closely to that of acute nephritis that we can refer almost entirely to the pre- 
ceding chapter. 

The main thing here is also regimen and symptomatic treatment. The patient 
must always keep himself warm, wear flannels, or stay in bed. Under some cir- 
cumstances climatic cures, like Italy, Egypt, etc., are indicated in the more chronic 
forms. A milk diet is to be carried out as far as possible. 

The treatment of dropsy follows entirely the methods previously described, and 
so does the treatment of any uraemic symptoms. 

In the more chronic cases with great anaemia preparations of iron, such as 
iodide of iron, are often to be used, and also frequently stomachics, cathartics, etc. 
The condition of the heart always deserves careful attention (digitalis !). The reti- 
nitis rarely demands a special treatment. 



804 



DISEASES OF THE KIDNEYS. 



CHAPTEE IV. 

CONTRACTED KIDNEY. 

(Genuine Contracted Kidney. Granular Atrophy of the Kidney. Granular Kidney. Renal 
Sclerosis. " Third Stage of BrighCs Disease" Chronic Interstitial Nephritis.) 

Definition and -Etiology. — The genuine contracted kidney is the result of an 
extremely chronic and very slowly but constantly progressive atrophy of the 
renal tissue. The term " chronic nephritis " is also used for contracted kidney, 
but the special inflammatory processes are very subordinate here, for the anatom- 
ical process consists essentially in nothing but a simple degenerative atrophy of 
the renal parenchyma, and in a corresponding gradual increase of the interstitial 
connective tissue. From a general pathological point of view the process is to be 
regarded as wholly analogous to the corresponding changes in the liver in cirrhosis 
of that organ, in the spinal cord in the chronic degenerations of the different sys- 
tems of fibers, etc. In all these cases we have a primary destruction of the special 
tissue-elements as a result of some deleterious action, and, following a general 
pathological law (Weigert), a partial replacement of the parts destroyed by a 
newly formed cicatricial connective tissue. 

In the "genuine" contracted kidney the atrophy of the renal parenchyma 
begins in a previously healthy kidney. Cell after cell of epithelium, islet after 
islet of tissue, are slowly attacked, while other parts still remain intact. It was 
therefore an error of the older pathologists to regard the contracted kidney as the 
" third stage of Bright's disease," as if every granular kidney were first found in 
the stage of acute inflammation, and then passed into the stage of chronic enlarge- 
ment, and lastly into that of contraction. This theory, of course, suits certain 
cases in part, for chronic nephritis at least may often finally pass into contraction, 
but these " secondary contracted kidneys " (vide supra) can clinically, and almost 
always anatomically, be differentiated from the genuine contracted kidneys. On 
careful examination, as it seems to us, the contracted kidney may of course arise 
from an acute nephritis in some cases, which perhaps are not very rare ; but then 
the process hardly ever passes through the three stages mentioned above, for the 
acute nephritis apparently recovers. A slight remnant of it is left — a little fire, as 
it were, glimmering under the ashes ; its work of destruction advances, wholly in 
secret, and perhaps only after many years do the symptoms of a pronounced renal 
contraction appear. 

If we inquire into the causes which produce the atrophy of the renal tissue in 
the ordinary cases of contracted kidney, which are chronic from the first, we are 
very often unable to make out any special causes. Of course, we must again bear 
in mind first the two great groups of injurious influences, the chemico-toxic and 
the organized parasitic, but at present only a small number of ^etiological factors 
have a more or less definite significance. 

Experience teaches us that there are three chemical substances to be mentioned 
which may favor the development of contracted kidney: alcohol, lead, and uric 
acid. Chronic alcoholism is often to be regarded as the most probable cause of 
renal contraction, especially in people who have " lived well " otherwise, and have 
become corpulent. This is the explanation of the combination of contracted 
kidney and cirrhosis of the liver repeatedly observed. The connection between 
contracted kidney and chronic lead-poisoning, in type-setters, painters, etc., is also 
incontestable. It is also a remarkable circumstance, and one not yet fully 
explained, that in these cases we very often see at the same time a genuine gout 
(arthritis iiratica). Gout, however, alone, without any co-existing chronic lead- 



CONTRACTED KIDNEY. 



805 



poisoning, often leads to the development of contracted kidney, " gouty kidney," 
in which we probably have to do with the noxious action of an abnormal amount 
of uric acid on the renal parenchyma. 

Infectious influences are, probably, first to be considered in those cases where 
the contracted kidney can be referred to a former infectious nephritis, as after 
scarlet fever. We may also mention here the appearance of contracted kidney 
sometimes observed after severe acute articular rheumatism. We may perhaps 
imagine a similar connection in the cases where contracted kidney is found com- 
bined with chronic endocarditis (valvular heart disease), or with chronic arthritis 
not of gouty origin. Of the chronic infectious diseases, which may probably some- 
times have a connection with the origin of contracted kidney, we may mention 
malaria and syphilis. The latter ought especially to be considered more than it is 
at present, because we may have either an immediate action of the syphilitic poison, 
or a renal atrophy as the result of specific disease of the renal arteries. 

We must here spend a little time in the general consideration of the connec- 
tion between renal contraction and primary disease of the vessels, which has been 
much discussed. It is true that we often find general arterio-sclerosis, and also 
atheroma, especially in the renal arteries, in the bodies of persons who have died 
from contracted kidney, but this frequent coincidence can not be remarkable in 
such cases, because contracted kidney is seen chiefly in advanced age, and in those 
persons in whom atheroma of the arteries is also a very common symptom. The 
theory advanced by the English authors, Gull and Sutton and others, that the vas- 
cular disease, " arterio-capillary fibrosis," always represents the primary process, 
to which the renal atrophy is only secondary, is, however, utterly untenable. We 
often find the most pronounced contraction of the kidneys without any vascular 
changes sufficient to explain the atrophy ; and where the latter can be found in 
the small renal arteries, we usually have not a primary but a secondary process — 
namely, the well-known obliterating arteritis, which is seen in almost all chronic 
inflammations and degenerative atrophies of various organs. 

Of course, it can not be denied that under some circumstances primary vascu- 
lar diseases of the renal arteries may lead to secondary atrophy in circumscribed 
spots by checking the blood-supply to certain parts of the tissue — " vascular con- 
tracted kidney" — just as indurated myocarditis arises after primary arterio-sclerosis 
of the coronary arteries. The " senile kidney " — that is, the granular kidney of old 
people — is also due to vascular changes like atheroma, as are also, which is worthy 
of special note, the rare cases of unilateral contraction of the kidney, which is 
observed chiefly in syphilis. 

The relation of contracted kidney to amyloid disease of the kidney, and to 
chronic diseases of the urinary passages, especially of the pelvis of the kidney, 
will be spoken of later in the appropriate chapters. 

Pathological Anatomy. — In the genuine contraction of the kidney, both kid- 
neys are always diminished in about the same degree. Their size is sometimes 
reduced to one half or even one third of the normal, so that it is almost difficult to 
find the little kidney in the very abundant and thick fatty capsule that is often 
present. The kidneys feel firm and dense, and show on their surface a very plain, 
coarse or fine, uniform or irregular, granulation. On pulling off the somewhat 
thickened fibrous capsule, these granulations become more prominent, and the cap- 
sule usually adheres quite firmly to the depressed portions. The raised portions 
are almost always darker and redder — that is, richer in blood — than the lighter 
and grayer depressions. Whether the whole kidney appears more red or more 
white depends only upon the amount of blood in the organ, and there is no reason 
for separating the " small red " from the " small white " contracted kidney. 

On section of the contracted kidney, we find the cortex much smaller, and pale 



806 



DISEASES OF THE KIDNEYS. 



atropliic streaks alternating with the darker portions. The pyramids are also 
somewhat smaller, and, as a rule, are darker than the cortex. In the pelvis of 
the kidney, which is often somewhat dilated, there are frequently a number of 
uric-acid concretions. Striated uric-acid infarctions in the pyramids are a very 
characteristic mark of the gouty contracted kidney. The microscope shows an 
advanced destruction of the renal parenchyma, which is replaced by a cicatricial 
connective tissue which is still granular or which has begun to be poor in granules. 
We can always make out signs of degeneration and atrophy of the epithelium, and 
the formation of casts in the uriniferous tubules which still remain, but which are 
always diseased. Atrophy, thickening of the capsule, etc., are found in many of 
the glomeruli. The uriniferous tubules that are still preserved in some places are 
often in part dilated. We can not here go more fully into the manifold histologi- 
cal details, especially the formation of cysts, the changes in the vessels (vide supra), 
the deposition of lime-salts, etc. Haemorrhages are only very rarely present. 

Thus the contracted kidney may be regarded as the form of chronic nephritis 
with by far the longest course (lasting from three to five years, and even much 
longer), and also the form with the widest extent. Its essential nature can in no 
way be contrasted with "chronic parenchymatous nephritis" as a "chronic inter- 
stitial nephritis " ; for we always find interstitial processes in the former, which 
have reached a far higher degree in the contracted kidney only because the slow 
atrophy of tissue is compatible with a much longer duration of life, and hence can 
attain a much greater extent. 

The anatomical changes in the other organs of the body beside the kidneys 
will be spoken of in connection with the symptomatology of contracted kidney. 

Clinical Symptoms. — Except in the comparatively rare cases where we can 
refer the origin of a contracted kidney to a previous acute or chronic nephritis, 
the clinical symptoms of contracted kidney develop as gradually and unnoticeably 
as the anatomical process itself. There is no doubt but that a contraction of the 
kidney may exist for years, without calling the patient's attention to his disease by 
a single serious subjective symptom. This follows in part from the chance dis- 
coveries on autopsy of a contraction of the kidney in people who have lost their 
lives in some other way, but especially from the cases where the severest symp- 
toms, like uraemia, cerebral haemorrhage, etc., which often lead immediately to 
death, suddenly come on in persons previously regarded as perfectly healthy, while 
the autopsy often shows quite a far advanced contraction of the kidney as the 
special cause of these symptoms. The less prominent the subjective symptoms of 
renal contraction are in the earlier stages of the disease, the more we should con- 
sider the objective changes, which in fact usually permit the diagnosis of the dis- 
ease quite early on careful examination of the patient. 

The condition of the urine is most important in this respect. As soon as 
changes have taken place in the epithelium in different parts of the kidneys, the 
results previously spoken of must make themselves manifest in the secretion of 
the urine, although still in a slight degree, and the diseased patient will secrete a 
urine diminished in amount and in solid constituents, but containing albumen. 
Since, however, many normal uriniferous tubules and glomeruli are still present, 
and since the whole process, as we have seen, develops only very slowly, the body 
gains time for the formation of one of those judicious compensatory contrivances 
which we recognize in so many pathological processes, and which we must regard 
in a teleological sense. This compensatory process consists of an increase in the 
arterial pressure, coming on as gradually as the renal contraction itself, and con- 
stantly increasing, and of a hypertrophy of the left ventricle dependent upon it. 
The blood therefore courses through the many normal glomeruli of the contracting 
kidney under an increased pressure, and the consequence is that in these portions 



CONTRACTED KIDNEY. 



807 



the secretion of the urine, especially of the water, is much more abundant. This 
is the reason why, as a rule, in contraction of the kidney, the patient passes an 
abnormally large amount of urine, which is more watery, and therefore lighter and 
of a lower specific gravity, and which contains only a slight amount of albumen 
coming from the diseased portions. The daily amount of urine is often seventy 
to a hundred and twenty ounces (2000-3500 c. c.) or more ; the urine looks light- 
yellow and clear, contains scarcely any morphological constituents, has a specific 
gravity of 1010-1005 or even lower, and gives, on heating, only a slight precipitate 
of albumen, the amount excreted in the twenty-four hours being about half a 
drachm to a drachm (two to five grammes). On careful microscopic examination 
of the urine, we usually succeed in finding a few hyaline casts, which only excep- 
tionally may be more abundant. The urine also frequently contains some white, 
and more rarely a few red blood-corpuscles. In rare but definitely attested cases 
it may happen that for a time, or even during the main part of the disease, the 
urine contains no albumen at all, or only a trace of it. This is probably explained 
by the fact that the diseased glomeruli have wholly ceased secreting, and that 
therefore the urine is secreted only by the healthy portions of the kidney. 

It is apparent of how great significance this abundant secretion of water, as a 
result of the abnormally high blood-pressure, must be for the whole morbid pro- 
cess ; for, in spite of the renal disease, there is now absolutely no retention of 
water in the body, and we therefore understand why there is no oedema in con- 
tracted kidney, even after a course of years. The secretion of the solid con- 
stituents of the urine is not quite in such a favorable condition as the secretion of 
water. It is self-evident that the percentage of the former decreases with the 
increased amount of urine, but the whole amount of urea, uric acid, phosphoric 
acid, etc. , eliminated is also at times somewhat less than normal in relation to the 
food. This diminution, however, is not very great, as long as the work of the 
heart is sufficient, and at certain times, especially in the earlier periods of the dis- 
ease, it may certainly be entirely absent. We accordingly see that the symptoms 
dependent upon an accumulation of the urinary constituents in the blood do not 
appear at all for a long time. Thus it happens that the patient may still feel per- 
fectly well up to a time when the objective examination of the urine discovers 
marked pathological changes. Many patients, of course, notice the polyuria, but 
often no further attention is paid to it, and it is attributed to drinking a good deal 
of fluid. The patient gets accustomed to it, even if, as often happens,' he has to 
pass his urine much more frequently than formerly, and even during the night. 

We need not go into detail here in regard to the special causes of cardiac 
hypertrophy (compare page 783). It was with regard to contracted kidney that 
Traube advanced his mechanical theory of cardiac hypertrophy, which, however, 
brought up the considerations previously mentioned, and therefore was properly 
replaced by the chemical theory, which was also very applicable to this form of 
renal disease. In its clinical relations it is especially important that the cardiac 
hypertrophy causes no subjective symptoms at all, as long as the heart can suffice 
for the work put upon it without strain, a condition which is perfectly analogous 
to that of any fully compensated valvular disease. We can usually recognize the 
condition correctly only by a careful physical examination of the heart and the 
vascular apparatus, although in contracted kidney the percussion and palpation of 
the heart are often rendered difficult by a co-existing pulmonary emphysema. 
We can often perceive, however, the displacement and the increased strength of the 
apex-beat, the extension of the cardiac dullness to the left, and almost invariably 
the abnormal tension of the radial pulse, and the accentuation of the aortic second 
sound. In the later stages of the disease a hypertrophy of the right ventricle is 
often added to that of the left (compare page 801). Complete, or almost complete, 



808 



DISEASES OF THE KIDNEYS. 



absence of the cardiac hypertrophy is observed, as we have said, in weak and 
cachectic patients. 

As long, therefore, as the high arterial pressure kept up by the cardiac hyper- 
trophy regulates the condition of the renal secretion in the way above described, 
the condition of the patient as a rule shows no special abnormality. At most it 
happens that certain cerebral symptoms now appear, especially attacks of head- 
ache and occasional vertigo, which are probably to be referred to active cerebral 
hyperaemia. Frequent nose-bleed is also sometimes the result of the abnormally 
high blood-pressure. 

The picture is quite different as soon as the first signs of a beginning cardiac 
insufficiency appear. Here, as in most diseases of the heart, the disturbance of 
compensation does not usually come on suddenly. Its results begin quite gradu- 
ally, disappear for a time, to come on afresh and to increase quite slowly. In the 
first place, the abatement of the heart's energy usually makes itself manifest by 
symptoms on the part of the heart itself, and of the lungs. The pulse loses in ten- 
sion, and becomes smaller, more frequent, and sometimes a little irregular toward 
the end of the disease. The patient begins to be short of breath, comparatively 
slight physical exertion affects him more than formerly, and there is often palpi- 
tation. Certain anatomical results of stasis may also temporarily or permanently 
develop in the lungs, especially a mild transitory catarrh, or a more obstinate and 
recurring bronchitis. In the more advanced stages of the disease the dyspnoea 
often comes on in pronounced paroxysms, which have an asthmatic character. 
This long-known asthma of renal disease, often termed, without reason, " uraemic 
asthma," does not always have the same origin. It usually depends distinctly 
upon the attacks of cardiac weakness, and is, accordingly, a genuine cardiac asthma, 
and corresponds precisely to angina pectoris in its different symptoms (see page 
296) ; but in other cases there is a transudation into the lungs from stasis, coming 
on as a result of the cardiac weakness, so that the dyspnoea is associated with the 
signs of an acute pulmonary oedema, and is sometimes accompanied by a copious 
expectoration of a frothy, serous, and often somewhat bloody sputum. This is the 
condition which may pass away again and be often repeated, which was formerly 
termed humid asthma. In the last stage of the disease the dyspnoea often becomes 
continuous, and forms the patient's chief disturbance. It is then usually due, not 
merely to the stasis in the lungs, but often, besides, to co-existing lobular pneu- 
monia {vide infra), to hydrothorax, etc. 

As a further sequel of the disturbance of compensation, oedema often appears 
in different parts of the body, in the later course of the disease. It has, indeed, 
been repeatedly observed that dropsy may be entirely absent in contracted kidney ; 
but this is the case only when death ensues from some intercurrent attack before 
the pronounced cardiac insufficiency. Otherwise oedema is by no means rare in 
contracted kidney. It usually appears first in the ankles, the eyelids, or the pre- 
puce, disappears again when the patient is in a quiet condition, and, after a longer 
or a shorter pause, comes on anew, until finally, in the last period of the disease, a 
high degree of general dropsy may develop. 

Among the results of the cardiac insufficiency on the internal organs we must 
first mention the cerebral symptoms. While at first, as we have said, these have 
more of an active hyperaemic character, the frequent and very violent headaches 
that come on later certainly depend mainly upon the passive hyperaemia of stasis, 
or the arterial anaemia of the brain. The pain sometimes shoots into the back of 
the neck, and sometimes is localized chiefly in one half of the head ; it is often 
associated with symptoms of vertigo, with a gloomy or morose disposition, with 
troubled sleep, etc. The stasis is also apparent in the abdominal organs. Chronic 
dyspeptic disturbances appear, the appetite fails, the bowels become irregular, and 



CONTRACTED KIDNEY. 



809 



we can even make out a moderate enlargement of the liver. The influence which 
the altered activity of the heart exerts upon the function of the kidneys them- 
selves is, however, particularly important. From what has been previously said 
of the dependence of the secretion of urine upon the arterial pressure, it follows 
directly that any compensatory activity of the still normal renal territory must at 
once experience a reduction, as soon as the blood -pressure can no longer be kept 
at the same level. Corresponding to this we see, in fact, that the secretion of 
urine also usually suffers a decline at the same time with the other symptoms of 
stasis already mentioned. The amount of urine is less abundant : it falls to forty 
or fifty ounces (1500-1000 c. c), and even lower; the specific gravity rises, rarely 
to a high figure, but still up to 1010 or 1012, or over. The urine often retains 
its clear color for quite a long time, but may finally more and more resemble the 
genuine urine of stasis. The point, however, which is especially to be considered, 
is the co-existing and increasing retention of the solid constituents of the urine in 
the blood, and the consequent allied possibility of the onset of uraemic symptoms. 

It must be stated that, in contracted kidney, the immediate exciting causes of 
uraemia are not always clear. Thus, it is a well-known and very important fact, 
clinically, that very severe and often fatal uraemic convulsions may sometimes 
attack the patient quite suddenly, apparently when in the best of health. Cases 
have been repeatedly seen, by other observers and by ourselves, where the daily 
amount of urine has shown no discoverable diminution in the days preceding the 
uraemia. The precise explanation of these cases must remaiu undecided ; we do 
not know whether there has been a previous retention of the solid constituents, in 
spite of the abundant secretion of water, or whether other changes, like oedema of 
the brain, are to be considered. It is certain, however, that in many cases at least, 
the onset of the uraemia is connected with the cessation of the secretion of urine, 
produced either gradually or suddenly by the cardiac insufficiency. In the former 
case the type of chronic uraemia (see page 780) develops with especial frequency ; 
this consists of headache, vomiting, diarrhoea, severe pruritus of the skin, etc., but 
these symptoms are, of course, often combined with the immediate symptoms of 
stasis, and are not always to be easily and distinctly separated from them. Such 
a condition of chronic uraemia, in patients with contracted kidney, often presents 
a very mournful picture, since the unrestrainable and constantly recurring vomit- 
ing, the headache, and the general mental anxiety may last for weeks. The 
severe acute uraemia either follows the preceding chronic uraemic symptoms, or 
comes on at once with the severest symptoms, general and often-recurring con- 
vulsions, and coma. The uraemia may pass off again, even in contracted kidney, 
but quite frequently it is the immediate cause of death {vide infra). 

Beside the symptoms so far described, we must now mention a set of anatom- 
ical complications which may appear in the course of contraction of the kidney. 
From its diagnostic and clinical importance the albuminuric retinitis, already 
known to us from the preceding chapter, takes the first place. It may come on 
at any time in the course of the disease ; but it often develops so early that the 
patient, up to this time, knows nothing at all of his other disease. He merely 
consults an oculist, who often first recognizes, from the ophthalmoscopic picture 
(see page 802), the special seat of the primary disease. Even in the cases where 
no subjective visual disturbance is present, the retinal examination sometimes 
shows a positive image. In general, the contracted kidney is that form of renal 
disease in which retinal changes are comparatively the most frequent. 

Another rarer but clinically important complication consists of the haemor- 
rhages of internal organs, whose cause is to be found either in the increased arte- 
rial pressure, or in an abnormal weakness of the walls of the vessels — arterio- 
sclerosis in older persons, defective nutrition of the vascular walls in young and 



810 



DISEASES OF THE KIDNEYS. 



anaemic patients. Haemorrhages into the brain are comparatively the most fre- 
quent. They cause both mild and severe apoplectic attacks, which pass off com- 
pletely or leave a hemiplegia behind, and sometimes they are the direct cause of 
death. Beside the haemorrhages into the brain itself, there may also be haemor- 
rhages on the inner surface of the dura mater — haeniatoma. Nose-bleed is also of 
significance ; in many patients it is frequent and very stubborn ; we have ourselves 
seen two cases where the fatal termination was caused directly by an unrestrain- 
able nose-bleed. Haemorrhages into the other organs are more rare, but they 
have also been observed in the skin, the stomach, the intestines, or the lungs. In 
a few cases, indeed, a sort of haemorrhagic diathesis seems to develop. 

Among the complicating inflammations of internal organs, pneumonia is the 
most frequent ; it appears in the lobar croupous form or in the lobular form pecul- 
iar to all varieties of nephritis. Inflammations of the serous membranes, pleurisy, 
or pericarditis, occur, but they are rare. The catarrhal inflammatory affections — 
laryngitis, bronchitis, gastric catarrh, intestinal catarrh — are either to be regarded 
as catarrhs from stasis, or they are perhaps connected with the retention of the 
urinary constituents in the body. We must also refer here to the acute exacerba- 
tions of inflammation in the kidneys themselves (acute recurrent nephritis), which 
is, of course, rare. 

Quite great variations appear in regard to the general nutrition. In most cases 
where the disease develops quite gradually in persons in middle or advanced life, 
the general nutrition for a long time shows no striking anomaly. The patient is 
often very well nourished, and even corpulent, at the period when the first cardiac 
symptoms begin. To the more practiced and attentive eye, of course, he shows 
a certain appearance of suffering, which later becomes more pronounced. He 
becomes emaciated, and has a faded and often somewhat cyanotic color to his 
skin. Marked anaemia usually develops only in younger patients, who then show 
the pallid exterior characteristic of so many patients with renal disease. 

General Course, Duration, and Termination. — The most important peculiarities 
in the course of renal contraction have already been spoken of above. We have 
stated that the disease may be latent for a long time; that the severest symp- 
toms — like uraemia or apoplexy — sometimes come on suddenly and unexpectedly; 
that in other cases the disturbances of compensation in the heart, dyspnoea, palpi- 
tation, or slight oedema, are the first symptoms ; that, under some circumstances, 
certain complicating conditions, such as retinitis, or frequent nose-bleed, first 
direct suspicion to a renal disease, and demand an examination of the urine ; while, 
finally, m a last class of cases, only general disturbances, loss of appetite, pallor, 
general physical weakness, and similar symptoms induce the patient to consult a 
physician. It is usually hard to decide how long the disease has lasted before a 
diagnosis is made. Beside any mild symptoms we must especially inquire into 
the existence of polyuria, which is often not observed, but which many patients 
notice. 

The further course may also vary according to the onset of complications, the 
external conditions under which the patient lives, etc. In general, as we must 
repeatedly emphasize, almost everything depends upon the heart's capacity for 
work and its staying qualities. If death does not ensue sooner from some inter- 
current disease, the last stage of the disease almost always presents itself under 
the picture of cardiac insufficiency with predominant symptoms of dyspnoea and 
general dropsy. 

As has been said, we usually can not determine with any accuracy the whole 
duration of the disease. It may, at any rate, last many years, probably sometimes 
even ten years or more, although there may be many variations in its course. It 
is not impossible that, during the earlier period of the disease, there may be a ces- 



CONTRACTED KIDNEY. 



811 



sation in the process of renal atrophy, but it is hard to decide with certainty. At 
all events, the disease must generally be termed completely incurable, although 
life may not only be preserved for a long time, but the patient may even exist 
without much discomfort. We need not refer especially here to the different 
intercurrent attacks, the possibility of which must always be kept in mind in 
regard to prognosis. 

Diagnosis. — The diagnosis of contracted kidney can be made with certainty 
only by examining the urine. We must, therefore, dwell again on the necessity 
of making this examination in all suspicious cases, because only in this way can 
we avoid overlooking the condition. The suspicion of a developing renal contrac- 
tion should demand an examination of the urine, especially in all cases where the 
patient complains of frequent headache, of congestive conditions, of palpitation 
and dyspnoea, asthmatic attacks, disturbances of vision, general dullness, and dys- 
peptic symptoms, without finding any other reason for these symptoms. The poly- 
uria, the clear urine of low specific gravity, containing a slight amount of albu- 
men, in connection with the signs in the circulatory apparatus, the tense pulse, 
and the hypertrophy of the left ventricle, permit us to recognize the disease cor- 
rectly in most cases. If retinal changes are present, they may sometimes be of 
much aid in confirming the diagnosis. The aetiological conditions — lead, gout, 
alcoholism, etc. — of course also merit attention. 

The diagnosis presents great difficulty in the quite rare cases where albuminuria 
is absent. In these cases we are sometimes able to reach the correct interpretation 
of the morbid condition only by repeated examinations of the urine. Otherwise 
we can scarcely avoid mistaking it for chronic affections of the heart, such as 
myocarditis or idiopathic hypertrophy. 

The diagnosis is also very difficult if the patient does not come under observa- 
tion until the stage of fully developed disturbance of compensation. The charac- 
teristic features of the urine of contracted kidney are then absent, the urine is 
scantier, darker, richer in albumen, and it is often scarcely possible to decide 
whether we have a primary renal affection with secondary cardiac hypertrophy 
or a primary heart disease with a secondary congested kidney. If general arterio- 
sclerosis or marked pulmonary emphysema is present at the same time, the judg- 
ment as to the condition is still more difficult. In such cases a correct diagnosis 
is possible only by very carefully balancing all the different symptoms, and con- 
sidering the whole course of the disease. 

Finally, the diagnosis of contracted kidney is very difficult in cases where the 
first examination of the patient is made during a sudden attack of uraemia or after 
an apoplectic seizure. Here the albuminuria is the symptom which points most 
to the existence of a renal disease, although, in spite of this symptom, the judgment 
as to the condition, and its differentiation from other acute cerebral affections, 
often presents great difficulties. 

Treatment. — As soon as the diagnosis of renal contraction is established, the 
whole hygienic condition of the patient must be regulated so as to prevent the 
advance of the affection in every possible way. In this respect two indications 
are to be fulfilled, to guard against any irritation which may have an injurious 
action on the kidneys, and to relieve the work of the heart as much as possible, in 
order to keep off cardiac insufficiency as long as we can. The diet must be care- 
fully regulated, and must be of scant measure or abundant and strengthening, 
according to the patient's physical constitution. In these cases, too, milk is the 
chief food to be considered. Alcoholic beverages are to be permitted only in a 
moderate degree. All physical over-exertion is to be avoided, although moderate 
methodical exercise is to be recommended for corpulent patients. We should 
always provide for regular evacuation of the bowels by appropriate remedies, 



812 



DISEASES OF THE KIDNEYS. 



dietetic prescriptions, fruits, bitter waters, etc. The general condition is often 
materially improved by proper air and recreation, and in this way the use of a 
bath may be of service, chosen according to the individual conditions, such as iron 
baths, Marienbad, Carlsbad, Kissingen, Ems, or Baden-Baden. 

If disturbances of compensation appear, the dietetic regime and the utmost 
bodily rest possible are still more strictly to be advised, and a symptomatic treat- 
ment should be instituted according to the prevailing symptoms. First of all we 
must try to excite the heart's energy anew by the exhibition of digitalis. The 
details of treatment here are almost precisely the same as are considered in the 
treatment of chronic heart disease (q. v.) and the other renal affections. 

At present it is impossible to influence the process of contraction in the kidney 
favorably by the direct use of drugs. The iodine preparations — iodide of potassium, 
and in anaemic patients iodide of iron — are alone recommended, and are worth 
trying in this respect. 

The prophylaxis of renal contraction is evident ; we should consider as far as 
we can the known setiological conditions. We may compare, in this regard, the 
chapters on gout and chronic lead-poisoning. 



CHAPTER V. 

AMYLOID KIDNEY. 

JEtiology. — The amyloid kidney is invariably a part of the more or less exten- 
sive amyloid degeneration of the organs in the rest of the body. In its clinical 
relations, however, it claims the most interest of all amyloid diseases, since it has 
by far the greatest significance for the whole clinical picture of amyloid degenera- 
tion. 

As is well known, we understand by amyloid degeneration a peculiar change 
which, under certain pathological conditions, is observed in the connective tissue, 
and especially in the smaller vessels. The walls of the vessels are thicker, they 
have a lustrous homogeneous appearance, and they show peculiar reactions on 
treatment with certain coloring agents. These reactions are due to the presence 
of an albuminoid substance — amyloid — which is either deposited in the tissue from 
the blood, or, as is much more probable, is developed in that place and spot from 
the albuminoid substances present. In marked amyloid degeneration the diseased 
organs often show macroscopically an altered " bacon-like " appearance, and 
assume a characteristic red-brown color on treating the affected parts with Lugol's 
solution of iodine. The microscopic examination alone affords more accurate 
conclusions as to the presence and distribution of the degeneration. Here we 
make use chiefly of staining the tissues with methyl-violet or gentian- violet. The 
amyloid portions thus take on a very characteristic and easily defined red color. 
In this way we can discover that the amyloid degeneration begins everywhere in 
the walls of the small vessels, that the interparenchymatous connective tissue may 
also be affected later, but that the parenchymatous cells proper, liver cells, renal 
epithelium, etc., almost always remain perfectly free. The latter often show 
atrophic and fatty degenerative changes (vide infra), but never amyloid degenera- 
tion. 

Nothing is known as to the special causes which effect that peculiar metamor- 
phosis of the albumen of the connective substance into amyloid. We know only 
that there are a number of primary diseases in which it is known empirically that 
amyloid degeneration quite frequently develops as a secondary condition in the 



AMYLOID KIDNEY. 



813 



different organs. These conditions have mainly the common feature that they go 
along with a general cachexia and weakness of the body. The following conditions 
(arranged in about the frequency of the occurrence of amyloid degeneration) are 
the special ones in which amyloid degeneration in general, and therefore amyloid 
kidney in particular, are chiefly observed : 

1. Chronic pulmonary tuberculosis, particularly the ordinary ulcerative phthisis. 
Tubercular ulcers of the intestines, with or without co-existing marked pulmonary 
tuberculosis, may also lead to amyloid disease. 

2. Long-continued chronic suppuration in the bones or soft parts, especially 
chronic fungous processes with fistulae into the bones or joints, empyema with 
fistulae, vertebral caries, etc. 

3. Constitutional syphilis, chiefly the cases with ulcerative and usually tertiary 
processes in the bones and mucous membranes. 

4. Other ulcerative processes or processes associated with chronic suppuration : 
saccular bronchiectases, chronic intestinal ulcers (for example, of dysenteric 
origin), purulent pyelo-cystitis, vesico-vaginal fistula, ulcerated new growths, like 
cancer, etc. 

5. In rare cases amyloid has also been observed in other chronic diseases, as in 
malaria, gout, and other chronic articular affections. In the medical clinique here 
at Leipsic we once saw a case of marked amyloid kidney in a girl of twenty-one 
with aortic insufficiency. 

6. Finally, in a small class of cases, of which we have ourselves seen some 
examples, no discoverable cause at all may be found at the autopsy for a usually 
quite extensive amyloid degeneration. In these cases there accordingly seems to 
be a primary amyloid disease. 

Pathological Anatomy. — Since the text-books on pathological anatomy have 
been referred to in regard to the anatomical conditions of amyloid in other organs 
(compare also page 468), we must here describe in detail only the pathological 
anatomy of amyloid kidney. 

In very slight and not extensive amyloid degeneration in the kidneys the latter 
present a perfectly normal appearance to the naked eye. Careful microscopic 
examination alone shows amyloid degeneration of the walls of different vessels in 
the cortex, and especially in the medullary substance. 

The commonest and most characteristic form of amyloid kidney is the so-called 
large white amyloid kidney (waxy kidney, lardaceous kidney). The kidney is 
usually enlarged, and the surface is smooth and of a grayish-white or yellowish 
color, and usually somewhat mottled. On section, the cortex is wider and also of 
a yellowish- white color, and the glomeruli may often be recognized with the naked 
eye as dull, lustrous, translucent points. Haemorrhages are scarcely ever seen. 
The medullary substance is either also pale or darker. In many cases the cortex 
may also have a darker reddish or mottled appearance, which is due merely to the 
greater amount of blood in the organ. The pale-yellow color is due either to the 
anaemia or to the fatty degeneration, while the amyloid spots show a more trans- 
lucent character with a bacon-like luster. 

If we examine the kidney microscopically, we find first the amyloid degenera- 
tion, which, in varying extent and combination, affects most frequently the glo- 
meruli and also the capillaries of the cortex, the vasa recta, and sometimes the 
membranae propriae of the uriniferous tubules. In pure amyloid kidney the rest 
of the renal tissue is normal, but in many cases we also find changes in the epi- 
thelium, fatty degeneration, desquamation and disintegration, and also not infre- 
quently interstitial cellular infiltration. 

Thus amyloid degeneration is often combined with degenerative inflammatory 
changes in the kidneys. If the process has lasted for a long time, it leads, as in 



814: 



DISEASES OF THE KIDNEYS. 



ordinary nephritis, to a complete atrophy of tissue in some parts, with a corre- 
sponding increase of connective tissue. Then the renal tissue sinks in at the 
affected parts, and there is a decided unevenness to the surface of the kidney. 
There is even a completely developed red or white contracted kidney, in which 
we find abundant amyloid, and which is, therefore, termed amyloid contracted 
kidney. In this form the parenchymatous and interstitial changes correspond 
precisely to those in ordinary contracted kidney, only the amyloid degeneration 
is added to them. 

At present differences of opinion prevail as to the precise connection between 
amyloid and the inflammatory degenerative processes in the kidney. Probably we 
have an actual combination of both conditions, sometimes perhaps even co-effects 
of the same cause. For since genuine nephritis, as well as amyloid kidney, occurs, 
as we have seen, in syphilis, tuberculosis, and other diseases, it can not be remark- 
able that in these diseases both sequelae, nephritis and amyloid, develop side by 
side, and that we may, therefore, find at the same time, beside the changes of an 
inflammatory large white kidney, of a secondary contraction, or of a genuine con- 
tracted kidney, a more or less extensive amyloid degeneration in the kidneys. On 
the other hand, it, of course, can not be questioned that the disturbance of circula- 
tion, which must arise in consequence of a marked amyloid of the vessels, is of 
influence on the nutrition of the renal tissue, and that, therefore, many changes in 
it, especially fatty degeneration of the epithelium, are, under some circumstances, 
the direct result of the amyloid disease. 

Clinical History. — If we consider the great differences which the distribution 
of the amyloid in the kidneys shows, and its manifold combinations with inflam- 
matory processes, it is clear from the outset that we can not set up a uniform 
picture of the symptoms of amyloid disease in general. To this we must add that 
the symptoms of amyloid disease, which is almost always a secondary condition, 
are also modified in various ways by the primary disease. 

We must first state that many cases, where the amyloid in the kidneys is of 
comparatively slight extent, can not be recognized by any clinical symptom. The 
albuminuria in particular may be entirely absent, as has been repeatedly proved 
(Litten and others), which is perhaps due to the fact that in such cases the vasa 
recta and not the glomeruli are chiefly affected by the amyloid degeneration. 

Except in these cases, however, the urine secreted from the amyloid kidneys 
shows marked changes, which, of course, present quite great variations according 
to the form of the individual case. The amount of urine is most frequently about 
normal, or somewhat diminished — in some cases much diminished — but in others it 
is decidedly increased, so that the patient may pass eighty to a hundred and twenty 
ounces (2500-3500 c. c.) in the twenty-four hours. We quite frequently see con- 
siderable variations in the amount of the urine in the same patient at different 
times. All these differences are easily explained if we remember how many cir- 
cumstances may act on the amount of urine — the presence or absence of inflamma- 
tory changes in the kidney, the presence or absence of cardiac hypertrophy, co-ex- 
isting perspiration, diarrhoea, oedema, fever, etc. 

The color of the urine is almost always light yellow. Only exceptionally, in 
amyloid nephritis, does it contain an abundant sediment ; usually it is entirely, or 
almost entirely, clear. The very considerable amount of albumen in the mine, 
which is often one or two per cent., is also characteristic of amyloid kidney. In 
many cases, of course, especially in amyloid contracted kidney, the amount of albu- 
men is but slight. It sometimes, but by no means regularly, happens that the 
urine in amyloid kidney contains a comparatively large amount of paraglobuline 
beside the ordinary serum albumen (Senator). 

The specific gravity of the urine varies very much according to the amount 



AMYLOID KIDNEY. 



815 



of water and albumen in it. It may be increased (1015-1020) or diminished 
(1010-1003). 

If we examine the urine under the microscope, we usually find only a few hya- 
line casts, and also most frequently a small number of white blood-corpuscles. In 
the combination of amyloid with more marked nephritic changes the sediment is 
more abundant, so that the urine is cloudy. The microscope then shows more 
numerous hyaline or moderately fatty casts, more abundant white blood-corpus- 
cles, sometimes a little renal epithelium, and in quite rare cases even red blood- 
corpuscles. Amyloid reaction occurs in the casts, but it is very rare, and therefore 
of no value in diagnosis. 

The other morbid symptoms which are observed in amyloid kidney depend 
either upon the change in the kidneys themselves, or upon co-existing amyloid 
degeneration in other organs ; or, lastly, upon the primary disease. The symp- 
toms of the latter are, of course, extremely varied, but in many cases they may be 
entirely subordinate. 

In regard to the directly resulting symptoms of amyloid kidney, their occur- 
rence is of interest, especially in comparison with the analogous conditions in 
acute nephritis. Dropsy of a moderate, or even a severe degree, is often present in 
amyloid kidney, but it may also be entirely absent. We must remember that an 
oedema independent of a renal affection may be produced by marantic venous 
thrombosis. Uraemic symptoms are distinctly rare in amyloid kidney, but they 
are sometimes observed, especially in their milder forms, such as vomiting. It is a 
very important point that a hypertrophy of the left ventricle is absent in most 
cases of amyloid kidney. This is because we have weak and cachectic individuals, 
in whom a cardiac hypertrophy can not develop for lack of an excess of nutritive 
material. Where there is no debility, a cardiac hypertrophy may doubtless develop, 
as we see especially in amyloid contracted kidney. At the autopsy we often find 
the heart, of course, in a condition of brown or simple atrophy. 

Albuminuric retinitis hardly ever appears in pure amyloid kidney. In the 
amyloid contracted kidney it has sometimes been observed, however, in cases 
where there has probably been originally a pure contracted kidney, with amyloid 
coming on later. The secondary inflammations in the internal organs, such as 
renal pneumonia, and the haemorrhages, like cerebral haemorrhage, are also rare. 

The patient's general condition is also dependent in part upon the renal disease, 
but usually upon the primary disease. The patient with amyloid kidney is usu- 
ally correspondingly cachectic, and shows in high degree a pallid, anaemic color 
of the skin. In some cases, however, such as syphilis, bronchiectasis, or unilateral 
contraction of the lung, the condition of the nutrition may remain tolerably good 
for a long time. 

The symptoms which point to a co-existing amyloid degeneration in other 
organs beside the kidneys are of great diagnostic significance. The symptoms in 
the liver ^enlargement, abnormal firmness, and a hard, sharp lower edge to the 
organ), the spleen (enlargement and hardness), and intestines (diarrhoea) are clin- 
ically important in this respect. The explanation of the diarrhoea is, of course, 
usually difficult, since it may often depend upon tubercular intestinal ulcers as well 
as upon amyloid of the intestines. 

We can scarcely make more general statements in regard to the whole course 
and the duration of amyloid kidney, since the form of the primary disease is to be 
especially considered in these cases. In regard to the time that it takes for an 
amyloid degeneration to develop in an existing primary disease, the degeneration 
is certainly present sometimes after a few months. Of course, it is hardly ever 
possible to determine its onset accurately, since the first beginnings of amyloid 
degeneration in the kidneys do not usually permit themselves to be recognized at 



816 



DISEASES OF THE KIDNEYS. 



once by the appearance of albuminuria (vide supra). The duration of amyloid 
kidney varies very much according 1 to the severity of the case ; it may last only 
a few weeks or months until death, while other cases have certainly lasted for a 
year, especially in amyloid contracted kidney. 

The prognosis of amyloid kidney is in most cases utterly unfavorable, which is 
due mainly to the incurability of the primary disease ; but trustworthy observers 
have repeatedly proved that, when the primary disease is curable, as with syphilis 
and many chronic suppurations, an already developed amyloid kidney can be 
completely restored. 

The diagnosis of amyloid kidney can be made with quite great certainty when 
the evident signs of a renal affection are added to those diseases which we know 
empirically often give rise to the development of amyloid degeneration. Whether 
in such cases we have a pure amyloid or a pure nephritis, or a combination of the 
two, can be decided with some certainty only from the condition of the urine : a 
clear urine, containing but few morphological elements, but rich in albumen, 
points to amyloid, while a large number of casts and red and white blood-corpus- 
cles in the urine, point to the presence of inflammatory changes in the kidney. A 
very characteristic symptom of many cases of amyloid kidney, and one that is 
therefore of diagnostic value, is the rapid and frequent change in the amount of 
the urine and in the amount of albumen in it (Wagner). An accurate diagnosis 
of the anatomical changes, however, is hardly ever to be made with certainty, and 
at most can be made only by attention to the whole course of the disease. 

A very material support for the diagnosis of amyloid kidney, and therefore one 
which should always be looked for, is the discovery of amyloid in other organs. 
We have briefly mentioned above the most important symptoms in the liver, the 
spieen, and the intestines referable to this point. 

Treatment. — Only the treatment of the primary disease can, of course, be con- 
sidered, both as a prophylactic and also as a causal indication. In many surgical 
cases, and also in the cases of amyloid in syphilis, there is a possibility of this (as 
by iodide of potassium) ; but otherwise we try to improve the primary disease as 
far as is possible. 

In other respects the treatment is purely hygienic and symptomatic. We must 
try to strengthen the patient as much as possible by good food and the exhibition 
of preparations of iron and quinine. The use of iodide of iron is to be recom- 
mended. In a symptomatic point of view the same remedies are used as in other 
renal diseases. 



CHAPTER VI. 

PURULENT NEPHRITIS AND PERINEPHRITIS. 

(Renal Abscess.) 

JEtiology. — Although in the forms of nephritis so far described the occurrence 
of interstitial accumulations of granular matter has been repeatedly mentioned, 
none of them ever come to genuine suppuration — that is, to a purulent liquefac- 
tion of tissue, a true abscess-formation. The origin of a purulent nephritis is, 
rather, always associated with the entrance of perfectly definite morbid irritants 
into the kidneys. These are invariably organized and their special peculiarity is 
to excite a purulent inflammation. 

There are two chief ways through which the morbid irritants may reach the 
kidneys — the arterial blood-current and the urinary passages. The first-mentioned 



PUEULENT NEPHRITIS AND PERINEPHRITIS. 817 



means of entrance is to be considered in all the cases of purulent nephritis which 
come on as one symptom of pyaemic processes and certain forms of ulcerative 
endocarditis (see page 101 on the point). Far more rarely purulent nephritis 
develops in this way as a complication in other diseases, such as dysentery. Puru- 
lent nephritis also occurs in actinomycosis (Israel). 

The excitants of inflammation take the second path in those cases where a 
purulent nephritis follows an inflammation of the lower urinary passages, the 
pelvis of the kidney, the bladder, etc. Here the bacteria, which almost always 
enter directly into the urinary passages (the urethra and bladder) from without, 
pass gradually upward from the bladder through the ureters to the pelvis of the 
kidney ; from this they enter the apertures of the collecting tubes and the urinif - 
erous tubules of the kidney, everywhere exciting a purulent inflammation. We 
therefore term these forms of purulent nephritis— with regard to their origin- 
purulent pyelo-nephritis. 

We must remark in conclusion that a purulent nephritis may arise in direct 
wounds of the kidney from infection of the wound; this is usually associated 
with a perinephritic suppuration (vide infra). 

Pathology. — Purulent nephritis shows quite characteristic peculiarities and 
differences according to its mode of origin. (We omit traumatic abscesses here.) 

The renal abscesses in pyaemia and analogous diseases are usually focal suppu- 
rations, which only exceptionally attain a great extent, but which are usually to be 
recognized with the naked eye as numerous little yellowish dots or lines, scattered 
over the whole kidney, about half a millimetre or a millimetre in diameter. On 
microscopic examination, these nodules prove to be genuine little abscesses, in 
whose territory the nervous tissue proper is completely destroyed. In the middle 
of them we often find the originating colony of micrococci, the " micrococci 
embolus," seated in a central vessel. The conditions are still plainer if we exam- 
ine the earlier stage of the process. We find vessels (the loops of the glomeruli, 
or the encircling capillaries), which are completely plugged with micrococci, and 
in whose vicinity the renal tissue is still perfectly normal. We further see analo- 
gous spots where the renal tissue is already necrosed in the vicinity of the colony 
of micrococci, and is infiltrated with emigrated cells. These nodules show, finally, 
a continuous transition to the completed abscess, which is often surrounded by a 
hypergemic or even a hsemorrhagic areola. 

In purulent pyelo-nephritis the renal abscesses appear somewhat different. 
The abscesses also have a characteristic striated appearance, corresponding to the 
distribution of the inflammation along the straight tubules. They often extend 
from the point of the renal papilla through the cortex to the surface of the organ, 
so that from the outside we see the abscesses, appearing through as yellowish 
points. The broader abscesses arise from the confluence of neighboring striae. 
The microscope shows that the purulent inflammation arises from the vessels of 
the interstitial tissue, in whose territory the uriniferous tubules are of course 
destroyed. The clusters of micrococci form the most interesting feature. These 
settle originally in the uriniferous tubules and are the special cause of the necrosis 
of epithelium and the inflammation. Pyelo-nephritis, indeed, was one of the first 
diseases for which Klebs discovered a bacterial origin. 

Clinical Symptoms. — We can speak very briefly here in regard to the clinical 
symptoms of purulent nephritis, since they can never be sharply separated from 
the symptoms of the primary disease. The pyaemic renal abscesses, and the 
abscesses in ulcerative endocarditis, hardly ever cause special clinical symptoms, 
so that their presence is first recognized on the autopsy-table. Since the abscesses 
do not usually communicate with the uriniferous tubules, there is usually not even 
a large amount of pus in the urine. 
52 



818 



DISEASES OF THE KIDNEYS. 



The clinical symptoms of pyelo-nephritis also depend less upon the nephritic 
abscesses than upon the previous and accompanying pyelitis and cystitis. We 
will therefore return to renal abscesses in the description of these diseases. 

Perinephritis Abscess. 

Perinephritic abscess is the name given to suppurations in the vicinity of the 
kidney, especially in its fatty capsule or in the peri-renal connective tissue. 
Apart from any traumatic origin for such abscesses, they develop most frequently 
as a result of purulent nephritis or purulent pyelitis. The escape of pus, which 
involves the surrounding tissue in the inflammation, may come from the ureter 
or pelvis of the kidney, or from the kidney. The special form of primary disease 
differs very much ; it may be either simple purulent pyelitis, or pyelitis from renal 
calculi, or sometimes tubercular processes and new growths that finally suppurate, 
such as cancer, or echinococci. The peri-renal suppuration may also take its 
start from the other organs in the neighborhood. Thus cases have been seen in 
which the perinephritis followed a perityphlitic abscess, a hepatic abscess, or a 
psoas abscess after vertebral disease. 

In many cases of this sort the accumulation of pus is so considerable that there 
is a protrusion in the lumbar region exactly like a tumor. This is at first only 
obscure ; but later the skin becomes cedematous there, it constantly protrudes more 
and more, it assumes an inflammatory hypersemic redness, until finally a definite 
fluctuation shows the advance of the abscess up to the skin. In other cases the 
inflammatory swelling extends forward into the iliac fossa; then there is also 
abnormal resistance and dullness above Poupart's ligament. The swelling may 
also extend upward toward the diaphragm, so that the diaphragm is crowded 
upward, giving rise to marked dyspnoea. The relations of the swelling to the 
descending colon are sometimes the same as in new growths of the kidney (com- 
pare Chapter VIII). 

Beside the swelling, there is almost invariably a very great pain in the 
affected region, either spontaneous or on pressure. If the swelling presses on the 
large nerve-trunks in the vicinity, it produces severe shooting pains in the leg of 
the same side, and sometimes a numb feeling and paresis. The leg is then often 
kept in a position similar to that in coxitis. 

The condition is almost always associated with fever, which shows the charac- 
teristic remitting or intermitting type of most suppurative fevers, and may be 
interrupted by occasional chills with a marked rise of temperature. The patient 
becomes very much debilitated and emaciated by the fever and the pain, and he 
may finally fall into a sad general condition. The urine contains pus only when 
the abscess communicates in some way with the urinary passages. 

Eecovery can take place only when the abscess is evacuated through some 
external channel. Except for operative procedures, the spontaneous escape of pus 
through the skin is the most favorable ; this most frequently takes place in the 
lumbar region, or more rarely, like a psoas abscess, under Poupart's ligament. 
Sometimes persistent fistulas are left after such a rupture. The rupture of the 
abscess into the intestine (the colon) has also been observed, with an evacuation 
of pus by the bowels, and also ruptures into the bladder, the pleural cavity, and 
the peritoneum. We need not here discuss in detail under what circumstances 
death may ensue ; it comes on, in many cases, after the disease has lasted a con- 
siderable time. 

The diagnosis is based chiefly upon the swelling, the tenderness, the fever, and 
a consideration of the setiological factors. The disease may be confused with 
hydro-nephrosis, psoas abscess, or solid renal tumors. The result of an explora- 
tory puncture is sometimes decisive in such cases. 



DISTURBANCES OF CIRCULATION IN THE KIDNEYS. 819 



The only treatment, apart from the fulfillment of any symptomatic indications, 
is surgical, and consists, if possible, in opening and draining the abscess. The 
success depends chiefly upon the patient's general condition, and the form of the 
primary disease. The details are to be found in the text-books of surgery. 



CHAPTER VII. 
DISTURBANCES OF CIRCULATION IN THE KIDNEYS. 

1. The Congested Kidney.— Although local impediments to the flow of venous 
blood from the kidneys, as from thrombosis of the renal veins, hardly ever attain 
a clinical significance, the participation of the kidneys in a general venous stasis, 
as it is chiefly seen in heart disease (compare page 280), pulmonary emphysema, 
etc., is of great diagnostic importance, since we possess in the condition of the 
urine quite an accurate measure of the intensity as well as of the increase and 
decrease of the stasis. 

The congested kidney is easily recognized anatomically. The organ is often 
somewhat enlarged, it feels firmer than normal, and shows, both on its surface 
and on section, a dark, bluish-red color — " cyanotic induration." The medullary 
substance is usually darker than the cortex. Under the microscope we see con- 
siderable dilatation and a tense fullness of the veins and capillaries. The paren- 
chyma is normal, but in more advanced cases it may show a beginning fatty 
degeneration of the epithelium, which is a result of the defective arterial blood- 
supply. Interstitial changes are usually absent. 

The clinical symptoms of congested kidney concern only the changes in the 
urine. The amount of urine diminishes, corresponding to the diminution of the 
arterial pressure and the diminished rapidity of the blood-current. Only twenty 
or twenty-five ounces (800-500 c. c), or less, are secreted daily. The urine is also 
more concentrated and darker than normal, and often has an abundant sediment 
of uric acid or urates. If nutritive disturbances have begun in the epithelium of 
the glomeruli as a result of stasis, the urine is also albuminous, but the amount of 
albumen in pure congested kidney is always slight — about one tenth to one sixth 
of the volume. The urine often contains, besides, a few hyaline casts, and a few 
white and red blood-corpuscles, the latter pointing to little congestive haemor- 
rhages. 

If the changes mentioned come on as one symptom of a general venous stasis, 
and are, accordingly, often associated with cyanosis, and dropsy, the diagnosis of 
congested kidney can be made with certainty. If we succeed in restoring the cir- 
culation by appropriate remedies, such as digitalis, the urine at once becomes more 
abundant and clearer and its albumen disappears. Otherwise the symptoms of 
the urine of passive congestion last until the patient's death. 

2. Embolic Infarction in the Kidneys.— Since the renal infarction, although it 
has great pathological interest, is hardly ever of clinical significance, we will limit 
ourselves here to a brief description of the most essential points. 

If one of the smaller renal arteries is plugged by an embolus in heart disease, 
the affected portion of the organ cut off from the circulation must perish, since 
all the renal arteries are terminal arteries. The epithelium undergoes the well- 
known changes of coagulation necrosis, disappearance of the nuclei of the cells, 
and disintegration, and the tissue becomes entirely or in part a hsemorrhagic 
infarction (compare page 280). In this way arise the characteristic wedge- 
shaped, red, hsemorrhagic infarctions in the kidney, or far more frequently the 



820 



DISEASES OF THE KIDNEYS. 



yellowish-gray, anaemic infarctions, often surrounded by a hemorrhagic areola, 
the base of which is at the surface of the kidney ; the base may reach a width of 
half a centimetre to a centimetre or more, while its apex extends a varying dis- 
tance into the cortex, or even into the medullary substance. Later on the gradu- 
ally disintegrated tissue of the infarction is absorbed, round cells emigrate from 
without into the region destroyed, and a shrunken connective-tissue cicatrix grad- 
ually develops in place of the former infarction. Many kidneys may have such a 
granular surface from numerous infarction cicatrices that they may be appro- 
priately termed " embolic contracted kidneys." 

The anatomical processes just briefly described cause in most cases no special 
clinical symptoms at all. Only in a few cases does a slight amount of blood in 
the urine seem to depend on the development of a haemorrhagic infarction in the 
kidneys, so that when a cause for embolic processes, like heart disease, is present, 
we may sometimes entertain the suspicion of the development of a renal infarction 
during life. In a few cases the development of a large renal infarction may be 
accompanied by a sudden severe pain in the renal region. 

The embolic processes in the kidney never demand special treatment. 



CHAPTER VIII. 

NEW GROWTHS IN THE KIDNEYS. 

Of the primary forms of tumor occurring in the kidney, two especially claim 
our interest : cancer of the kidney and congenital sarcoma. The latter is of great 
importance in regard to the general theory of tumors, since it points definitely to 
the development of the new growth from scattered portions of embryonic tissue. 
Striped muscular fibers have been repeatedly found in tumors consisting otherwise 
of round or spindle cells, from which the name of " rhabdomyoma " has been 
chosen for these tumors. Since there are no muscular fibers in the kidney itself, 
their occurrence in the tumors points undeniably to disturbances of development. 
This theory obtains a further interesting confirmation from our own observation 
of the development of left-sided, and, probably, congenital renal sarcoma in two 
brothers. Both children died when between two and three years of age, and the 
autopsy gave almost precisely the same lesion in both : numerous metastases in 
the liver and lungs, beside a new growth almost as large as a child's head in place 
of the left kidney. 

Renal cancer is also remarkably frequent, comparatively speaking, in children 
under four years of age, and about equally common in the two sexes, although, of 
course, we find renal cancer in persons of more advanced years. Usually only 
one kidney is affected, chiefly the left, as it seems, but the new growth has some- 
times been found in both kidneys. In its character, renal cancer belongs either to 
the denser or to the softer, medullary form. It may permeate the whole kidney 
and change it to a large tumor, weighing fifteen or twenty pounds (five or ten 
kilogrammes). Softening and haemorrhage very often take place within the 
tumor. The proliferation has been repeatedly observed to extend to the neighbor- 
ing parts, especially the pelvis of the kidney, and metastases also form in other 
organs, as in the liver or the lungs. 

The clinical symptoms of renal tumor are entirely absent, or of a very indefi- 
nite nature, in the first period of the disease. Dull pain in the renal region is 
repeatedly given as the first symptom, but, of course, this is hardly ever of definite 
significance. The diagnosis almost always first takes a definite direction by the 



NEW GROWTHS IN THE KIDNEYS. 



821 



appearance of a palpable tumor. This develops in the lumbar and lower lateral 
abdominal region, constantly extending from this point upward and inward. As 
stated above, both carcinoma and sarcoma of the kidney may cause enormous 
tumors, especially in children, which may make the whole abdomen protrude to 
a marked degree. The tumor feels dense, and either smooth or rough, and it 
does not move with the respiration. The relation of the tumor to the descend- 
ing colon in left-sided renal tumors is not unimportant in diagnosis. Since the 
latter is pressed forward by the growth of the tumor, and thus gets into a position 
between the new growth and the anterior abdominal wall, we can often succeed in 
making out by percussion, and sometimes even by palpation, that the affected por- 
tion of intestine, and sometimes even a loop of small intestine besides, is drawn 
forward over the tumor ; the percussion may vary as the large intestine is empty 
or full. In right-sided renal tumors analogous conditions may also be present, 
but they are rarer. The liver is then sometimes pushed to the left. 

In many cases of renal tumor the urine shows no abnormal conditions at all, 
since its secretion is performed compensatorily by the other healthy kidney. In 
carcinoma of the kidney it sometimes presents, however, one valuable sign for 
diagnosis — namely, an admixture of blood. This hsematuria often comes on very 
early, even before there is any tumor to be felt. It is repeated either frequently 
or only rarely in different cases, and sometimes it is entirely absent. The haem- 
orrhage is associated with colicky pains only when large clots have to pass through 
the urinary passages. It is a remarkable fact that in a few cases the blood, as it 
seems, may come from stasis in the healthy kidney, which is very hyperaemic. 
Sometimes, but very rarely, small particles and shreds of tissue from the disin- 
tegrated new growth may be found in the urine. 

The general symptoms are often very late at first, especially in children ; but 
finally a general condition of marasmus almost always develops. A constant and 
great frequency of the pulse is often strikmg. We must also mention the peculiar 
symptoms several times observed, that in girls with congenital renal tumors there 
is an abnormally early development of the pubic and axillary hair, and sometimes 
a peculiar pigmentation of the skin (Kuhn). We need not mention in detail the 
symptoms of compression of neighboring organs by the tumor, which may develop 
in different ways. 

The diagnosis of renal tumor may be made with quite great certainty in many 
cases. The position of the tumor, its immobility, its relation to the large intestine, 
and, especially, our general experience as to the occurrence of renal tumors in 
children, lead us at once to think of the correct diagnosis. In older people renal 
haemorrhages, which are otherwise inexplicable, must direct our suspicions toward 
the possibility of a renal cancer. Renal tumors may, of course, often be mistaken 
for retroperitoneal glandular tumors, ovarian tumors, large psoas abscesses, or 
splenic tumors. The differential diagnosis must accordingly be carefully con- 
sidered in every case. 

The prognosis is, of course, always unfavorable. The disease sometimes lasts 
only a few months, sometimes a year or two, rarely longer. 

The treatment must in most cases be purely symptomatic. The only expecta- 
tion of success lies in the operative removal of the new growth, the details of 
which are to be found in the later writings on renal surgery. 



.822 



DISEASES OF THE KIDNEYS. 



CHAPTER IX. 

PARASITES OF THE KIDNEYS AND OF THE URINARY PASSAGES. 

CHYLURIA. 

Echinococcus of the Kidney.* — Echinococcus cysts have been repeatedly found 
in the kidney, although much more rarely than in the liver. Usually only one 
kidney is affected, and the parasite is generally situated in the renal substance 
itself, only exceptionally between it and the capsule of the kidney. The size of 
the echinococcus cysts may be very considerable, the diameter reaching to twenty 
centimetres or more. 

Clinical symptoms usually first appear when the tumor can be felt through the 
abdominal walls. Subjective symptoms may even then be entirely wanting. Pain 
on pressure develops gradually later. The tumor usually has an approximately 
globular shape. Its relations to the neighboring organs, especially to the colon, 
are the same as we have learned to recognize in the preceding chapter, in the 
description of cancer of the kidney. The feeling of the so-called " hydatid thrill," 
from a sudden impulse on the tumor with the palm of the hand against it on 
palpation, is characteristic of echinococcus, but, unfortunately, it is but seldom 
manifest. 

It happens rather frequently that the sac of the echinococcus bursts into the 
pelvis of the kidney. Then single echinococcus cysts, or at least bits of membrane, 
hooks, etc. , are passed with the urine, usually with severe colicky pains, which are 
exactly like the renal colic from the passage of a calculus. Such attacks may be 
often repeated, and may form a very severe type of disease by obstructing the 
urinary passages — the bladder and urethra. In such cases the symptoms of a sec- 
ondary pyelitis and cystitis are often added. 

Perforations in other directions are much rarer. The rupture of a renal echi- 
nococcus into the bronchi has sometimes been observed, the patient coughing up 
echinococcus cysts. 

Sometimes, especially after injuries, the sac of the echinococcus inflames, sup- 
purates, and thus leads to a general pyaemic condition. 

The diagnosis of renal echinococcus is possible only when a tumor can be made 
out belonging to the kidney, and when portions of echinococcus are passed with 
the urine, or through an exploratory puncture. They are most frequently con- 
founded with hydronephrosis {vide infra), and, in women, with ovarian tumors. 

The prognosis is not wholly unfavorable. Permanent recovery has been 
repeatedly observed, especially after the rupture, or single or repeated evacuations 
of the sac of the echinococcus; but, of course, echinococcus of the kidney may 
also be attended with numerous dangers, such as suppuration of the sac. The 
whole course of the disease is always very tedious. 

A radical treatment is possible only by surgical means. Symptomatically, ice 
and local blood-letting are used when there are symptoms of local inflammation; 
and morphine, warm baths, and sometimes mechanical aids, like the catheter, when 
there are symptoms of colic. 

2. Distoma Haematobium (see Fig. 105) is a parasite, occurring frequently in 
Egypt and Abyssinia; it is one of the fluke-worms (hematodes), and has its seat 
in the branches of the portal vein, the splenic vein, the vesical plexus, etc., and 
is nourished by the blood. Its eggs are often deposited in great numbers in the 
mucous membrane of the pelvis of the kidney, the ureters, and the bladder, and 



In regard to the general natural history of the echinococcus, compare page 464. 



PARASITES OF THE KIDNEYS AND URINARY PASSAGES. 823 



there cause very intense inflammation, ulceration with subsequent stricture, deposit 
of concretions, etc. Many cases of the so-called tropical hematuria are caused by 
the distoma. The diagnosis of the disease can be made with certainty by finding 
the eggs in the urine. 




Fig. 105.— Distoma haematobium (from Leuckart). a. Male and female, the latter in the canalis gynse- 
cophorus of the former. Ten diameters, b. Egg with a terminal spine, c. Egg with a lateral spine. 
150 diameters. 

3. Strongylus or Eustrongylus Gigas (palisade worm) is a parasite occurring 
in the pelvis of the kidney in many animals — the dog, the wolf, the marten, and 
very rarely in man. In size and color it is not unlike an ordinary earth-worm. 
It may produce symptoms of severe pyelitis, with haemorrhages, and colicky 
pains. 

4. Filaria Sanguinis Chyluria.— The blood filaria of man, belonging to the 
round-worms, has obtained a special clinical interest, since it is recognized, from 
the investigations of Wucherer in Bahia in 1868, and of Lewis in the East Indies 
in 1870, as the cause of the tropical chyluria and some allied diseases, such as 
lymph scrotum, elephantiasis Arabum, and chylous ascites. 

The full-grown filaria, "filaria Bancrofti" a very thin worm, about three or 
four inches long, has been found only a few times in man. Its seat is in the 
larger lymphatics, where it gives rise to chronic stasis of the lymph with its conse- 
quences — chronic hyperplasia of the connective tissue, etc. In the affection which 
here especially interests us, chyluria, the parasites are probably situated in the 
main branches of the thoracic duct — at any rate, in such a place that a stasis of 
the lymph ensues in the lymphatics of the bladder, or perhaps, in some cases, of 
the pelvis of the kidney and the other urinary passages. If the distended lymph- 
sac ruptures, the lymph or chyle is poured out into the urinary passages and is 
evacuated with the urine. Since this process may be often repeated, the inter- 
mittent course of chyluria is thus explained. The individual attacks of the disease 
may come on during years at intervals of weeks or months. They are often asso- 
ciated with pain and febrile symptoms. 

The condition of the urine, which in many cases may look almost exactly like 
milk, is most characteristic. A creamy layer of fat forms upon the surface. If we 
shake the urine with ether, the greater part of the fat can be removed, and the 
urine rendered clear. The fat in the urine may amount to two or three per cent. 
The chyluria is often associated with a hematuria coming, from the ruptured 
veins. The urine then looks bloody red, and shows under the microscope many 
red blood-corpuscles beside the fat-drops. Large clots often form in the urine. 

The embryos of filaria, found in the urine in very many cases, although not in 
all, form the most important diagnostic feature in the urine. These (see Fig. 106) 
are objects two to three tenths of a millimetre long, with a diameter about equal 
to that of a red blood-corpuscle. They are usually imbedded in a very delicate 
sheath, which often projects at the end of the animal, and show a constant, vigor- 



824 



DISEASES OF THE KIDNEYS. 



ously vibrating motion. They have 




Fig. 106.— (From Scheube.) Embryos of 
filaria. 



also been found in the blood of the patient, 
as well as in the urine, and, strange to say, 
especially during the night. 

The course of the filaria disease may 
vary considerably. Many patients reach 
an advanced age ; in others, severe general 
symptoms, like anaemia and emaciation, 
finally come on. The different forms in 
which the disease occurs — chyluria, ele- 
phantiasis, etc. — are combined in manifold 
ways. 

The region of the geographical distribu- 
tion of the disease lies almost wholly in 
hot countries. It has so far been most fre- 
quently observed in Brazil, the Antilles, 
the East Indies, China, Japan, Egypt, Cape 
Colony, and . Australia. Nothing definite 
is yet known of the precise mode of inva- 
sion of the parasites. According to Man- 
son's investigations, mosquitoes play an im- 
portant part here. 

In regard to treatment, apart from any 
surgical interference, we may try picro- 
nitrate of potassium, three to ten grains 
(grm. 0*2-0 "5), in pills or capsules, several 
times a day (Scheube). 



CHAPTER X. 

MOVABLE KIDNEY (FLOATING KIDNEY, REN MOBILIS). 

JEtiology.— Although under normal conditions the kidney is fixed firmly in its 
position by its fatty capsule, over which the peritoneum is tightly drawn, and by 
the diaphragm, there is not infrequently a pathological condition, in which the 
kidney shows quite a high degree of displacement and mobility. The causes of 
this anomaly are not always quite clear, and there are probably different factors 
which may give rise to movable kidney. 

First, perhaps, a congenital predisposition is often to be considered ; this may 
be based chiefly upon an abnormally loose character of the tissue surrounding the 
kidney, and also upon an abnormal length of the renal artery ; but in later life 
it is chiefly the factors that lead to a marked distention and laxity of the abdomi- 
nal cavity, which further the development of a movable kidney. Frequent 
pregnancies are especially unfavorable in this respect, which explains the fact 
that floating kidney is very much commoner in women than in men. Severe 
and persistent bodily labor may also give rise to floating kidney ; in some cases, 
too, injuries which affect the abdomen, and especially the region of the kidney, 
also play a part. Too tight lacing has been repeatedly accused of gradually caus- 
ing a mobility of the kidney. Finally, a loss in the general nutrition, by which 
the fatty capsule of the kidney undergoes a reduction, sometimes seems to favor 
the occurrence of movable kidney. 

We have just mentioned the frequent occurrence of floating kidney in women, 



MOVABLE KIDNEY. 



825 



but some cases have also been observed in men and even in children. It is 
remarkable that the right kidney shows the anomaly in question much oftener 
than the left, which is possibly connected with the fact that the right kidney may 
be more easily displaced by the respiratory movements of the liver. Movable 
kidney can be confirmed in the cadaver only when the kidney is found in an 
abnormal position — for instance, in front of the vertebral column. 

Clinical Symptoms are not necessarily present in every case of movable kidney. 
If we examine old women with special regard to this point, we not very rarely 
find movable kidneys without any symptoms caused by them. In other cases, 
however, the floating kidney gives rise to a whole set of symptoms which are 
inexplicable except by the discovery of their cause. Drawing and pressing pains 
in the abdomen are the most frequent; these may shoot into the epigastrium or 
into the sacral and lumbar region, and may sometimes assume almost a colicky 
character. They are also frequently associated with nausea and even vomiting. 
All these disagreeable sensations usually increase still more as the patient moves, 
in walking, or riding, while they are slightest or even disappear entirely when the 
patient lies down. 

In many cases of floating kidney more severe attacks come on periodically, 
often at the time of the menses, which have been termed by Dietl " incarceration 
symptoms. " They consist of the sudden onset of pain, chills, which may increase 
almost to a rigor, vomiting, and symptoms of general collapse. Diuresis is usu- 
ally diminished during this period, and increases only when the attack ceases — that 
is, three or four days later. The special cause of these symptoms is to be found 
partly in circumscribed inflammatory changes in the vicinity of the kidney, but 
chiefly in a sudden urinary stasis from bending or twisting the ureter. There 
then arises an acute hydronephrosis, whose attendant symptoms disappear when 
micturition has again become possible. In some cases floating kidney seems to 
cause persistent hydronephrosis, with secondary pyelitis. 

We find quite frequently in women with floating kidney a line of general 
nervous " hysterical " symptoms— headache, backache, mental irritability, parses- 
thesise, etc. It is often hard to decide whether these symptoms are due to floating 
kidney or are only co-ordinate with it. They often arise, at any rate, only as a 
result of the mental alteration, for the mere idea of possessing a " floating kidney " 
may be enough in nervously disposed women to provoke a host of subjective sen- 
sations. Hence we must be cautious in informing the patient of the diagnosis. 

Movable kidney also seems able sometimes to produce certain resultant condi- 
tions by pressure on neighboring organs. Thus Bartels has claimed that many 
cases of dilatation of the stomach are due to a compression of the descending 
part of the duodenum by the movable kidney. In an analogous way, jaundice 
may arise from pressure on the gall-ducts, constipation from pressure on the 
colon, oedema of the legs from pressure on the inferior vena cava, and finally it 
has been stated that floating kidney in women may be the cause of abortion. All 
these accidents, at any rate, are only rarely to be considered. 

The diagnosis of floating kidney can be made only by its objective discovery. 
It is rather a theoretical assumption, which is only rarely of value in practice, 
that we can recognize the displacement of the kidney from its normal position, 
by the sinking in of the affected lumbar region (almost always the right), and 
by the abnormal clearness of the percussion-note there. The only certain proof 
is feeling the kidney as a movable tumor of the proper size and shape beneath 
the edge of the right ribs or toward the umbilicus or the inguinal region. Occa- 
sionally we can succeed in feeling the pulsation of the renal artery: Palpation 
of the movable kidney, however, is not always equally easy, and generally 
demands a certain amount of practice. Bimanual palpation and counter-pressure 



826 



DISEASES OF THE KIDNEYS. 



in the lumbar region with, the left hand is very advisable. If we can reach the 
kidney with the fingers, we can push it about and often bring it back into its 
proper place. 

In general, the diagnosis is not very difficult in patients whose abdominal walls 
are lax, if the attention is directed to the possibility of .floating kidney. Of course 
a positive result is alone decisive, while a negative result, or finding it only once, 
proves nothing. In many cases, of course, floating kidney is confused with other 
sorts of tumors, with pedunculated ovarian cysts, faecal tumors, enlargements of 
the gall-bladder, or echinococci. 

The prognosis is so far favorable that the patient's life is never threatened by 
an uncomplicated floating kidney. The symptoms are of course very obstinate, 
and may resist any therapeutic attempts for years. In advanced age they often 
cease of themselves. 

Treatment. — If there are severe disturbances or " incarceration symptoms " on 
the part of a floating kidney, a quiet dorsal decubitus is to be prescribed, and, 
if the kidney does not return to its proper place of itself, we should try artificial 
reposition, which can be performed in many cases, and is then attended with 
success. If we can not relieve the symptoms in this way, prolonged warm 
baths, warm poultices, and opium must be used as indicated. Various bandages 
provided with pads and supports are recommended to guard against a new dis- 
placement of the kidney ; these of course sometimes do good service, but they are 
often useless. At all events, they should be tried. The hope of " removing the 
laxity of tissue" by a "tonic treatment, 1 ' iron preparations, cold rubbing, etc., 
must be illusory; nevertheless, these remedies are very much recommended in 
practice, since they often act very favorably, especially on the general nervous 
symptoms, as mental remedies. Certain general hygienic measures, especially the 
avoidance of any great bodily movements, and care for easy dejections, are also of 
service. 

In cases with very severe, distressing symptoms, surgeons who are fond of 
operations have repeatedly performed extirpation of the movable kidney, some- 
times with success, sometimes, too, with an undesired termination. At any rate, 
the indication for operation is furnished only when the symptoms are very 
marked, and when all other remedies have been unsuccessful. 



APPENDIX. 

THE DISEASES OF THE SUPRA-RENAL CAPSULES AND ADDI- 
SON'S DISEASE (BRONZED SKIN). 

In the year 1855 the English physician Addison published for the first time a 
list of cases in which, beside the symptoms of a general bodily weakness and 
anaemia, a peculiar dark pigmentation of the skin had gradually developed. 
Since disease of the supra-renal capsule was found at the autopsy in all cases, 
Addison concluded that this was the immediate cause of the bronze coloring of the 
skin. Observations similar to Addison's were soon made in greater numbers, so 
that the fact itself can not be doubted ; but even at present nothing definite is 
known as to the special cause of the disease or the theory of this remarkable con- 
nection between disease of the supra-renal capsules and pigmentation of the skin. 

Attempts* have been made in different quarters to obtain an explanation from 
experiments on animals ; but up to the present time these attempts have remained 
quite fruitless, and even lately Nothnagel, in spite of having destroyed both supra- 



ADDISON'S DISEASE. 



827 



renal capsules in a large number of puppies, has not succeeded a single time with 
certainty in provoking the symptoms of the disease artificially. The anatomical 
lesions in man are up to the present time not calculated to add clearness to the 
case, since they seem to contradict one another in various points. In the first 
place, some observations must be mentioned in which the supra-renal capsules 
were found perfectly normal in spite of an existing pigmentation of the skin. 
Such cases, however, prove little, since it of course can not be put in question that 
a staining of the skin may sometimes develop from some other reasons beside 
disease of the supra-renal capsules. On the other hand, it has been asserted that 
extensive changes are sometimes found in the supra-renal capsules on autopsy 
without the existence of the symptoms of bronzed skin during the patient's life ; 
but these cases are also open to the objection that the disease has perhaps not been 
extensive and intense enough to cause the bronze coloring of the skin. The con- 
tradictions just mentioned, however, have led to many other attempts at an 
explanation of Addison's disease, of which one especially deserves considera- 
tion. According to this the symptoms met with are produced not by the disease of 
the supra-renal capsules themselves, but by the invasion of the solar plexus and 
the semilunar ganglia of the sympathetic by the morbid process (Kisel, Burger, 
and others). According to this theory, the symptoms of Addison's disease may 
arise when the aforesaid nervous parts are diseased independently, or by the 
extension of a pathological process from some other neighboring organ. A num- 
ber of anatomical lesions are cited to favor this view, but it is not certainly 
proved, and the internal connection between the symptoms is by no means clear 
by this hypothesis. 

Pathological Anatomy and iEtiology of Addison's Disease.— Addison himself 
has pointed with emphasis to the fact that the special form of disease in the supra- 
renal capsules is by no means always the same. At any rate, the disease named 
from him is not to be regarded as a definite anatomical affection, but rather as a 
particular group of symptoms. By far the most frequently it is tuberculosis 
of the supra-renal capsules which lies at the bottom of Addison's disease. The 
capsules then are either enlarged and studded with caseous tubercular new 
growths, or they are in part cicatricially contracted. Other tubercular affections 
are almost always present in the body at the same time, especially caseation of 
the mesenteric lymph-glands and pulmonary tuberculosis. Other morbid pro- 
cesses beside tuberculosis may also be found in the supra-renal capsules : simple 
chronic inflammations, enlargement of the organ (which Yirchow has called 
" strum a of the supra-renal capsules "), haemorrhages, new growths like cancer, and 
even echinococci. It is self-evident, from what has been said above, that in every 
case we must consider some implication of the neighboring sympathetic ganglia, 
by compression, cicatricial contraction, or chronic inflammation. Both supra- 
renal capsules are almost always diseased at the same time, rarely only one. 

Of the lesions in other organs we must also mention that Peyer's patches and 
the solitary follicles of the intestine are as a rule swollen. The spleen is some- 
what enlarged in some cases, but not in others. There is no striking pigmenta- 
tion of the internal organs. The changes in the skin and in certain mucous 
membranes will be mentioned below. 

Considering the variety of the anatomical causes there can be no question of a 
uniform aetiology of the disease. Among the causal factors, those most frequently 
reported are defective nutrition, care and anxiety, and finally traumatic action on 
the abdomen. The majority of cases are met with in the male sex and in middle 
life. Addison's disease, however, must be regarded as a rare affection of which 
but few cases are observed even in the larger cliniques. 

Symptomatology. — The purest type of Addison's disease appears in those cases 



828 



DISEASES OF THE KIDNEYS. 



where the symptoms are apparently primary in their development, and do not 
come on in the course of some other disease, such as phthisis or cancer. 

The first symptoms of the disease are usually of a general nature, and are 
referable to a gradually increasing anaemia, and to general weakness and phys- 
ical lassitude. The anaemia shows itself objectively through the pallor of the skin 
and the diminution in the number of red blood-corpuscles, but without other 
definite anomalies of the blood that can be made out. A number of symptoms 
appear besides, which are due secondarily to the anaemia, especially to the 
anaemia of the brain. Among them are mental lassitude and loss of energy, 
frequent headaches, attacks of vertigo and faintness, and tinnitus aurium. The 
patient's general nutrition often suffers very considerably ; but it must be added 
that in Addison's disease, as in other anaemias, the fatty layer, especially over the 
abdomen, often remains remarkably well developed. 

Beside the anaemic symptoms, there very often are disturbances of the stomach. 
The appetite is poor, and there is very often vomiting. The latter may sometimes 
be almost unrestrainable, and then is one of the most distressing symptoms of the 
disease. It is usually due, not to an anatomical change in the stomach, but prob- 
ably to the anaemia of the brain, or to other nervous influences. Cardialgic 
symptoms are also frequent. The bowels are sluggish as a rule, but there is some- 
times diarrhoea. We sometimes hear functional murmurs in the heart, but as a 
rule its sounds are low and pure. The pulse is usually moderately accelerated. 
The liver and spleen present no constant changes. Albuminuria is only excep- 
tionally found, and is due to complications, such as amyloid kidney. 

The special characteristic symptom, which alone renders the diagnosis possible, 
is the gradual onset of a peculiar pigmentation of the skin. This usually shows 
itself first in the face and on the backs of the hands, and also in those parts which 
normally present a greater pigmentation, the areola of the nipples, the axillae, 
and the genitals, or which are exposed to greater pressure by the clothing, as 
the hips and shoulders. It is especially noteworthy that dark pigmented spots 
usually develop on the mucous membrane of the lips and mouth. The 
intensity of the coloring differs in different cases. It usually increases as 
the general condition grows worse. In the most intense cases the whole skin 
may become dark brown or black, like a mulatto or negro. Sometimes, however, 
the pigmentation remains limited to separate large or small spots, and in other 
parts of the skin there may then be even a marked loss of pigment. The nails 
and the sclera always remain white, and frequently the palms of the hands and 
the soles of the feet also. The pigmentation of the skin usually increases during 
the whole disease ; only exceptionally does the skin become light again in the 
later stages. 

The course of Addison's disease is almost always chronic, and may last for 
years, but cases have been described with a more acute course. The disease some- 
times begins with violent initial febrile symptoms, vomiting and diarrhoea. The 
disease then has a comparatively rapid termination after a few months, or a second 
chronic stage may follow the first acute one. 

The final termination of Addison's disease is always unfavorable. Temporary 
remissions are often observed, but the disease always becomes worse again after 
them. Death usually ensues gradually amid the signs of increasing general 
uraemia and weakness. In some cases severe nervous symptoms also come on 
toward the end of the disease — coma, delirium, or epileptiform attacks. Such 
conditions may sometimes develop quite rapidly and unexpectedly. 

Treatment. — There can be no question of a specific treatment of Addison's dis- 
ease, especially considering the differences in the primary diseases and in the com- 
plications. Tonic remedies, strengthening diet, iron, quinine, and arsenic, are most 



INFLAMMATION OF THE PELVIS OF THE KIDNEY. 829 

indicated, although iodide and bromide of potassium, electricity, etc., have been 
tried by some physicians. Otherwise the treatment is purely symptomatic ; the 
vomiting-, diarrhoea, and nervous attacks demand special measures. We know, 
by experience, that great caution is to be used in prescribing cathartics, since 
patients have repeatedly been observed to grow considerably worse after them. 



section n. 

Diseases of the Pelvis of the Kidney and of the Bladder, 

CHAPTER I. 

INFLAMMATION OF THE PELVIS OF THE KIDNEY. PYELITIS. 

iEtiology. — Isolated primary pyelitis hardly ever occurs as an independent dis- 
ease. Pyelitis is rather in most cases either a complication or a result of other 
diseases, and in such cases often claims but little clinical interest. 

We sometimes find a usually moderate pyelitis in the bodies of persons 
who have died of severe general infectious diseases, typhoid fever, small-pox, 
diphtheria, or pyaemia. The affection depends, in all probability, upon the elimi- 
nation by the kidneys of substances that excite inflammation, and is thus to be 
regarded as analogous to the renal changes which often co-exist. Toxic sub- 
stances, like cantharides, and copaiba, which pass through the kidneys, may also 
cause pyelitis as well as other disturbances. 

Pyelitis very often arises from a direct extension of inflammation from the 
neighboring organs. In many cases of acute and chronic nephritis the pelvis of 
the kidney takes part in the inflammation to a greater or less degree ; but an 
ascending extension of the inflammation from primary diseases of the urethra or 
bladder is still more common. Any urethritis or cystitis may, if it lasts long, 
advance upward to the ureters and the pelvis of the kidney, so that in severe cases 
we often find an inflammation of the whole urinary tract, a pyelo- cystitis, and 
even a "ureteritis." We have already stated (compare page 816) that the inflam- 
mation may extend still farther to the kidneys themselves, and this exten- 
sion will be repeatedly spoken of. 

Another frequent cause of pyelitis is the presence of foreign bodies in the 
pelvis of the kidney, which act as direct mechanical irritants. Among these are, 
in the first place, renarl calculi {vide infra), and also retained coagula, parasites 
(see page 822), etc. The pyelitis arising as a result of retention of urine in the 
pelvis of the kidney {vide infra, hydronephrosis) does not belong here directly, 
since it first develops from a decomposition of the urine. 

Whether there is a primary independent pyelitis, arising in ways other than 
those so far mentioned, is doubtful, as we have said. The occurrence of a primary 
pyelitis after exposure to cold especially lacks confirmation. The pyelitis coming 
on in women in childbed, or following different sorts of diseases of the sexual 
organs, may in all cases be referred to an infection of the pelvic mucous mem- 
brane from the bladder or from the kidneys. 

Pathological Anatomy. — In simple catarrhal inflammation the mucous mem- 
brane of the pelvis of the kidney is reddened, swollen, and covered with an abun- 
dant secretion, which contains varying amounts of pus-corpuscles and epithelium. 
In severer inflammations we often find quite numerous little haemorrhages in the 



830 DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



mucous membrane, and sometimes little gray nodules, which correspond to the 
swollen lymph-follicles. 

In severe cases, which are seen almost solely as a complication of a more 
extensive affection of the urinary passages, like pyelo-cystitis, we have a puru- 
lent, ulcerative inflammation, which may even assume a diphtheritic character. 
In these cases the kidneys are almost always coincidently involved — pyelo- 
nephritis. If the nephritic abscesses break into the pelvis of the kidney, there 
arises an ulcerative destruction of the renal tissue, so that the pelvis of the kidney 
is filled with pus and bounded by extensive ulcers, which often penetrate deeply 
into the substance of the kidney — pyo-nephrosis. The usually striated, pyelo- 
nephritic abscesses reaching- to the surface of the kidney have already been 
described in the previous section (see page 816), where their bacterial origin has 
also been mentioned. 

The condition differs when the kidney is involved, as in many cases of chronic 
pyelitis. This appears most frequently as a result of retention of urine, and hence 
it is usually associated with a dilatation of the pelvis of the kidney. In these cases 
we sometimes find pronounced processes of contraction in the kidneys — that is, a 
partial atrophy of the renal tissue, increase of the interstitial connective tissue, 
and evident cicatricial depressions on the surface — in a word, a secondary con- 
tracted kidney, arising as a result of pyelitis, which differs from genuine contrac- 
tion of the kidney only in its aetiology. 

Clinical Symptoms. — Since in most cases pyelitis develops only as one symptom 
of a more extensive morbid process, its clinical symptoms are usually but slightly 
prominent in the whole course of the disease. In what follows, therefore, we can 
not give any complete description of the clinical course of pyelitis, but we must 
mention only those symptoms from which, when there is an affection of the urin- 
ary passages, we can conclude that the pelvis of the kidney is involved. 

The most essential sign which the urine presents in all inflammatory affections 
of the urinary passages, the presence of mucus and pus, will be described more fully 
in the chapter on cystitis (vide infra). In pyelitis, also, the muco-purulent secretion 
of the pelvic mucous membrane must mix with the urine, and in every severe 
purulent inflammation the amount of pus in the urine must be quite considerable. 
We can never decide with certainty, from the mere presence of pus in the urine, 
as to the place where the pus mixes with the urine, whether in the pelvis of 
the kidney or in the bladder, or even in the urethra. Only when the urine con- 
tains other characteristic morphological elements beside the pus-corpuscles can 

we decide upon the portion of the urinary 
tract which must be especially affected. 
Among these morphological constituents is, 
first of all, the epithelium, which in the pel- 
vis of the kidney shows in part another 
shape than in the bladder. If we find in 
the urine, then, the triangular, long caudate 
pelvic epithelium (see Fig. 107), with its cells 
Fig. 107.— Pelvic epithelium. sometimes laid over one another in the form 

of tiles, we may assume that the pelvis of 
the kidney is involved in the inflammation. Of course, the reverse of this law 
does not obtain; for, even in severe purulent pyelitis and pyelo-nephritis, we 
often fail entirely to find the caudate epithelium in the urine. We must also 
add that similar forms of epithelium are also found in the bladder, so that great 
caution is always to be enjoined in estimating the diagnostic value of the epithe- 
lium found. Blood is only rarely found in the urine in simple pyelitis, but it is 
common in pyelitis calculosa (see the following chapter). The reaction of the 




INFLAMMATION OF THE PELVIS OF THE KIDNEY. 831 



urine in pyelitis is usually acid, but it is not correct to assume that there is in this 
a comprehensive mark of distinction between pyelitis and cystitis, in which the 
urine is often alkaline. 

Another symptom, to be referred directly to the pyelitis, is the local pain in 
the region of the kidney, which sometimes passes from this point down along the 
ureters to the bladder. This symptom has not, therefore, a great diagnostic value, 
because only its presence is in favor of pyelitis, while its absence proves nothing 
against the existence of the disease. 

All the other symptoms may be directly dependent upon the pyelitis, but 
they may usually be referred in great degree to the other co-existing affec- 
tions. First among these is fever, which either shows an irregularly remitting 
course, or appears in single high elevations of temperature, usually associated with 
rigors. The fever, however, seldom shows this latter pysemic character except in 
the severe purulent forms, where we usually also have the formation of renal 
abscesses — that is, a pyelo-nephritis. Beside the fever there are often, in severe 
cases, general nervous symptoms, like headache, delirium, and sopor, which are 
to be referred partly to the general pysemic infection of the body and partly, per- 
haps, to the absorption of ammonia from the urine decomposing in the blood — the 
" ammoniaemia " of Treitz and Jaksch. 

The whole course of pyelitis differs so much according to the primary disease 
present that nothing of general application can be said about it. The milder 
forms, which often pass off rapidly, are found most commonly in childbed, and 
sometimes in acute infectious diseases, poisonings, and as a result of mild cystitis. 
The severe forms occur chiefly as cysto-pyelitis and pyelo-nephritis, as a result of 
strictures of the urinary tract {vide infra), of severe cystitis in diseases of the 
spinal cord, and in other severe diseases of the kidney and of the pelvis of the 
kidney, like new growths, and parasites. They usually form then a very tedious 
and often incurable affection, which lasts until the patient's death. 

The signs of pyelitis which are important in diagnosis have already been men- 
tioned above. The main point is always to pay careful attention to the aetiology 
of the case, and, next to that, to the changes in the urine. If the whole condition 
points to a severe affection of the urinary tract, we can often decide correctly on a 
pyelitis or a pyelo-nephritis without the presence of direct signs of these diseases, 
because we know by experience that such an extension of the affection is the rule 
in all severe and long-continued cases. 

The implication of the kidneys is sometimes shown directly by the presence of 
casts in the urine in addition to the pus-corpuscles. In the cases above mentioned, 
where a chronic cysto-pyelitis is complicated with a contracted kidney, the condi- 
tion of the urine is the same in many respects as in genuine contracted kidney. 
It is abundant, usually has a low specific gravity, and contains, beside the pus- 
corpuscles, a few short hyaline casts. 

Treatment. — The treatment of pyelitis coincides mainly with the treatment of 
the primary disease, and therefore it needs no detailed description here. Ordi- 
narily only the accompanying cystitis {vide infra) is accessible to a direct local 
treatment, and here an important prophylactic factor is discovered, since by a 
timely treatment of the cystitis we can certainly hinder the advance of the inflam- 
mation to the pelvis of the kidney. 

Among the internal remedies to which we ascribe a favorable influence on the 
mucous membrane of the urinary tract, and which are, therefore, used in like 
manner both in pyelitis and in cystitis, we may mention the astringents, tannin, 
alum, and acetate of lead. Balsams, such as copaiba, are sometimes prescribed, 
and also antiseptic substances, such as salicylic acid and chlorate of potassium. 
The details in regard to all these remedies will be found in the treatment of 



832 DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



cystitis. The copious ingestion of fluids sometimes acts favorably, especially 
the use of certain mineral- waters, among which the waters of Carlsbad, Vichy, 
Ems, Neuenahr, and Wildungen, have obtained the most reputation. A method- 
ical milk cure is also greatly to be recommended, especially when there are symp- 
toms of irritation, such as pain on micturition. 

Local applications to the region of the kidneys, warm poultices, or exception- 
ally local blood-letting, are indicated only when there is severe pain, where of 
course narcotics must also be used under some circumstances. In this respect 
warm baths also do good service at times. 



CHAPTER H. 

NEPHROLITHIASIS. 

{Renal Calculus. Renal Gravel. Pyelitis Calculosa.) 

Occurrence, Chemical Composition, and JEtiology of Renal Concretions— The 

precipitated concretions of the urinary constituents which form in the pelvis of 
the kidney, and which, under some circumstances, may be passed from it with the 
urine, are designated, according to their size and nature, as renal sand, a fine, 
pulverized precipitate; renal gravel, gravel-like, granular concretions about the 
size of the ordinary coarse grains of sand, which can usually pass through the 
ureters without special difficulty; or renal calculi, the larger concretions. The 
latter are about the size of a pea or bean, but larger stones are occasionally seen 
which may even resemble actual casts of the pelvis of the kidney. We usually 
find a calculus only in one kidney, although both kidneys may be affected. 

In regard to the chemical nature of renal concretions, they consist most fre- 
quently of uric acid. They then have a brown-red or blackish color, and have a 
crystalline breakage, which, in large stones, is usually plainly laminated ; and, on 
the whole, a smooth, although irregular-shaped, surface. More rarely the renal 
concretions consist of calcic oxalate. The oxalate calculi are extremely hard, 
have a dark -brown color and a rough surface, often furnished with many 
prickles, from which reason they are often called "mulberry calculi." Their 
breakage sometimes has a radiated, but never a laminated arrangement. Stones 
are also frequently seen, which consist of alternating layers of uric acid and calcic 
oxalate, or which have a nucleus of uric acid and a coating of calcic oxalate. The 
phosphatic calculi are another variety of renal concretions. We only very rarely 
have to do, however, with stones which consist exclusively of basic calcic phos- 
phate or animomo-magnesic phosphate, but we usually have secondary deposits of 
layers of phosphate which are precipitated on uric acid or mulberry calculi in 
urine which has become alkaline. The phosphatic calculi have a grayish- white 
color, and are comparatively soft. The largest examples of them are found, not 
in the pelvis of the kidney, but in the bladder. The cystine and xanthine calculi 
are the rarest of all. 

But little definite is known as to the exact causes for the origin of all these 
concretions. We must suppose for the deposition of uric acid an abnormally 
great acidity of the urine, but we are not in a position to state by what circum- 
stances (the patient's food and manner of life, acid fermentation of the urine 
within the urinary tract ?) this may be provoked. It is a very probable theory 
that some solid body usually affords the nucleus and the first cause for the 
formation of at least the larger stones, among these bodies being mucous 
coagula, shreds of epithelium, and perhaps bacteria. The oxalate, cystine, and 



NEPHROLITHIASIS. 



833 



xanthine calculi are also deposited from acid urine, but scarcely anything is 
known as to the precise conditions to be here considered. We can point only to 
the fact that with the close chemical alliance between uric acid and oxalic acid 
the origin of the latter from uric acid seems possible, and the frequent co-existence 
of the two substances in the calculi therefore seems plausible. We have already 
indicated above that the cause of the deposition of phosphatic concretions can be 
found only in the existence of an alkaline reaction in the urine. 

In regard to the predisposing causes of calculus formation we must mention, 
first of al], that they are often found in children, and next in frequency in ad- 
vanced life. Men show a greater disposition to renal calculi than women. Hered- 
ity also seems to play a certain part, since the disease has been repeatedly observed 
in different members of the same family. The many relations which have been 
imagined between the formation of calculi and certain conditions in the manner 
of life and in the food taken, all lack accurate foundation. In regard to this the 
chief blame is laid upon an excessive meat-diet, drinking copiously of new sour 
wines, and drinking water containing lime. In regard to the occurrence of uric- 
acid concretions in gouty patients, compare the chapter on arthritis uratica. 

The Anatomical Changes caused by Renal Calculi.— The most frequent change 
which the presence of concretions in the pelvis of the kidney excites is pyelitis. 
This may exhibit all degrees, from a simple catarrhal inflammation to a diphthe- 
ritic or severe purulent inflammation of the pelvic mucous membrane. As a 
result of the mechanical irritation, there are quite frequently large or small 
haemorrhages. 

If a severe purulent pyelitis has developed, this may bring with it all the 
sequelae with which we have previously become acquainted. In severe cases the 
process may involve the kidneys, and there arises a pyelo-nephritis, with a puru- 
lent breaking down of the renal tissue, and, under some circumstances, even a 
peri-nephritis, with extensive suppuration into the vicinity of the kidney, and with 
occasionally perforation into the neighboring organs. If the renal calculi have 
previously passed outward, they are not found at the autopsy, although they form 
the special starting-point of the disease. Sometimes, however, the pus-cavity is 
entirely filled with calculi. 

A second important sequel of a renal calculus which sometimes develops is 
hydronephrosis {vide infra). It arises when a large stone blocks the passage from 
the pelvis of the kidney into the ureter, or when a smaller stone remains fast 
in the ureter and completely shuts off the passage of the urine. In the latter case 
there may also arise a pressure necrosis and perforation of the ureter. It goes 
without saying that mflammation and hydronephrosis or pyonephrosis may be 
combined with each other. 

Clinical Symptoms. — If there is merely the formation of renal sand or renal 
gravel in the urinary tract, this condition is sometimes associated with no symp- 
toms at all. The little granules are washed away by the urine and evacuated, 
and at most they may give rise to slight pain in the region of the kidney. 
Larger stones, however, may sometimes be wholly, or almost wholly, without 
symptoms, if from their position and their smooth surface they can cause no special 
bad results. 

The characteristic clinical symptoms of nephrolithiasis do not appear until the 
results of mechanical irritation of the pelvis of the kidney arise, or until there is 
an incarceration of a calculus in the ureter. It is the latter circumstance which, 
after the analogy of gall-stones, causes the most important symptom in the diag- 
nosis of renal calculi — the pains, the so-called renal colic. Such an attack of colic 
sometimes comes on quite suddenly and unexpectedly ; in other cases it is pro- 
duced by some exciting cause — jumping, running, walking, or riding. The pain 
53 



834: DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



often attains an uncommonly severe intensity ; it shoots from the lumbar region 
along the course of the ureters, but sometimes extends still farther, to the testicles, 
the thighs, or the back. In severe attacks there may be a general state of collapse 
with a small rapid pulse, cold sweat, and attacks of fainting. The temperature may 
be somewhat raised. We often see nausea and repeated vomiting. The urine 
is sometimes entirely normal, inasmuch as it comes exclusively from the other 
free kidney ; but oliguria, or even complete anuria, with its consequences, invari- 
ably sets in, if both ureters are stopped. Even when one kidney remains nor- 
mal, the evacuation of urine may be inhibited by a reflex spasm of the bladder. 
Sometimes the urine passed contains pus and blood. The duration of renal colic 
depends upon the duration of the incarceration ; it may last for a few hours or 
several days. The attack often ends with the passage of the stone outward. 

The other symptoms occurring in nephrolithiasis refer mainly to the results of 
the mechanical irritation of the pelvis of the kidney. The urine then shows an 
admixture of pus, and contains pelvic epithelium and often blood. The frequent 
appearance of blood in the urine, which usually has its cause in purely mechanical 
lesions of the mucous membrane, is a characteristic symptom of pyelitis calculosa. 
If we find, as sometimes happens, the urine at many times perfectly clear and 
normal, but at other times containing pus, we may suspect an occasional blocking 
of the ureter coming from the diseased kidney by a renal calculus. 

The symptoms are much more severe if the trouble goes on to a severe purulent 
pyelitis and pyelo-nephritis. We need not describe the details again here — the 
pain, fever, swelling, and perforation internally or externally — since they agree 
completely with what has been said before (see the previous chapter and Chap- 
ter VI in the previous section). A special chapter is devoted below to the symp- 
tomatology of hydronephrosis. 

The whole course of nephrolithiasis is, as a rule, very tedious. Since the dis- 
position to the formation of calculi usually persists, and since also the sequelae 
which have once developed may last for a long time, a very chronic state often 
develops, which, in varying ways and with manifold exacerbations and remis- 
sions, is composed of attacks of colic, haemorrhages, and symptoms of pyelo- 
cystitis. 

In many cases, of course, complete recovery may finally ensue. The calculi 
present are passed, new ones are not formed, the pyelitis that has arisen disappears, 
and, of course, all the morbid symptoms cease ; but, on the other hand, nephro- 
lithiasis has also a number of dangers in itself, which threaten life very seriously. 
These are, beside the rare occurrence of uraemia, first of all, the development of 
pyelo-nephritis and of still more extensive suppurations, with a general decline in 
strength, pyaemic states, etc. There is also a possible danger in such chronic sup- 
purations that there may be the appearance of a general amyloid degeneration of 
the internal organs. 

Among the complications occurring in other organs, only one circumstance 
has especial interest: that gall-stones and renal calculi are found quite fre- 
quently in the same individual. We, of course, can not well speak of a compli- 
cation with vesical calculi, since a great part at least of the vesical calculi are 
originally formed in the pelvis of the kidney, and undergo merely a further 
growth in the bladder. 

Diagnosis. — The diagnosis is made perfectly certain only by finding the special 
corpora delicti in the urine. For this purpose the urine must always be examined 
as soon as possible after its passage, and it is best to pour it through a fine sieve. 
In many cases, however, we can diagnosticate nephrolithiasis quite certainly, 
without the direct evidence of concretions, from the characteristic symptoms, espe- 
cially from the periodical renal haemorrhages and from the attacks of colic. Of 



NEPHROLITHIASIS. 



835 



course, it may be confused with renal cancer, parasites of the kidney like echino- 
cocci, and similar affections, but this does not happen very often because renal 
calculus is a far commoner affection than the diseases just mentioned. Finally, 
we must state that these diseases may comparatively often be combined with 
nephrolithiasis. 

Treatment. — Since the uric-acid concretions are by far the commonest, the 
methods of treatment most in use for nephrolithiasis refer first to these; but they 
are to be used in like manner in the allied oxalate calculi. 

If the tendency to the formation of urinary gravel is confirmed in a patient, or 
if the severer symptoms of nephrolithiasis have already appeared, we must first 
give a number of general dietetic directions, which check the formation of uric 
acid in general, and aid the solubility of the uric acid already formed as far as 
possible. Without entering too much on theoretical reasoning, we will give in 
what follows the measures which have been proved practically and quite gener- 
ally acknowledged. In the first place, the patient must avoid any immoderate 
indulgence in food in general, and particularly too great indulgence in meat. 
We should recommend for him a diet mainly, though not exclusively, vegetable, 
with a moderate supply of meat ; milk is also a proper food. Alcoholic beverages 
should be taken only in slight amount, and acid foods and drinks, except lemon- 
ade, should not be taken at all. It is a good plan to control the supply of food by 
weighing the patient regularly, in order to avoid any further addition to the 
weight in all persons in a state of normal nutrition and to obtain a loss of weight 
in the corpulent. We should also aid the using up of tissue by regular physical 
exercise and muscular work, gymnastics, sawing wood, or gardening, and, finally, 
the urine must be diluted by an abundant supply of fluid, and its soluble power be 
thus increased. 

This latter indication will usually correspond at the same time with those 
which diminish the acid reaction of the urine by a supply of alkalies and thus 
hinder the deposition of uric acid as far as possible. From this comes the very 
extensive use of the alkaline mineral- waters in nephrolithiasis. The simplest plan 
is to dissolve some alkaline salt in a large amount of plain water, soda-water, or 
lemonade, and let the patient drink it. Among these salts we may mention sodic 
phosphate, one to four drachms (grm. 5-15) a day, or, better, sodic carbonate, one to 
two drachms (grm. 5-10), or carbonate of lithium, which has lately been especially 
recommended, two to five grains (grm. 0"l-0'3) several times a day. Of course, 
the special mineral-waters enjoy a greater reputation ; these may be used in con- 
formity with the treatment at home, or especially at the appropriate springs. The 
following springs enjoy the greatest reputation in this respect: Carlsbad, Vichy, 
Salzbrunn, Tarasp, Neuenahr, Ems, and Wildungen. 

The symptomatic treatment is also very important. In so far as this relates to 
the accompanying pelvic and vesical catarrh, we may refer to the appropriate 
chapters in this book, while the surgical methods of treatment in the severer 
sequelae — hydronephrosis, pyonephrosis, or perinephritic abscess — are to be found 
in the special treatises. Against renal haemorrhages some internal remedies, like 
ergotine or tannin, have been recommended, but their action is quite doubtful. 
The treatment of the attacks of colic is of greater practical significance. The 
chief remedies are the narcotics, opium, and morphine, internally, or, with very 
severe pain, better subcutaneously. Warm baths, warm poultices, or narcotic 
embrocations, like chloroform liniment, also frequently give relief. Local blood- 
letting is only rarely indicated. An abundant supply of fluid is always advisable, 
in order to aid the washing out of the incarcerated stone by an increased secretion 
of urine. 

As we have stated, what has thus far been said obtains chiefly in the treatment 



836 DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



of uric-acid and oxalic-acid calculi. "We know no special prescriptions to be con- 
sidered for the occasional cystine calculi. When there are phosphatic calculi, 
however, which can be deposited only from alkaline urine, the use of acids has 
been recommended, especially of lactic acid, seven to fifteen grains (grm. 0*5-1), 
internally in an aqueous solution. The main thing, of course, is always the treat- 
ment of the catarrh of the urinary tract, which usually lies at the bottom of the 
calculus formation. 



CHAPTER HI. 

TUBERCULOSIS OP THE GE NIT O -URINARY APPARATUS. 

iEtiology and Pathological Anatomy.— It does not seem remarkable that, with 
the presence of many tubercular processes in the body, tubercle bacilli should quite 
easily reach the kidneys by way of the blood-current, and there give rise to an 
eruption of tubercle. Accordingly, we quite frequently find a few or many mili- 
ary tubercles in the kidneys in acute miliary tuberculosis, in pulmonary tubercu- 
losis, etc., which are distributed over the whole kidney, or sometimes only in the 
territory of one arterial branch. 

While miliary tuberculosis of the kidney, however, is without any clinical sig- 
nificance, there is also an extensive local tuberculosis of the kidney, which is so fre- 
quently combined with tuberculosis of other parts of the genito-urinary apparatus 
that the disease mentioned is properly classed under the name of genito-urinary 
tuberculosis. It is possible that the infection here may sometimes arise through the 
blood-current, but in some cases we probably have an entrance of tubercle bacilli 
into the urinary tract from without. In this way the place of the first anatomical 
manifestation of the tubercular poison may be very diverse. The kidneys often 
seem to be first diseased, in other cases the bladder, and quite frequently, as it 
seems, the prostate, and sometimes perhaps the vesiculae seminales or the testicles. 
From the organ first affected the process then extends continuously or by leaps to 
the neighboring parts. If the cases come to autopsy, the tuberculosis is often so 
extensive that we can no longer make out with certainty the place where it first 
began. In women the urinary apparatus is only very rarely affected by tubercu- 
losis, while uterine and ovarian tuberculosis represents a localization of the tuber- 
cular poison of clinical importance (compare the chapter on tuberculosis of the 
lungs). 

In the kidneys the tubercular infiltration develops either chiefly from the pel- 
vis of the kidney, or in the renal substance itself. Yellow cheesy nodules arise 
which finally break down and thus lead to an actual "nephrophthisis." The 
infiltrated renal papillae are usually first destroyed, from which the whole pelvis 
of the kidney is changed into an ulcerating surface covered with necrotic tissue 
and cheesy detritus. In very advanced cases almost the whole kidney is 
destroyed. The process is usually bilateral, but it is often more advanced on one 
side than on the other. 

If the process invades the ureters, their walls are also infiltrated with tubercle, 
and hence are thickened, while the mucous membrane is often changed in great 
part to a necrotic ulcerating surface. Precisely analogous conditions are found 
in the bladder, and in some cases even in the urethra, while in the prostate, the 
vesiculae seminales, and the testicles there is more frequently the formation of 
cheesy nodules, and more rarely disintegration and perforation. 

Clinical Symptoms. — The picture of genito-urinary tuberculosis corresponds in 
most of its details completely to that of a severe chronic pyelo-cystitis. The occa- 



TUBERCULOSIS OF THE GENITO-URINARY APPARATUS. 837 



sional local symptoms are pain in the region of the kidneys and bladder. This 
may sometimes assume great severity, like colic, if the ureter becomes plugged by 
a broken-down, crumbling mass ; yet in other cases the pain is but slight during 
the whole disease. 

The urine shows the most important changes. It almost invariably contains 
an abundant sediment, consisting of pus-corpuscles and detritus. Its amount 
usually remains normal for a long time, its reaction is faintly acid, but in severe 
cases it may become alkaline through complication with an alkaline fermentation 
of the urine. The discovery of shreds of tissue in the urine, elastic fibers and 
connective tissue, is sometimes possible, and is of diagnostic value because it is 
direct evidence of an ulcerative process. The discovery of tubercle bacilli in the 
purulent urinary sediment (Rosenstein and others) is, however, far more impor- 
tant. This is performed by the same method as in the sputum ; it succeeds in 
almost all cases, and is an infallible and absolutely decisive sign in diagnosis. 
Admixtures of blood in the urine are also seen in genito-urinary tuberculosis, but 
they may often be entirely absent. 

The local objective examination of the kidneys usually gives a negative result. 
Only in a few cases have we been able to feel the diseased kidney as a tumor 
through the abdominal walls. This is usually due less to the tubercular infiltra- 
tion than to the dilatation of the pelvis of the kidney from hydronephrosis. We 
can sometimes feel the thickened walls of the bladder. The local examination of 
the prostate and the testicles is far more important in diagnosis. Especially in 
the latter we often feel the hardening corresponding to the tubercular infiltra- 
tion, and manifesting itself chiefly in the epididymis. 

Among the general symptoms we must mention, first of all, fever, which is 
only exceptionally absent, and usually shows a pronounced remitting, hectic char- 
acter. The other general symptoms are the same as in most of the other tuber- 
cular diseases — anaemia, emaciation, loss of appetite, increasing bodily weakness, 
etc. We have a special sign in the occasional co-existence of other tubercular 
diseases in the body, the lungs, the intestines, the bones, etc., which may also be 
wholly absent, so that we have to do with a purely local genito-urinary tuber- 
culosis. 

The course of the disease is steadily progressive. Recovery does not occur, at 
least not in any cases where the disease has attained any extent. The disease 
lasts from a few months to a year or two, rarely longer. The fatal termination 
usually ensues from the increasing general weakness, more rarely under the 
symptoms of ammonisemia, or sometimes from a miliary tuberculosis or some 
other tubercular disease, such as pulmonary tuberculosis. 

Diagnosis. — The diagnosis of genito-urinary tuberculosis is now usually no 
longer difficult in fully developed cases, since it can be made with complete cer- 
tainty by the discovery of the tubercle bacilli joined to the presence of pus in the 
urine. Of course this gives no information as to the more special extent of the 
process. In order to judge of this, we must add the local symptoms and the phys- 
ical examination of the different organs. We are aided in the confirmation of 
our first suspicion of a tubercular disease chiefly by the consideration of the gen- 
eral condition and the habit of the patient, the discovery of a hereditary taint, or 
at least the approximate possibility of tubercular infection, and also the discovery 
of other tubercular affections, especially in the testicles, the hectic fever and the 
tedious course, upon which nothing has a favorable influence. 

Treatment. — Since we do not know at present any efficient remedy to combat 
the tubercular process, the treatment has merely the task of improving the patient's 
general condition as far as possible, and also of undertaking a local symptomatic 
treatment in the same way as in ordinary pyelitis and cystitis (q. v.). 



838 DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



CHAPTER IV. 

HYDRONEPHROSIS. 

(Dilatation of the Pelvis of the Kidney.) 

iEtiology. — If a contractiou arises in any part of the urinary tract and checks 
the now of urine, there is a stasis of the urine in the portion hehind the stenosis, 
which gradually leads to a constantly increasing dilatation of the tract as a result 
of the pressure of the retained fluid. If the obstacle is situated in a ureter, the 
pelvis of the kidney, as well as the part of the ureter, dilates, and there arises a 
so-called hydronephrosis. If, however, the obstacle has its seat in the urethra, 
the bladder and both ureters gradually dilate, and there finally arises a bilateral 
hydronephrosis. 

A closure of the ureter arises most frequently in adults from impacted renal 
calculi, and also from new growths in the vicinity, in the uterus or ovaries, which 
compress the ureter from without. So great a pressure may also be exerted on the 
ureters by the gravid uterus as to be followed by a hydronephrosis, which is usu- 
ally bilateral. Cicatricial strictures, valve-formations and bends, also are found 
in the ureter, and form an obstacle to the flow of urine. Finally, in cancer of 
the bladder the lower opening of the ureter may be contracted or entirely closed. 

Constrictions of the urethra, which finally lead to a bilateral hydronephrosis, 
arise most frequently from strictures as a result of gonorrhoea, and also from 
enlargements of the prostate. In rare cases a phimosis may even form the 
obstacle. 

It is worthy of note that hydronephrosis may also be congenital, and then it is 
usually due to congenital defects of development in the ureters or other urinary 
passages. In later life hydronephrosis is in general more frequently observed in 
women than in men. 

Pathological Anatomy. — The pathological anatomy of hydronephrosis is on 
the whole very simple. We have a dilatation of the pelvis of the kidney, which 
is associated with a pressure atrophy of the renal tissue. The papillae are flattened, 
the uririiferous tubules and the glomeruli are gradually more and more obliterated, 
and, finally, the whole kidney may be changed to a connective-tissue sac filled 
with fluid. The size of such a hydronephrotic sac may sometimes be so large as to 
contain ten or twenty quarts (litres) of fluid. The latter consists, of course, at first 
of urine, but the farther the atrophy of the kidney advances, the more it contains 
merely the secretion of the mucous membrane. Inflammatory conditions are 
found in hydronephrosis only when they have existed previously, as in pyelitis 
calculosa, or when excitants of inflammation in addition have reached the pelvis 
of the kidney. 

Clinical Symptoms. — Since the whole type of the disease is, of course, depend- 
ent in many respects upon the nature of the primary disease, we have here to 
describe only those symptoms which point particularly to the development of 
hydronephrosis. Such a condition often causes no special clinical symptoms at 
all, so that we can at most suspect its existence from the presence of an aetiological 
cause. 

The appearance of a visible and palpable tumor is the first definite point in the 
diagnosis of hydronephrosis. This first shows itself in the region of the affected 
kidney, but then it gradually enlarges toward the hypochondrium and the median 
line of the body, and may finally show very considerable dimensions. The tumor 
is not movable on respiration. Its resistance is usually quite considerable, but 
sometimes a marked feeling of fluctuation may be present. On percussion, the 



HYDRONEPHROSIS. 



839 



tumor gives a dull note, from which the tympanitic note of the colon in front of 
the tumor is sometimes distinct (see page 821). It is an important diagnostic sign 
if the tumor shows variations in its size at times, since it decreases in size with a 
co-existing increase in diuresis, and increases again when the amount of urine 
becomes smaller. 

In doubtful cases an exploratory puncture of the tumor may also be of signifi- 
cance in diagnosis. It of course favors the existence of hydronephrosis if urinary 
constituents, especially urea, can be found in the fluid evacuated ; but, if the hydro- 
nephrosis is of long standing, its contents, as we have said, will be simply sero- 
mucous, and then chemical examination gives no definite data for distinguishing 
hydronephrosis from ovarian tumors, or other cystic tumors of the kidney. In 
regard to the procedure first devised by Simon, which is also important in regard 
to palliative therapeutics — namely, catheterization of the ureter in women after 
having previously dilated the urethra artificially, and in this way confirming the 
diagnosis — the details may be found in the special works on surgery. 

The secretion of urine in unilateral hydronephrosis may be completely normal 
if the other healthy kidney acts vicariously. In stricture of the urethra, and also 
in bilateral constrictions of the ureters, however, there is, of course, an obstacle for 
the passage of urine, so that the amount of urine may be abnormally small. There 
may be at times complete anuria, and even uraemic symptoms. The composition 
of the urine depends entirely upon the form of the primary disease. If only the 
healthy kidney secretes, the urine passed is normal. If there is at the same time 
pyelitis or cystitis, the urine may contain pus or blood. If the urine can also 
come from the diseased kidney at one time and not at another, the urine also 
exhibits a varying composition, as we have said before (page 834). 

In many cases of hydronephrosis quite severe local symptoms are present; 
there are frequently severe pains in the tumor, which shoot chiefly toward the 
thigh. Of course, these local symptoms are sometimes only slight. In regard to 
the symptoms on the part of other organs, gastric disturbances appear most fre- 
quently, such as nausea, loss of appetite, vomiting, and eructations. In some*cases 
the bowels are constipated, in others there is obstinate diarrhoea. 

The whole course of the disease is always chronic. There are often variations 
in its course, but no general statements can be given, because the conditions vary 
in the different cases according to the form of the primary disease. Most cases of 
hydronephrosis end fatally, either in consequence of the primary disease or in 
consequence of secondary pyelo-nephritic or perinephritic inflammations, from 
uraemia, etc. Recovery takes place in rare cases, especially if one kidney is per 
fectly normal, and there is no incurable primary disease. Recovery may ensue 
spontaneously from perforation or obliteration, or it may be brought about arti- 
ficially from operative procedures. 

In the diagnosis of hydronephrosis, the points especially to be considered have 
already been mentioned. The diagnosis is usually not easy, especially if the aetio- 
logical factors are unknown; and the disease is often confused with other renal 
tumors and echinococci of the kidneys, with ovarian tumors, and even with splenic 
and hepatic tumors. 

Treatment. — Except for the symptomatic treatment of the pain and any accom- 
panying pyelo-cystitis, an efficient treatment of hydronephrosis can be attempted 
only by surgical means. Puncture, incision, extirpation of the kidney, and the 
establishment of a renal fistula, are the methods of operation most in use — the 
details of which are to be found in the special surgical treatises. 



840 DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



CHAPTER V. 

CYSTITIS. 

(Vesical Catarrh ) 

iEtiology. — In most cases of vesical catarrh the agents of inflammation reach 
the bladder from without through the urethra. The most unequivocal experiment 
in this regard is, unfortunately, often made by the physician himself, when he 
excites a cystitis by the use of an insufficiently purified and disinfected catheter 
or bougie. The development of the vesical catarrh is generally aided in such cases 
by the fact that there is usually a defective evacuation of urine, from stricture of 
the urethra or paralysis of the detrusor, and that there is at the same time reten- 
tion of urine, in which the bacteria can develop undisturbed. The agents of 
inflammation may also enter from the urethra into the bladder in incontinence 
of urine. On account of the imperfect closure of the sphincter, a stagnating 
column of urine, directly connected with the contents of the bladder, forms in the 
urethra, and to this column the air and the bacteria that excite decomposition of 
the urine have direct access. In this way many cases of cystitis arise in patients 
with nervous disease who have paralysis of the bladder, and also many of the 
frequent cases of cystitis in persons who are severely ill and stupid from some 
other disease, such as typhoid fever. 

Cystitis often follows diseases of the neighboring urinary tract. Gonorrhoea! 
urethritis is the most common, and this invades the bladder directly and leads to 
a gonorrhceal cystitis. In women, the agents of inflammation may quite easily 
enter the bladder from the vagina through the short female urethra. Thus arise 
especially the frequent cases of cystitis in childbed. In some cases communica- 
tions may develop between the bladder and certain neighboring organs, as in 
vesico-rectal or vesico-vaginal fistulae, by which again access to the bladder is 
open to the agents of inflammation. 

Another group of cases is due to the presence of foreign bodies, which irritate 
the vesical mucous membrane mechanically. Among these is, first of all, the 
cystitis which so often accompanies stone in the bladder. It must be stated, how- 
ever, that many cases of the vesical catarrh which here exists are not directly 
dependent upon the calculi, but are first excited by examination with catheters, 
and sounds. 

In distinction from the methods of the origin of cystitis so far described, the 
production of inflammation by way of the blood-supply is much rarer. Certain 
chemical substances, already mentioned (page 829), which are eliminated by the 
kidneys and provoke an inflammation of the urinary tract, are the most important 
in this respect. Cantharides shows the most intense action of this sort, and it may 
cause an actual croupous cystitis. Slight irritative states of the bladder also fre- 
quently appear after taking certain foods and drinks, as after drinking new beer. 
Infectious substances only rarely come under consideration in this regard. Most 
of the cases of cystitis in severe acute infectious diseases are secondary complica- 
tions {vide supra). It can not be doubted that in some cases an apparently idio- 
pathic primary cystitis appears after exposure to cold, but it is very rare. In such 
cases we usually have to do with acute exacerbations of an old chronic cystitis — 
for example, of gonorrhceal origin. 

It has been stated in the previous chapters how frequently cystitis is only one 
symptom of a more extensive disease of the urinary tract. As cystitis may 
further invade the pelvis of the kidney through the ureters, so on the other hand 
can any pyelitis of primary origin extend downward and involve the bladder. 



CYSTITIS. 



841 



Pathological Anatomy. — The pathological anatomy of cystitis presents the 
same conditions as the inflammation of any other mucous membrane. In simple 
catarrhal cystitis the mucous membrane is swollen and covered with pus, and is 
often studded with haemorrhages. In old chronic cystitis the mucous membrane 
often takes on a slaty grayish-black color as a result of the haemorrhages. The 
severer forms of cystitis, such as are often observed in diseases of the spinal cord, 
are termed vesical diphtheria. These cases come to a necrotic destruction of the 
superficial layers of the mucous membrane, ulcerations, etc. In such severe cases 
submucous and pericystitic abscesses sometimes develop, which may perforate into 
the surrounding parts in various ways. The incrustation of the mucous mem- 
brane with urinary salts, especially with ammonio-magnesic phosphate, is also 
frequently found in chronic cystitis, and is worthy of mention. 

Clinical Symptoms. — The local symptoms in the bladder are sometimes quite 
severe in cystitis, but in other cases they are only slight. In general, they show 
a greater intensity in acute cases than in chronic cystitis. The pain in the region 
of the bladder is rarely entirely continuous ; it usually comes on only on micturi- 
tion, but it is often very distressing then, and shoots to the opening of the urethra. 
Since the inflamed vesical mucous membrane shows an increased irritability, and, 
since the morbidly altered urine {vide infra) also exerts an abnormal irritation 
on the mucous membrane, there is very often an increased desire to micturate. 
The patient has to empty the bladder much oftener than normal, and in severe 
cases there is an almost constant, painful " vesical tenesmus," from which, at any 
attempt to micturate, only a very small amount of urine is passed with severe 
burning. As a result of the increased irritability of the vesical mucous membrane, 
there sometimes comes on a very troublesome reflex spasm of the sphincter, by 
which the symptoms are increased. 

Only the character of the urine is decisive in the diagnosis. This is secreted in 
a perfectly normal amount and character, in case there is no complication on the 
part of the kidneys ; but in the bladder it is mixed with the products of the dis- 
eased mucous membrane, and it is here exposed to the action of the bacteria in a 
way that will presently be described. The abnormal admixtures in the urine con- 
sist chiefly of pus-corpuscles and bladder epithelium, and sometimes of some of 
the mucus produced by the mucous membrane. The specific action of the bacteria, 
which have reached the bladder from without, consists of the so-called alkaline 
fermentation of the urine — that is, in the fermentative change of urea into car- 
bonate of ammonia. This process is associated entirely with the presence of cer- 
tain micro-organisms, the "urine torulaceoe 11 and the "micrococci urece" and 
the retention of urine as such never leads to an alkaline fermentation. The reten- 
tion is only a factor, which greatly aids the whole process, since the activity of 
the bacteria, as we have said, can develop much better here than if the bladder 
were to a certain degree constantly purified and washed out by the urine that is 
always coming afresh. As soon as a part of the urea is changed to carbonate of 
ammonia, the acid reaction of the urine must be less. The urine has a faintly acid 
or neutral reaction, and sometimes it is even already decidedly alkaline when 
passed. The latter, however, is only rarely the case, but it is often simulated by the 
fact that the urine is not examined until it has stood for some time. Since during 
this time the alkaline fermentation which has once begun makes rapid progress, 
the cystitic urine that has stood is very often alkaline. Many crystals of ammonio- 
magnesic phosphate and urate of ammonia then form in it ; the former are easily 
recognized by their " coffin-lid shape," and the latter by their " thorn-apple shape " 
(see Fig. 108). 

If we then briefly put together what has been said, the urine is passed in about 
the normal amount in cystitis. It usually looks clear, and has an abundant sedi- 



842 DISEASES OF PELVIS OF THE KIDNEY AND BLADDEE. 



ment, which, can often be recognized as purulent with the naked eye, and in 
which, microscopically, we can find pus-corpuscles, often bladder epithelium, and 
constantly innumerable bacteria — usually short rods in vigorous motion. The 
alkaline fermentation may usually be recognized by the strong ammoniacal odor, 

and also, as we have said, by the reaction 
of the urine. In the severe diphtheritic 
forms of cystitis we find entire shreds of 
necrotic tissue in the urine. If there are 
haemorrhages in the bladder, the urine 
often contains red blood-corpuscles and 
sometimes even large blood-clots. The 
mucus in the urine appears in milder cases 
as a cloudy opacity — "nubecula." The 
viscid masses which can be drawn out into 
threads, and which are usually abundant 
in the urine in severe cystitis, are not the 
special product of the mucous membrane, 
mucine, but they arise from the pus-cor- 
puscles and the epithelium dissolved in 
the alkaline urine, and hence give the 
Fio. 108,-Crystais of triple phosphate and am- reactions for albumen. It goes without 
momc urate. (From Funkk.) saying (compare page 773) that every 

cystitic urine is albuminous from its mix- 
ture with pus-serum. The presence of slimy threads in the urine — the so-called 
"clap-threads" (Tripperfaderi) — is characteristic of gonorrhceal cystitis. 

There can be no doubt that the decomposing alkaline urine acts as a chemical 
excitant of inflammation on the vesical mucous membrane. Hence cystitis often 
arises perhaps in this way, that the bacteria which have entered the bladder first 
excite only an alkaline fermentation, and that then the mucous membrane is 
affected by the irritation of the ammonia salts that are formed. It is, however, 
at present hard to decide, and it is also without special practical interest, whether 
the bacteria as such can not directly excite inflammation. 

The other morbid symptoms associated with cystitis usually depend only in 
part upon the disease itself and in part upon some existing primary disease. The 
most important symptom is the fever, which is often to be referred directly to the 
cystitis. In severer cases it may be very intense, and often assumes a pysemic 
intermittent character, especially if there have arisen pericystitic suppurations or 
if the cystitis has extended to the pelvis of the kidney and the kidneys (see page 
831). An acute cystitis may also begin with a chill and high fever. If the escape 
of the purulent urine, however, always remains undisturbed, the fever may be 
entirely absent in spite of the existence of cystitis. 

Sometimes in severe cystitis with a marked alkaline fermentation certain nerv- 
ous symptoms appear, such as headache, vertigo, stupor, and nausea. The idea has 
been advanced that in these cases we have to do with an auto-intoxication of the 
body, since ammonia and perhaps other products of decomposition, like sulphu- 
retted hydrogen (?), are absorbed from the bladder into the blood (ammoniaemia), 
and in this way excite the symptoms of poisoning mentioned. 

According to the course of the disease we distinguish an acute and a chronic 
cystitis. The former, which may come on, for example, after catheterization, in 
gonorrhoea, etc., often passes off favorably after a few days. The amount of 
mucus and pus in the urine remains slight. Chronic cystitis is observed especially 
as a complication in other diseases of the urinary tract, like stricture, in chronic 
diseases of the spinal cord with paralysis of the bladder, etc. It is very often 




CYSTITIS. 



843 



incurable because the primary disease is incapable of improvement and the cause 
of the disease therefore persists. The longer a cystitis lasts, the nearer is the 
possibility of the development of more severe and dangerous complications, espe- 
cially the development of a pyelo-nephritis, and the formation of pericystitic sup- 
purations. In this way cystitis, especially in chronic nervous diseases, may become 
the immediate cause of death. 

Treatment. — The dangers last mentioned must urgently impress upon us the 
prophylaxis of cystitis. Fortunately, a good deal can be done in this respect, in 
the first place, by the avoidance of all unnecessary use of bougies and catheters, 
by the greatest care for cleanliness in the use of all instruments of this sort, and 
by the timely treatment of all those conditions which may lead to cystitis. 

The treatment of cystitis is, in the milder and acute cases, hygienic and medi- 
cinal, but in the severer cases only a careful local treatment can be useful. 

In any severe, and especially in any acute cystitis, the greatest bodily rest (if 
possible rest in bed) is urgently desirable, since otherwise an increase of the symp- 
toms and a prolongation of the course of the disease is the almost inevitable 
result. The diet must be mild and unirritating. Spiced food and alcoholic drinks 
are to be avoided, but we should recommend an abundant supply of fluid, by 
which the urine is diluted and the bladder washed out. We have the patient 
drink plenty of ordinary water, tea, or a suitable mineral-water, like Wildunger, 
Selters, or Fachinger. A diet mainly of milk is very good; by it the cystitic 
symptoms often very rapidly cease. 

Among internal remedies those are to be considered which are eliminated with 
the urine, and are thus able to act on the diseased mucous membrane, or directly 
upon the agents of inflammation. One of the most efficient drugs, which never 
does harm with necessary caution, is chlorate of potassium, of whose favorable 
influence on vesical catarrh we have often convinced ourselves. It is prescribed 
in an aqueous solution, forty to seventy-five grains a day (grm. 3-5), and 
should never be taken on an empty stomach. Salicylic acid is sometimes used 
with good results in doses of half a drachm to a drachm (grm. 2-4) a day in 
ten-grain (grm. 0'5) capsules. The two remedies mentioned have largely replaced 
tannin, which was formerly in great favor. At present a decoction of uva ursi is 
still more frequently prescribed, 10 or 15 to 150, whose active principle, arbutine, 
in doses of forty-five to sixty grains a day (grm. 3-4) in an aqueous solution, 
seems worthy of further trial (Lewin and others). In more advanced stages of 
vesical catarrh, if the initial symptoms of irritation have ceased, the resinous 
drugs are to be used, of which oil of turpentine and balsam of copaiba especially 
sometimes show a very good action. Both are best given in gelatine capsules. 

If there are severe local symptoms, we prescribe warm compresses and poul- 
tices to the region of the bladder. In robust persons with acute cystitis, local 
blood-letting, three to six leeches to the perineum, sometimes has a decidedly 
favorable symptomatic action in such a case. In other respects narcotics, especially 
subcutaneous injections of morphine, are the best remedy where there is severe 
pain and tenesmus. Camphor, extract of belladonna, etc., are much more uncer- 
tain in their action. The frequent use of protracted warm baths may, however, 
be greatly recommended. 

In chronic cystitis all the remedies previously mentioned are also to be con- 
sidered ; but they are usually not sufficient alone, and at any rate they are far less 
effective than a methodical local treatment. This consists in washing out the 
bladder regularly every day by the aid of an elastic catheter, to which a T-tube is 
fastened by means of rubber tubing, one arm being connected with an irrigator 
and the other with the escape-tube. We thus let a moderate amount of fluid, 
eight or ten ounces (200-300 c. c), run into the bladder and run out again, fre- 



844 DISEASES OF PELVIS OF THE KIDNEY AND BLADDEE. 



quently repeating the process, until it comes away perfectly clear. For this pur- 
pose we use either pure warm water, or, better, a dilute solution of plumbic 
acetate (1 to 1000), permanganate of potassium (1 to 1000), boric and salicylic water, 
and the like. By such a treatment many cases of chronic vesical catarrh may 
recover, and others may at least be kept constantly in check. 

Attention to the causal indication is sometimes very important also in chronic 
vesical catarrh — for example, the treatment of any strictures, the removal of cal- 
culi, or the improvement of paralytic states of the bladder. 

In pericystitic suppuration surgical treatment is only rarely possible. We 
must, therefore, confine ourselves to purely symptomatic procedures. 



CHAPTER VI. 
NEW GROWTHS IN THE BLADDER. 

Primary new growths in the bladder are quite rare. The commonest is the 
so-called villous cancer (which is properly a papillary fibroma), which may attain 
the size of a walnut, and is usually situated in the lower portion of the bladder 
near the entrance of the urethra. Since the tumor is usually very vascular, there 
are often haemorrhages into the bladder, and repeated hematuria is therefore one 
of the commonest symptoms of vesical papilloma. In this affection the blood- 
clots often assume a peculiar long, worm-like shape, from their passage through the 
urethra. Severe symptoms on micturition sometimes appear, since portions of 
the tumor may lie in front of the opening of the urethra. A definite diagnosis of 
a villous tumor is possible only when single portions of the tumor are thrown off, 
and are found in the urine passed. Examination of the bladder by the catheter 
may also give information as to the presence and seat of the tumor. 

Primary carcinoma of the bladder is rare. It is usually spread diffusely over 
the wall of the bladder, and leads to so considerable a thickening of it that we can 
often feel the bladder from without through the abdominal walls. Otherwise the 
symptoms are the same as in severe chronic cystitis. The urine contains much 
pus, and is sometimes bloody. The general cancerous cachexia developed rather 
late in the cases which we have seen, of which one was in a man still quite young. 
The diagnosis is not always easy. Except from attention to the general course of 
the disease and any vesical tumor that may be felt, it must aim to be based chiefly 
upon the discovery of particles of cancer in the urine. 

A secondary invasion of the bladder by carcinomatous new growths from the 
uterus, rectum, and vagina is quite frequently observed. 

The treatment can usually be only symptomatic, since surgical procedures are 
possible only in rare cases. 



ENURESIS NOCTURNA. 



845 



CHAPTER Yn. 

ENURESIS NOCTURNA. 

{Nocturnal incontinence of Urine.) 

Enuresis nocturna is a nervous affection of the bladder by no means rare in 
children of both sexes, and therefore quite important in its practical relations. 
Of course, in small children there is no sharp boundary to be drawn between 
normal and pathological conditions ; but it is decidedly pathological if larger chil- 
dren, from four to ten years of age and even older, pass their urine in bed more 
or less frequently during sleep, in spite of well-developed reasoning powers and 
professedly the best intentions. This anomaly may extend to the years of puberty 
and even beyond it, and then it frequently produces a very depressing mental 
affection for the patient. Special causes for it are not to be discovered in most 
cases. We are compelled to assume either an abnormal weakness of the sphincter, 
which is probably sometimes congenital, or an abnormal irritability of the detru- 
sor. At any rate, in wetting the bed at night the process of micturition comes on 
in a purely reflex way, but it is often accompanied by certain ideas in dreams 
referable to micturition. It does not hold in all cases that the sleep is especially 
deep. Many patients, of course, first notice the trouble in the morning, but others 
almost always wake directly after. The involuntary micturition usually occurs 
in the first hours after going to sleep, but sometimes it is later, and even first 
toward morning. By day micturition is often perfectly normal ; but in many 
cases there is even then a noticeable weakness of the bladder, so that the child has 
to make water oftener than usual, and sometimes wets its clothes even by day. 

Although, as we have said, we can usually find no special cause for the trouble, 
still, in some cases, certain morbid changes in the urinary organs may give rise to 
the incontinence. We should, therefore, in every case at least think of the pos- 
sibility of stone in the bladder, of congenital phimosis and adhesions of the pre- 
puce to the glans penis, of ascarides, and of inflammatory conditions, and make a 
special examination of these points. We must also bear in mind polyuria caused 
by diabetes or renal disease, and finally, of course, in the diagnosis of a purely 
nervous nocturnal incontinence of urine, we must exclude the existence of any 
actual anatomical spinal affection. 

In all the cases just mentioned, the treatment must of course refer first to the 
primary disease ; but in the ordinary nocturnal incontinence the treatment must 
first take into consideration the prevention of the appearance of nocturnal mic- 
turition as far as possible. The child must take only a very little fluid in the 
evening, and he should be made to empty his bladder immediately before going 
to sleep, and once again later. He should not be covered up too warmly, and, if 
possible, he should not lie on his back during sleep. Tying a brush to the back is 
therefore a well-known domestic remedy. A somewhat strict mental treatment is 
often effective, since thus the attention to the process is increased, although uncon- 
sciously, and the child often learns to wake up at the right time. The use of the 
rod is of course on the whole only rarely admissible. On the contrary, we often 
have to protect the child against unreasoning parents. 

Internal remedies, especially belladonna and tincture of nux vomica, which 
were formerly recommended, rarely avail. Iron preparations are indicated only 
in anaemic children. Electrical treatment, however, is often, if not always, very 
effective. We put the broad anode over the lumbar cord, and the smaller 
kathode over the region of the bladder or on the perineum, and let quite a strong 
constant current pass through for two or three minutes. Then we pass the wire 



84:6 DISEASES OF PELVIS OF THE KIDNEY AND BLADDER. 



end of a conducting cord, which, we make the kathode, into the mouth of the 
urethra for one or two centimetres, and let quite a strong and somewhat painful 
faradic current act for one or two minutes (Seeligmiiller). The sittings must at 
first he repeated daily. It is also a very good plan to let the whole body be well 
rubbed with cold water before going to sleep. 

The prognosis of these forms of incontinence, which have no organic disease 
at the bottom of them, is almost always favorable, since in the worst case the 
anomalous condition usually disappears gradually of itself with increasing years. 

[In the experience of the editor, belladonna has given much better results than 
it would seem to have given in that of the author. The drug can be given in the 
form of the tincture or extract by the mouth, or in suppository. If the enuresis is 
only nocturnal, a full dose at bed- time is often sufficient ; if it is also diurnal, the 
remedy should be given also during the day, and pushed till its physiological 
effects are fully felt before it is abandoned as useless.] 



) 



DISEASES OF THE ORGANS OP LOCOMOTION. 



CHAPTER I. 
ACUTE ARTICULAR RHEUMATISM. 

JEtiology. — Acute articular rheumatism is an infectious disease. This is shown 
by all the clinical and anatomical peculiarities of the disease ; and, although the 
specific organic pathogenetic poison can not yet be demonstrated, still this view of 
the disease, which was first brought forward by Hiiter, is the only one which ena- 
bles us properly to understand its symptoms and course. 

Like many other infectious diseases, acute articular rheumatism is often indis- 
putably endemic and epidemic. According to Hirsch, the disease is most preva- 
lent in the temperate zones, being much rarer in cold and tropical latitudes ; but 
even in Europe it is by no means uniform in its frequency, and certain districts of 
England, Belgium, and Russia are said to be almost exempt from it. It is also 
possible to observe epidemic influences with regard to the frequency of its appear- 
ance, as already intimated. Here in Leipsic, where articular rheumatism is one 
of the most frequent of acute diseases, we have observed for years that at certain 
times there are only a few cases, while at others there is a striking increase in 
then number. Usually attacks are most prevalent in the winter and spring 
months, but again it is sometimes in summer that the disease is especially 
common. 

Among the exciting causes of the disease, taking cold is always mentioned as 
of first importance; and in fact it can not be denied that the influence of cold does 
often seem to contribute to the occurrence of the disease. 

This result, however, seldom follows a single severe exposure, but it rather 
follows persistent causes, and in particular the long-continued influence of wet 
and cold, as in certain occupations — for example, washing and scrubbing, or inhab- 
iting unhealthy damp dwellings, and the like. This explains why those who follow 
certain callings are especially subject to articular rheumatism; thus servant-girls 
and coachmen are frequently victims to the disease. And yet it is possible to 
regard all these injurious influences as being merely indirect causes, inasmuch as 
they favor the development of the specific micro-organisms ; and, furthermore, it 
is by no means exceptional to see a case of articular rheumatism where no history 
of exposure to cold can be obtained. 

Sex exerts no special influence upon the frequency of the disease. As to age, 
acute articular rheumatism is most frequent in young adults between fifteen and 
thirty-five years of age. In later life, and particularly in old age, it is much 
rarer. In children six years old or more the disease is not especially infrequent, 
but in younger children it occurs only exceptionally. We may be permitted to 
mention a single interesting case which we met with here in Leipsic, where a 
child who died when only a few days old, and whose mother at the time of its 



848 



DISEASES OF THE OEGANS OF LOCOMOTION. 



birth, was suffering from a severe attack of acute articular rheumatism, was found 
to have multiple purulent arthritis. 

Much has been said with regard to the relations of acute articular rheumatism 
to other acute diseases. We must, therefore, call particular attention to the fact 
that the joint diseases, whether simple or multiple, which occur after scarlet fever, 
gonorrhoea, or in connection with puerperal and septic diseases, as well as recent 
cases of secondary syphilis, have nothing to do with genuine acute rheumatism. 
In cases of this sort the trouble in the joints is merely a special localization of the 
general disease ; and, indeed, the circumstance that the joints are a favorite point 
of attack for infectious diseases may be brought forward as another proof that 
acute articular rheumatism is of infectious origin. There is, however, a single 
affection, namely, chronic endocarditis, about which the facts are different. This 
disease is setiologically identical with acute endocarditis, and therefore with acute 
rheumatism {vide infra). At least this is true in many cases, although probably 
not in all. It may be regarded as a proof of this connection between the two dis- 
eases that patients with chronic cardiac disease are especially liable to attacks of 
acute articular rheumatism. Here, therefore, we have a genuine articular rheu- 
matism as a symptom of more general disease. It may be regarded in some sense 
as a fresh acute exacerbation of this disease, localized mainly in the joints. 

A very noteworthy fact is that acute articular rheumatism can not be num- 
bered among those infectious diseases which usually occur but once in the same 
individual. This disease, on the contrary, resembles pneumonia and erysipelas, in 
that it is very apt to occur repeatedly in the same person. Acute rheumatism, 
therefore, even when it ends favorably and leaves behind it no evident lesions, 
seems to render the patient more liable to the disease than he was before. 

Symptomatology. — The chief symptom of acute articular rheumatism is an acute 
febrile synovitis, which almost always affects several joints. The synovitis is 
associated with the usual local phenomena of swelling and tenderness in the parts 
affected. Often this articular affection is the first symptom, and, indeed, it may 
be the only symptom of the disease. It is, however, by no means exceptional for 
the arthritic trouble to be preceded by certain prodromal or initiatory symptoms, 
as is true of other infectious diseases. These prodromata consist either of a slight 
general ma]aise, or of certain local symptoms. It is not rare to have sore throat, 
or, as we have repeatedly had opportunity to observe, laryngitis. These pre- 
monitory symptoms are, however, generally insignificant, and may, as we have 
said, be entirely absent. 

The articular disturbance is almost always very rapid in its development. 
Some of the larger joints are usually first affected, and perhaps those of the lower 
extremities somewhat oftener than those of the upper. It is extremely exceptional 
for all the joints that are affected to be attacked at one and the same time. It is 
somewhat characteristic of acute articular rheumatism that it " jumps from one 
joint to another." To-day this joint will be affected and to-morrow that, while the 
joint first attacked may still remain diseased or undergo rapid recovery. Thus, 
there may be either a few joints affected or many, in varying sequence, and they 
may sometimes be affected rapidly and at other times more slowly. In many 
of the milder cases the disease is an extremely temporary one, while in others it 
may attach itself most persistently to some one or more joints. 

There is usually fever in addition to the arthritis ; but it is not usually very 
high, seldom exceeding 103° (39*5° C). The fever, on the whole, corresponds with 
the arthritic phenomena, and does not present a curve which is at all typical, but 
one which is irregularly remittent. We have scarcely ever seen the disease begin 
with an initial rigor, nor are the so-called " general febrile symptoms " of headache, 
stupor, and subjective feeling of heat as a rule at all marked in acute rheumatism. 



ACUTE AKTICULAR KHEUMATISM. 



849 



This indicates that the constitutional infection does not as a rule attain great 
severity. The skin is noticeably inclined to perspiration, but the perspiration is 
not at all a result of any sudden fall in temperature such as is seen in other dis- 
eases. 

The course of the disease is marked by alternate ameliorations and aggrava- 
tions of the local symptoms and of the fever, and lasts, particularly if it is not 
treated, one or more weeks, or a still longer period. Then, as a rule, the symp- 
toms gradually abate and convalescence begins ; but it generally is tedious and 
frequently interrupted by relapses. In other cases, however, the disease contrasts 
strongly with this simple course, for articular rheumatism is notoriously subject 
to numerous complications and peculiarities in its course. The protean character 
of the disease will be evident upon a perusal of the following description of the 
symptoms referable to the different organs of the body. 

Symptoms referable to the Different Organs, and Peculiarities in the Course of 
the Disease. 1. Joints and Sheaths of the Tendons. — The favorable termination 
of most cases of acute articular rheumatism prevents us from often examining the 
anatomical changes in the affected joints ; but there can be no doubt that in most 
instances the trouble is merely a simple serous synovitis — that is, an inflammation 
of the synovial membrane, with an exudation into the cavity of the joint composed 
mainly of serum with but little admixture of fibrine and pus. The synovial mem- 
brane itself, in the cases which do come to autopsy, is usually very little affected. 
It is somewhat injected, opaque, and thickened. Necrosis of the cartilages is seen 
only in severe cases, or in those which have lasted a rather long while. From a 
clinical standpoint, the articular disturbance is noticeable chiefly for the pain 
which it causes the patient upon every movement of the joint and any pressure 
upon it. The painfulness is often in striking contrast with the slight apparent 
change in the structure of the joint, for a joint which is extremely sensitive may 
appear to be scarcely at all diseased. Usually, however, the joints exhibit the 
signs of synovitis. The effusion into the joint produces an evident swelling, 
which can be seen particularly well in the knees, but also in the joints of the 
ankle, wrist, shoulder, and elbow, and sometimes even in the smaller joints of the 
fingers and toes, particularly the great toe. It is rather exceptional to detect swell- 
ing of the hip-joint. It should be remembered, however, that the swelling in the 
region of the joint, particularly the ankle or wrist, is often less the result of a 
synovial effusion than of an inflammatory periarticular oedema. This oedema, 
for example, may extend over almost the whole posterior surface of the hand. 
The joints are by no means invariably the only parts attacked. Not infrequently 
there are analogous inflammatory changes visible in the sheaths of the tendons, 
the bursse, and perhaps, in many cases, even the fasciae and muscles. The skin 
over the affected joints often has an inflammatory blush, which is usually pale 
red and spotted, and can be best seen at the ankle, knee, and wrist. It has been 
maintained that the cutaneous sensibility is diminished over the joints affected, 
but we regard this as a mistake. 

As might be expected, the number of joints attacked and the sequence in which 
they are attacked differ greatly in different cases; but almost invariably a number 
of joints suffer, so that any monarticular arthritis should not be regarded as rheu- 
matic except after careful deliberation {vide infra, diagnosis). It should be said 
that, in mild cases, there may be only two or three joints affected, these being 
usually some of the larger joints of the extremities ; and of these, one may be so 
much worse than the others that their participation in the trouble can be ascer- 
tained only by careful questioning and examination. In severe cases, on the other 
hand, the number of joints attacked is often very great. Such patients become 
extremely helpless, because any movement is possible, if at all, only under the 
54 



850 



DISEASES OP THE OKGANS OF LOCOMOTION. 



penalty of very severe suffering. The patient usually lies with bended knees and 
feet curved so as to be concave on the plantar surface, and screams with pain at 
any attempt to change his position. The joints of the trunk sometimes participate 
in the disease, but hardly ever except in the severe cases. The articulations of the 
vertebrae, the ster no-clavicular joint, the articulation of the lower jaw, and the 
symphysis pubis, are particularly apt to be affected. The fugitive character of 
the arthritis has been spoken of as characteristic of acute articular rheumatism, 
and, indeed, it is not infrequently the case that comparatively large swellings of 
the joints soon abate and yield to new disturbances in other joints ; but, on the 
other hand, the disease may persist very obstinately in a single joint. In this case 
one joint, or rarely several, are attacked with marked severity, either from the 
start or subsequently to milder affections of other joints, and often remain for 
weeks swollen or painful long after a]l other symptoms have vanished. 

2. Cardiac Symptoms. — The condition of the heart in acute articular rheuma- 
tism is next in importance to that of the joints. The physician should therefore, 
in every case, even the mildest, maintain a continuous watch over this organ. In 
1836 Bouillaud made careful auscultatory investigations in this disease, and was 
thus the first to discover that the course of acute articular rheumatism is, with 
noticeable frequency, accompanied by endocarditis, and sometimes even by peri- 
carditis. Complications of this sort may occur in any case, whether mild or severe, 
or may be absent in any case, even the worst. They may develop at the beginning 
or later on in the course of the disease. Their development is often unattended 
by any subjective symptoms, so that they can be recognized only by careful phys- 
ical examination. In many cases, however, the onset of cardiac disease is marked 
by a fresh exacerbation of the fever, or possibly by palpitation, or by painful sen- 
sations in the prsecordia, or by dyspnoea. 

We will consider first rheumatic endocarditis. This is almost always the benign 
verrucous variety (see page 259). 

It is far more prone to attack the mitral than the aortic valves, and is accord- 
ingly usually betrayed by a blowing systolic murmur at the heart's apex. Uncer- 
tainty may be cast upon the diagnosis by the fact that functional murmurs are 
not very infrequent at the apex of the heart in cases of acute articular rheuma- 
tism. We once observed a case of " hyperpyretic rheumatism " {vide infra) where 
there was an evident murmur of this sort during life, and yet at the autopsy we 
were able to assure ourselves of the complete integrity of the cardiac valves. 
Even an expert may for a time be in doubt as to the significance of many cardiac 
murmurs, and this explains in part the conflicting statements as to the frequency 
of cardiac complications in acute rheumatism. In general, one may say that such 
complications occur in 25 to 33 per cent, of the cases. The ultimate results of this 
endocarditis we do not need to describe over again in this connection (see the chap- 
ters on acute and chronic endocarditis ) . Complete recovery is possible. Often, how- 
ever, the lesion gives rise to a chronic endocarditis — that is, to a cardiac valvular 
disease, which lasts through life. 

The close connection between endocarditis and the arthritis must formerly 
have seemed very puzzling, despite the many hypotheses made to explain it. If, 
however, we regard acute articular rheumatism as an infectious disease, this 
obscurity vanishes. Acute articular rheumatism is plainly not a merely local 
disease, but the result of a general infection. The specific pathogenetic matter is 
not only present in the joints affected, but it also circulates in the blood. It is there- 
fore easy to understand why the valves of the heart should be attacked by it, as is 
the case in so many infectious diseases (see page 257). Often the specific properties 
of the micro-organisms in question produce a typical endocarditis. The endocar- 
ditis, therefore, is not strictly a " complication," but a symptom of the disease. 



ACUTE ARTICULAR RHEUMATISM. 



851 



Rheumatic pericarditis is not infrequent, although less common than endocar- 
ditis. The only certain way to recognize it is by a characteristic friction-sound ; 
and even when this is heard there may be a doubt as to its significance, inasmuch 
as functional murmurs are not infrequently heard at the base of the heart. The 
pericarditis is of a sero-fibrinous nature. Sometimes it is of slight severity ; but it 
may be extremely severe, with a large effusion and the most urgent dyspnoea 
(see page 300). In rare instances this pericarditis proves fatal. Usually, however, 
recovery ensues, although in severe cases there may be obliteration of the peri- 
cardial sac, with the consequences described on page 303. 

With regard to the origin of the pericarditis, it may be said that it would not 
be impossible for the pericardium to be directly infected by the blood. We have 
reason, however, to believe that in most cases the infection proceeds from the 
endocardium, and probably in the great majority of cases from the aortic valves 
(see page 279). It is not always possible to prove that an endocarditis precedes the 
pericarditis, but yet this does not overthrow the opinion we have expressed, inas- 
much as many cases of acute endocarditis do not betray themselves by any audi- 
ble murmurs. 

We should also mention that there may be functional cardiac derangement 
without any grave anatomical lesion. We have already spoken of the functional 
murmurs. There may also be a rapid and irregular pulse, and, in rare instances, 
attacks of angina pectoris of apparently purely nervous origin. 

3. Serous and Mucous Membranes. — The pleura and peritoneum, as well 
as the pericardium, may be affected in articular rheumatism ; so that it was for- 
merly often maintained that acute articular rheumatism is a disease of the serous 
membranes of the body in general, inclusive of the joints. Rheumatic pleurisy is 
much rarer than either endocarditis or pericarditis ; and rheumatic peritonitis is 
rarer still. The pleurisy, at least in most instances, is propagated directly from 
an inflamed pericardium; and in the same way the peritoneum may become 
infected from the pleura by way of the diaphragm. Few of these severe cases, pre- 
senting a simultaneous inflammation of several serous membranes, occur, now 
that the salicylic-acid treatmeut has been introduced. We do not say that it is 
absolutely impossible for a pleurisy or a peritonitis to occur in rheumatism with- 
out inflammation in any other serous cavity, but such an occurrence is extremely 
rare. 

The mucous membranes are seldom greatly affected in acute articular rheuma- 
tism. As has already been stated, a catarrh of the pharynx or larynx sometimes 
occurs in the beginning of the disease. Bronchitis is often spoken of by the older 
authors ; but it is probably in many cases not due directly to the rheumatism, but 
it is a complication, just as in any disease attended by great prostration. The 
stomach and intestinal canal are seldom especially affected. 

4. Skin. — Cutaneous phenomena are not infrequent in the course of acute 
articular rheumatism. A prominent symptom of the disease is the tendency to 
profuse perspiration. The perspiration often has a strongly acid odor and reac- 
tion. Many patients exhibit an abundant crop of sudamina, the back in particu- 
lar being sometimes entirely covered. Sometimes there are other cutaneous 
eruptions. In a whole series of cases we observed erythema nodosum. This 
affected the lower extremities more than the upper. Urticaria is not very infre- 
quent, while herpes labialis has been very rare in our experience. It is well 
known that arthritic affections and the so-called " hgemorrhagic diseases " are in 
many ways related to each other ; and it is therefore an interesting fact that 
extensive hsemorrhagic disturbance of the skin also occurs in connection with 
acute articular rheumatism, as we have repeatedly had opportunity to observe. 
We have seen several cases of haemorrhagic urticaria : wheals appear upon the 



852 



DISEASES OF THE ORGANS OF LOCOMOTION. 



skin, and a haemorrhage takes place into their centers and spreads gradually. 
There may also be simple cutaneous ecchymoses. These may in severe cases be 
merely one symptom of a general hsemorrhagic diathesis, with haemorrhages 
from mucous membranes. The occurrence of these symptoms again points most 
clearly to the infectious character of acute articular rheumatism. 

5. The Muscles Am> Nervous System. — In most cases of acute articular rheu- 
matism there are no nervous symptoms whatever ; but occasionally the latter may 
assume very great importance. 

Among the milder symptoms are rheumatic atrophy of the muscles and paraly- 
sis. It is a universal law that certain definite trophic relations exist between 
the joints and the muscles which correspond to them, such that any grave 
and persistent derangement of a joint necessarily involves atrophy of the corre- 
sponding muscles. This atrophy has long been recognized, and was formerly 
regarded, particularly by surgeons, as merely the result of inactivity of the mus- 
cles — " atrophy from disuse " — but this view is certainly erroneous. "We do not 
know its precise cause, but it is without doubt the result of the disease of the joint, 
and may therefore be termed "muscular atrophy of arthritic origin." If an 
attack of acute articular rheumatism affects any one joint for a long period there 
is a secondary atrophy of the corresponding muscles. This is seen most often, and 
in its most typical form, where there is obstinate trouble in the shoulder-joint, the 
deltoid becoming extremely atrophied. This atrophy of the muscles may con- 
tribute largely to the sum-total of functional derangement. We have repeatedly 
seen cases where the patient could hardly lift his arm at all, although the inflam- 
mation of the shoulder- joint had passed away, and that without leaving any 
anchylosis. It is therefore entirely justifiable to speak of a rheumatic paralysis. 
Many authors have attempted to explain its occurrence by saying that the inflam- 
mation of the joint is propagated to the nerves and muscles ; but this is not very 
probable. At least it is noteworthy that the atrophied muscles respond promptly 
to the faradic current, and never exhibit the reaction of degeneration. This indi- 
cates that the atrophy is not due to neuritis. 

Chorea (vide supra, page 739) may be a sequel of acute articular rheumatism. 
This complication is seen most frequently in children. Endocarditis may accom- 
pany it, but it does not always do so. 

There are certain peculiar cases of acute articular rheumatism which excite the 
greatest interest. In these, very severe cerebral symptoms are developed, and often 
most acutely. They are therefore called " cerebral rheumatism " ; or, as they are 
almost always characterized by an extraordinarily high temperature, another name 
is "hyperpyretic articular rheumatism." In these cases the disease may exhibit 
severe nervous symptoms from the start, particularly delirium ; or it may at first 
ran an apparently favorable course, and not change for the worse until after sev- 
eral days, or even at a later period. The change may be quite abrupt. The tem- 
perature rises to 104° or 106° (40°-41° C). There are great uneasiness, delirium, 
and sometimes also signs of motor irritation, such as general convulsions, or tonic 
spasm of the extremities, or trismus. The face grows pale and cyanotic, the pulse 
small and extremely rapid. With slight interruptions, the temperature continues 
to rise, and attains 107"5° to 109'5° (42°-43° C'). This great rise is most apt to occur 
just before death, and there may be a still further increase of temperature after 
death occurs. As has been implied, the termination is usually unfavorable. It 
is only in exceptional cases that recovery takes place. 

It has been stated that cerebral rheumatism attacks mainly hard drinkers and 
other individuals whose nervous system has been previously impaired ; but our 
own experience does not confirm this view. No case is absolutely secure from the 
occurrence of hyperpyrexia ; but it is a very rare phenomenon, occurring perhaps 



ACUTE ARTICULAK RHEUMATISM. 



853 



once in several hundred cases. On post-mortem examination, the brain seldom 
shows any change in these cases of cerebral rheumatism. We are therefore 
obliged to regard the condition as the result of an unusually severe infection, 
affecting chiefly the intellectual, motor, and thermal centers. Cases have also 
been reported where there have been actual anatomical lesions of the brain — in 
particular, purulent meningitis. Probably, however, most of these cases, were 
falsely diagnosticated, the observer having confounded articular rheumatism with 
epidemic meningitis, pyaemia, and similar diseases. Of course, if there is endocar- 
ditis, cerebral embolism is possible. Mental derangements deserve a brief men- 
tion. They rarely occur during the course of the disease, but are somewhat more 
frequent after it has terminated. We may have either melancholia attended with 
marked excitement or anxiety, or a more general insanity. The prognosis is usu- 
ally favorable. 

6. Other Viscera. — Other parts of the body than the heart, the serous mem- 
branes, and the brain, are seldom much affected in articular rheumatism. Lobar 
pneumonia occurs only in especially severe cases, but in such may attain quite a 
considerable development and occasion great dyspnoea. It usually requires quite 
a long while to recover from it. Lobular inhalation-pneumonia may also occur 
in severe cases. Acute nephritis has certainly sometimes occurred, but it is ex- 
tremely rare. The spleen may be somewhat swollen, but it is not the rule to find 
a splenic tumor, such as is present in other acute infectious diseases. 

7. General Symptoms. — In many cases the general condition of the patient is 
but little affected, but in others the disease seems to exert a peculiar influence 
upon the constitution. This may show itself in a striking anaemia; and we have 
observed this repeatedly where there was no cardiac complication. Another 
much more dangerous, but extremely rare, complication has already been briefly 
referred to, namely, the occurrence of a general haemorrhagic diathesis. This is 
almost always associated with high fever and great prostration, and is usually 
fatal. 

Course, Duration, and Prognosis. — Acute articular rheumatism may be described 
in general as a benign disease, for it usually terminates in recovery. It is only in 
a very few cases that an unfavorable termination takes place immediately, Avhether 
as the result of pericarditis or other severe cardiac complication, or from hyper- 
pyrexia, or the development of a general haemorrhagic diathesis. The entire dura- 
tion of the disease varies greatly according to its severity. There are mild cases 
which terminate in a few days ; and, on the other hand, the disease may be very 
tedious, lasting for weeks and months, and finally merging into chronic articular 
rheumatism. Quite often the violent symptoms experienced at first disappear 
quite rapidly, but only to be replaced by such milder ones as pain and stiffness of 
the joints — these latter persisting for a long while. It is a general rule that the 
severity and persistency of the case correspond with the number of joints affected ; 
but to this rule there are numerous exceptions. The disease may persist with 
great obstinacy in a single joint. It need hardly be said that the duration of the 
disease is greatly modified by the occurrence of complications, cardiac or other- 
wise, and such sequelae as muscular atrophy, anchylosis of the joints, or chorea. 
The most important of all sequelae is cardiac disease, and this must always be 
considered in giving a prognosis ; for, although the disease as such does in most 
instances terminate in recovery, yet too often it gives rise to a tedious and usually 
incurable disease of the heart. It is, however, true that complete recovery from 
the acute endocarditis seen in articular rheumatism is possible, but in a large 
majority of cases recovery is not complete, and the acute passes into a chronic 
endocarditis. In these cases the cardiac symptoms may be developed directly, so 
that the patient at once begins to complain of palpitation and shortness of breath ; 



854 DISEASES OF THE ORGANS OF LOCOMOTION. 



or lie may seem to regain his health completely, and a murmur which the phy- 
sician alone can detect be the only sign of the incurable injury which the body 
has suffered. The patient may feel perfectly well for years after, and then at last 
begin to suffer from the failure of compensation (see page 264 et seq.) 

Diagnosis. — Most cases of articular rheumatism can be easily recognized, for 
the acute occurrence of pain and swelling in several joints is sufficiently charac- 
teristic of the disease. It shou]d, nevertheless, be borne in mind that articular 
swelling may also take place in the course of other diseases, and that mistakes in 
diagnosis are by no means impossible. "Where there are grave constitutional 
symptoms, with fever, from the start, we should not forget the possibility of 
pyaemia, or of acute osteomyelitis, since these affections occasionally give rise to 
the swelling of several joints. In such cases, however, careful attention to the 
further course of the disease will generally enable us to see that we can not be 
dealing with a simple acute articular rheumatism. Again, after childbirth there 
may be swelling of the joints, of septic origin, and therefore entirely independent 
of any genuine rheumatic infection. 

If a single joint is attacked, the diagnosis of articular rheumatism must be 
made with extreme caution. These monarticular inflammations often prove to be 
something entirely different, namely, fungous disease of the joint, or an osteo- 
myelitis. The arthritis which follows gonorrhoea is also sometimes monarticular 
(affecting especially the knee-joint), or at any rate it is confined to the lower extremi- 
ties ; and, in conclusion, it should be stated that it is not very rare to observe pain 
and swelling in various muscles and joints at the commencement of the secondary 
stage of syphilis, simulating an acute articular rheumatism. 

Sometimes the diagnosis is doubtful in those cases which present cutaneous 
ecchymoses (purpura and peliosis) and erythema nodosum, because we may be 
unable to determine which should be regarded as the primary symptoms and 
which the secondary ; but in these cases, after all, it is often merely a question of 
nomenclature, and the best way is to follow the rule that the greater should include 
the less. 

Genuine gout (q. v.) can usually be readily diagnosticated from articular rheu- 
matism by its localization in the toe, and by the gastric and other symptoms 
which attend it. 

Treatment. — Acute articular rheumatism is one of the few diseases for which 
we possess an undoubtedly specific and universally accepted remedy. Kolbe sug- 
gested its use, and since 1876 it has been largely employed upon the recommenda- 
tion of Strieker, Buss, and others, for articular rheumatism. This remedy is sali- 
cylic acid. Although this medicine does not in all cases produce its surprisingly 
favorable results with equal rapidity and completeness, yet it almost invariably 
does produce a decided and beneficial effect upon the disease. "We might even 
say that this influence is so constant that where salicylic acid proves entirely 
inefficient in a fresh case, such failure throws doubt upon the correctness of the 
diagnosis. Thus, where there is monarticular arthritis dependent upon some local 
cause, the remedy has hardly any beneficial influence. The same is true with 
regard to affections of the joints connected with gonorrhoea, pyaemia, and similar 
troubles. In genuine acute articular rheumatism, on the other hand, the salicylic- 
acid treatment is so superior to any other that it is the first duty of the physician 
in every case to give this remedy a fair trial. 

There are but two preparations of salicylic acid used in rheumatism — the pure 
acid and its sodium salt, salicylate of sodium. Each of these two remedies has its 
peculiar advantages ; but the specific influence of each is about the same. Sali- 
cylic acid should never be prescribed in solution, but always in capsules, usually 
containing ten grains (grm. 0'50). In this way the salicylic acid can be taken by 



ACUTE ARTICULAK KHEUMATISM. 



855 



almost any patient quite easily, especially if a little water or milk be drunk after 
each dose. Adults should receive ten grains every hour until about one or two 
drachms (grm. 5-8) have been administered. Usually there will by this time be a 
very decided abatement of the articular pain and swelling, while, on the other 
hand, there will also usually be such toxic " salicylic symptoms " (vide infra) as 
to forbid its further use. The salicylate of sodium is best exhibited in single large 
doses of a drachm to a drachm and a half (grm. 4-6), each dose being given 
with about an ounce (grm. 20-30) of peppermint-water. The quite disagreeable 
taste of the medicine is only exaggerated by the addition of such things as syrup 
or fluid extract of licorice, added for the sake of elegance ; but the simple solution 
in peppermint- water is quite well taken, at least by most patients. The advan- 
tage of the salicylate over the pure acid consists in its being possible to give a 
larger dose at one time, so that it need not be taken more than two or three times 
a day. In general, the amount given in twenty-four hours should not exceed two 
and a half drachms (grm. 10) ; one and a half to two drachms (grm. 6-8) may 
suffice. For children the dose is, of course, smaller, say five grains of salicylic 
acid (grm. 0*30), or half a drachm to a drachm (grm. 2-4) of the sodium salt. 

Which of these two preparations shall be employed is, as has been stated, of 
little consequence. We ourselves usually prescribe, at first, capsules of salicylic 
acid to be taken hourly, as being most agreeable to the patient ; but, if our first 
visit is made in the evening, we prescribe a single large dose of a drachm to a 
drachm and a half (grm. 4-6) of salicylate of sodium, so that the patient may not 
be disturbed every hour through the night in order to take medicine. It is often 
possible to give the two remedies in alternation. This is a good way later on in 
the disease, when the patient has already acquired a distaste for the medicine. 
In such cases also it may be desirable to give the salicylate of sodium as an 
enema. About two and a half drachms should be given, in two ounces of water 
(grm. 10 and 60). There is no doubt that the specific effects can be obtained in this 
manner. 

The benign influence of this remedy upon the disease is apparent in many 
fresh cases as early as ten to eighteen hours after treatment begins ; and it is often 
astonishing to see how soon a patient, who before lay helpless and complaining, 
becomes free from pain and able to move his limbs. It must be confessed, how- 
ever, that, apart from its taste, salicylic acid may produce disagreeable incident- 
al effects. In the first place, there may be nausea with epigastric distress, and 
even vomiting. Tinnitus aurium may be exceedingly troublesome, and may be 
attended with marked vertigo. In somewhat rarer instances the mind is pecul- 
iarly affected. Young girls in particular are often peculiarly excited ; but the 
frame of mind is, however, in general a cheerful one. After large doses there 
maybe an actual " salicylic delirium." It should also be said that respiration 
may be affected, becoming very deep and rapid (salicylic dyspnoea). All these 
incidental effects, and particularly the nausea and ringing in the ears, render 
difficult the employment of the remedy in those large doses which alone are of 
any benefit. This is the more unfortunate, as it is often very desirable to employ 
salicylic acid persistently. 

Although it is not exceptional to have the symptoms almost entirely vanish 
at the end of one or two days, yet it is only in the minority of cases that the 
entire process ends with this release from pain. There is very often, sooner or 
later, a relapse, with fresh pain or even fresh swelling in one or more joints. It 
has been recommended to continue the salicylic acid in smaller doses for some 
time, in order to avert such relapses ; but of late we have abandoned this method, 
for the reason that these small doses do not prevent the return of the disorder, but 
are calculated to give the patient a strong dislike to the remedy, and lessen his 



856 



DISEASES OF THE OEGANS OF LOCOMOTION. 



confidence in it. We therefore recommend to stop the medicine entirely as soon 
as the pain ceases, and to guard the patient as much as possible from relapses by 
preventing his catching cold {vide infra). If there is fresh pain, we should at 
once resume the acid or its salt in large dosas, and thus we will very frequently 
be able to cut short the relapse at once. 

[One other salicyl compound deserves mention — the oil of wintergreen ; this 
has been used largely by Kinnicutt, who finds it efficacious, easy to take, and not 
likely to produce the unpleasant symptoms which sometimes follow the com- 
pounds in more general use. It is given in doses of m, x-xv every two hours, 
either in milk, on sugar, or in capsules. 

The salicylic treatment markedly diminishes the pain and fever, shortens the 
time spent in bed by four or five days, does not shorten the time spent in hospital, 
and seems to have little or no influence on the cardiac complications. The full 
alkaline treatment does not curtail the pain and fever in the same degree, but 
does seem to afford some protection against the heart affection, and to shorten the 
stay in hospital several days. 

Consequently, a combination of the two methods deserves a more extended 
trial than it has yet received. Fenwick recommends beginning with a free purge, 
followed by twenty-grain doses of salicylate of sodium hourly for six hours ; an 
interval of twelve hours is then to be allowed without medicine, after the expira- 
tion of which time thirty-grain doses of citrate of potash are to be given every 
four to six hours until the saliva becomes alkaline. 

It has seemed to me distinctly useful to envelop the painful joints in cloths 
kept wet with laudanum and water, either in equal parts or with a larger propor- 
tion of water, according to the intensity of the inflammation ; as the pain and 
swelling subside, cotton batting, held in place by a few turns of roller bandage, 
can be substituted.] 

Despite the admirable qualities of salicylic acid, it must be confessed that we 
can not always bring about a rapid and complete cure of the disease by this rem- 
edy. There are cases where, although at first evident improvement follows its 
use, relapses continually recur, or the disease fastens itself obstinately in single 
joints. In such, the continued use of salicylic acid proves almost unavailing, and 
indeed the patient can hardly be persuaded to take it. These cases deserve the 
name of subacute. There are still other internal remedies which should be tried, 
but the effects of which are rarely satisfactory. Most important among these are 
iodide of potassium and the preparations of colchicum (tincture of colchicum, 
twenty-five to forty drops several times a day). Numerous other remedies have 
been recommended, and were formerly largely employed, but at present they are 
almost abandoned. Among these are large doses of the alkalies (such as bicar- 
bonate of soda), trimethylamine, veratrine, and quinine. Local treatment of the 
diseased joints is far more important and effective in such cases. Properly exe- 
cuted massage deserves special mention, as its effects are often very brilliant. 
Electricity also may have a beneficial effect, particularly the galvanic current. 
We would caution against the too early use of warm baths, as these often aggra- 
vate the pain instead of mitigating it. Steam baths are sometimes very beneficial, 
but may also do harm, and should therefore be given only when the acute inflam- 
matory symptoms have entirely vanished, leaving behind only stiffness and ten- 
derness in the joints. 

The application of an ice-bag in genuine articular rheumatism is seldom neces- 
sary, but it may sometimes be desirable where there are violent and obstinate symp- 
toms of acute inflammation. Warm, moist applications are useless if not harmful 
in acute cases. In the advanced stages of subacute cases, a wet pack may afford 
some relief. Painting the skin over the joints with tincture of iodine produces no 



ACUTE ARTICULAR RHEUMATISM. 



857 



effect in acute cases ; and even in the chronic ones it is probably mainly a subject- 
ive remedy. Some observers report that injections of carbolic acid beneath the 
skin of the affected joints greatly relieve the pain. A Pravaz's syringeful (thir- 
teen minims) of a one-per-cent. solution may be injected one to three times a 
day. We have had no personal experience with this remedy. In all severe cases 
careful attention should be given from the start to maintaining a correct position 
of the diseased joints, because of the possibility of anchylosis. Before salicylic 
acid was introduced, " the treatment of articular rheumatism with splints " was 
largely and very advantageously employed. The use of salicylic acid has greatly 
diminished the necessity of such procedure, but even now it is sometimes required. 
It is often possible to give the patient great relief by applying a suitable paste- 
board or wooden splint to an affected extremity. 

General hygienic and dietetic treatment should not be undervalued. An 
equable temperature should be carefully maintained in the sick-room, inasmuch 
as cold, or draughts, or moisture have very often been found to exert an evil 
influence upon the disease and excite fresh pain. The patient should, therefore, be 
kept warm, and it is sometimes advantageous to wrap up the affected joints in cot- 
ton batting. It is of great importance that even in the mildest cases the patient 
should be strictly confined to bed, and should by no means get up too soon. If 
possible, we keep our own patients in bed for a week after the pain has ceased. 
Getting up too early will very often bring on a relapse. With regard to diet, 
milk is the best food. We may also allow soup, eggs, and a little meat. In 
France, great weight is laid upon an exclusive milk diet ; but this would seem to 
us an extreme view. 

We do not need to speak at length about the treatment of the complications 
and sequelae, since we should merely repeat what has already been said in the 
appropriate chapters of this work. There has been much said on both sides as to 
the influence of salicylic acid in preventing complications, particularly cardiac 
complications. This much is certain, that cardiac complications are not absolutely 
prevented by the salicylic treatment, and that they too frequently occur while it 
is being employed ; but we do believe that this treatment decidedly shortens the 
course of the disease as a whole, in many instances, and thus lessens the liabil- 
ity to endocarditis. If, however, a cardiac complication has made its appear- 
ance, salicylic acid does not apparently exert any appreciable influence upon it. 
Another important question is in regard to the efficiency of salicylic acid in the 
graver forms of articular rheumatism, particularly in cerebral rheumatism. It 
may be stated, in the first place, that here in Leipsic cerebral rheumatism has 
apparently become much less frequent since the salicylic treatment was intro- 
duced. At any rate, not a single case of hyperpyrexia has occurred in the clinique 
in this city out of many hundred cases treated, where the salicylic acid was prop- 
erly employed from the first. We had an opportunity to observe a case in which 
hyperpyretic symptoms had already appeared when we first saw it, and which had 
not been treated with salicylic acid. Here large doses of that remedy produced 
no effect. We should nevertheless be inclined to employ it, first of all, in such 
cases ; and the energetic use of cool baths would probably be the most speedy way 
of modifying the dangerously high temperature. Stimulants, in particular cam- 
phor, are also required in these severe cases. 

In the severe haemorrhagic varieties of rheumatism we should also give sali- 
cylic acid a trial. The milder haemorrhagic cases (haemorrhagic urticaria) do well 
under ordinary methods of treatment. 

If the acute affection merges into a chronic condition of stiffness and swelling 
of certain joints, such as the wrist or shoulder, we must employ the same reme- 
dies as in chronic articular rheumatism. Massage furnishes the best results. 



858 



DISEASES OF THE ORGANS OF LOCOMOTION. 



Warm baths may also be ordered in such cases (see the following chapter). The 
patient might be sent to Teplitz or Wiesbaden. 

Prophylaxis requires, first of all, that one should avoid cold or wet, and other 
" rheumatogenous influences." Persons who have already had one attack of 
articular rheumatism must be especially careful, inasmuch as they are more than 
ever liable to the disease, as has already been said. It is not inconsistent, how- 
ever, with the exercise of due caution, to endeavor to lessen the sensitiveness of 
the skin by such procedures as cold sponging, followed by friction. 



CHAPTER II. 

CHRONIC ARTICULAR RHEUMATISM (CHRONIC POLYARTHRITIS) 
AND ARTHRITIS DEFORMANS. 

iEtiology. — The two diseases known as " chronic articular rheumatism " and 
"arthritis deformans" are considered together here, because it is impossible to 
draw a sharp distinction between them. It is, indeed, not unlikely that the above 
names are sometimes applied to diseases which differ essentially from each other ; 
but, as we do not yet understand the nature or the aetiology of many chronic dis- 
eases of the joints, we must provisionally be guided by the external changes they 
produce. We shall, therefore, embrace all chronic inflammatory processes affect- 
ing the joints under the name of chronic arthritis. Traumatic arthritis it is not 
intended to include, much less those chronic affections of the joints which are evi- 
dently of tubercular origin, and which have ordinarily been termed fungous 
arthritis. These belong to the domain of surgery. We would also exclude 
chronic syphilitic diseases of the joints, about which, indeed, there is still less 
known than about the tubercular affections; besides, they are extremely rare. 

The aetiology of those cases of chronic arthritis where the disease is a direct 
sequel of acute articular rheumatism is evident enough. It is hardly possible to 
doubt that the same specific poison which excited the acute arthritis maintains 
possession of the joints, and produces the chronic inflammatory changes. Cases 
of this sort especially deserve the name of chronic articular rheumatism. They 
are not very infrequent, and may be of slight or great severity. The worst cases 
produce macroscopic changes which fully justify the other appellation of arthritis 
deformans. 

It is also possible that many cases which are chronic from the start have the 
same setiological origin — that is, are due to the same pathogenetic agents. This 
might be inferred from analogy with numerous other diseases, and is rendered 
still more probable by the fact that the same exciting causes which promote acute 
articular rheumatism often play a conspicuous part in chronic arthritis. Such 
causes are exposure to cold and wet, and working in cold or draughty places, or 
dwelling in newly built and damp houses. This explains why those who follow 
certain callings — for instance, washer-women — are more apt to suffer from the 
disease than others, and why arthritis deformans has, with some justice, been called 
a disease of the poor, in contrast with the gout of the wealthy. Many of the laity, 
and even some physicians, believe that gout and arthritis deformans are in some 
way related, but this view is erroneous. 

It is very questionable whether all cases of chronic multiple arthritis are refer- 
able to the causes already enumerated. Such other influences, however, as are 
concerned in its production are not at all understood. Various authorities have 
maintained that arthritis deformans is the result of a primary disease of the nerv- 



CHRONIC RHEUMATISM AND ARTHRITIS DEFORMANS. 859 



eras centers, and in particular of the spinal cord. We regard this statement as 
entirely uu warranted. It originated at a time when there was a tendency to 
ascribe all sorts of ills to disease of the " trophic centers," but there is no doubt 
that this tendency was carried very much too far. We may state in this connec- 
tion that a careful microscopic examination of the spinal cord in one case of 
very severe arthritis deformans yielded an entirely negative result. 

Predisposing Influences. — Chronic arthritis is mainly a disease of advanced 
years. Certain monarticular varieties, about whose aetiology, it must be confessed, 
we know little as yet, have been termed arthritis senilis — in particular the malum 
coxce senile. Even the common and, in a certain sense, typical form of arthritis 
deformans {vide infra) is not apt to occur in people under thirty-five years of age. 
This rule, however, has exceptions, and we have ourselves seen a few perfectly 
characteristic cases of arthritis deformans in children between ten and fifteen 
years of age. Women are much oftener attacked than men. It is often said that 
trouble, anxiety, and other emotional influences favor the outbreak of the disease ; 
but the proof of this is lacking. The disease does not often seem to be hereditary. 

Pathology. — The process is described as simple chronic arthritis so long as it is 
confined mainly to the synovial membrane of the joint and the periarticular con- 
nective tissue. These parts often undergo decided inflammatory thickening ; the 
synovial membrane becomes cloudy ; and the amount of synovial fluid is more or 
less increased — that is, we have chronic dropsy of the joint. Sometimes different 
parts of the synovial membrane are connected by adhesions, which considerably 
interfere with the movements of the joint. There may even be complete anchy- 
losis : for example, in the shoulder or knee. 

Chronic synovitis may pass imperceptibly into arthritis deformans. In this, 
not only the capsules of the joint, but the articular cartilages and the articular 
extremities of the bones, are so much affected as to produce the most striking 
deformity. These changes almost always originate in the articular cartilages. 
The cartilage is roughened and worn away ; its free borders and surfaces undergo 
proliferation and then disintegration ; or become polished on the surface, while 
deeper in the newly formed layers of cartilage undergo ossification. The under- 
lying bone undergoes inflammation and degeneration. Sometimes, also, the 
periosteum near the joints undergoes ossific periostitis. On microscopic examina- 
tion, we find fibrous disintegration of the matrix of the cartilage, and prolifera- 
tion and subdivision of the cartilage-cells, at the same time that there is destruc- 
tion of the newly formed cells by simple or fatty degeneration. Analogous 
processes of proliferation and destruction also affect the bony structures. The 
synovial membrane is invariably affected in cases of any severity. Usually the 
most striking change is a great proliferation of the joint villi, which may cover 
the walls of the cavity like great fringes. 

Of course the normal structure of the joint is at last completely destroyed by 
these various processes. The articular extremities of the bones waste away more 
and more, and take new relative positions, as the parts which impinge upon each 
other are worn away. Externally, the joint usually becomes larger and larger ; 
and this is the more evident because the surrounding muscles undergo great 
atrophy. Often there is no synovial fluid whatever {arthritis sicca), but some- 
times there is a considerable effusion : for instance, in the knee-joint. 

Clinical History. — The symptoms of chronic arthritis are usually quite simple 
and uniform. They are almost exclusively referable to the local disturbances 
and their results. 

Except in the cases which are preceded by acute articular rheumatism, the dis- 
ease usually begins quite gradually and insidiously. The first subjective symp- 
toms are stiffness and pain in the joints, the latter being aggravated by pressure 



860 



DISEASES OF THE ORGANS OF LOCOMOTION. 



/ 



I 



or movement. The stiffness is most noticeable when the joint has remained quiet 
for some time previous, and is therefore ordinarily greatest on waking up in the 
morning. The pain often shoots from the joints upward and downward, and is 
of a burning character, or less often neuralgic. Even in advanced cases, the pain 
usually occurs only when the affected joints are moved, although then it may be 
very severe. When the body is entirely at rest there is little or no pain. Motion 
is impaired very early. This is due at first to the pain, and to a certain reflex inhi- 
bition and ataxia of the muscles ; to which are later added the purely mechanical 
hindrances and the ever-increasing atrophy of the muscles. 

The objective changes in the affected joints begin to appear soon after the 
symptoms just mentioned, at least in cases of any severity. The joints seem 
enlarged and thickened. If we attempt to move them, we not only cause pain, 

and meet with mechanical obstruction, 
I but we may hear and feel the cracking 

'\ and grating produced by the rubbing 

/ of the denuded and uneven surfaces 

upon each other. This is often noticed 
by the patient himself. As the disease 
gradually progresses, there are usually 
developed certain characteristic defor- 
mities, which are apt to be most strik- 
ingly exhibited in the hands (see Fig. 
109). The metacarpophalangeal joints 
are thickened and swollen, and are 
made all the more prominent because 
the interossei upon the back of the 
hand are atrophied. The bases of the 
first phalanges are directed obliquely 
toward one side, so that the Angel's as- 
sume more and more the appearance of 
subluxation. They are bent over to- 
ward the back of the hand, and are also 
displaced toward the ulnar side, so that 
they often actually come to rest one 
upon the other. The palm of the hand 
is often deeply hollowed out. Often 
the phalangeal joints are also distorted, 
so that, for example, there will be an 
obtuse angle on the dorsal surface of 
the fingers between the first and second 
phalanx, while the terminal phalanx is 
apt to be flexed, although the second 
phalanx preserves a position of extension. Despite these changes, many patients, 
if only their thumb remains tolerably movable, are able to use their hands for 
quite delicate work, although at the expense of much time and effort. The feet 
exhibit analogous deformities, but seldom to the same extent as the hands. The 
knees and elbows are likewise enlarged. At the hip-joint, subluxation is not 
infrequent, the head of the femur slipping upward. The motion of the shoulder- 
joint, and as a consequence the use of the arms, is gradually more and more im- 
paired. If the joints of the lower extremities are affected, of course it becomes 
painful and difficult either to get up or to walk. It may finally be necessary 
for the patient to have the help of some other person, or of crutches. 

There are monarticular and polyarticular forms of the disease — the name indi- 




Fig. 109.— Appearance of the hand in a case of pro- 
tracted arthritis deformans. 



CHRONIC RHEUMATISM AND ARTHRITIS DEFORMANS. 861 



eating' that one or several joints are affected. The monarticular form is usually 
regarded as a surgical trouble, and is most often located in the hip- joint {malum 
coxae senile), or more rarely in the knee- and shoulder- joints. The polyarticular 
form is the characteristic one. In most of the typical cases it begins in the small 
joints of the hand and fingers. At a later period the larger joints are also invaded, 
one after the other, the invasion taking place symmetrically on both sides of the 
body, although the disturbance is not infrequently greater on one side than on the 
other. In severe cases, the joints of the spinal column are also involved. This 
impairs particularly the movement of the head. The articulation of the lower 
jaw is usually very little affected, if at all. 

In less frequent instances the arthritis is confined principally to the lower 
extremities, while the upper escape intact for a long while, or even permanently. 
It is very possible that such cases often have a different aetiology from ordinary 
arthritis deformans ; and the same is true of the cases which are confined mainly 
to the vertebral column, and are termed spondylitis deformans. A remarkable 
and, as it seems to us, unique disorder may be mentioned in passing. It leads 
very gradually and painlessly to a complete anchylosis of the entire spinal column 
and the hip-joints, so that head, trunk, and thighs are firmly united and com- 
pletely stiffened, while all the other joints retain their normal mobility. It need 
scarcely be said that this necessarily causes a peculiar modification of the carriage 
and gait of the sufferer. We have ourselves seen two cases of this peculiar affec- 
tion which resembled each other very closely. 

There is hardly any affection of parts of the body other than the joints in 
arthritis deformans. The muscles should be excepted, for they always undergo 
that muscular atrophy which we have already described {vide page 852) as the 
result of joint disease. This atrophy is most marked in the interossei and in the 
muscles of the calf and thigh. Sometimes the skin over the wrist and other 
affected joints appears peculiarly wrinkled and flabby. The internal organs 
almost always perform their functions in a perfectly normal manner. Appetite 
and digestion remain good, although there is often some tendency to constipa- 
tion. Rarely there is valvular disease of the heart, but usually only in such 
cases as originated in an acute articular rheumatism. Once in a while it is 
seen in cases chronic from the start. This last fact is not without interest from 
an setiological point of view. Sometimes there are certain nervous symptoms 
to be observed, such as headache, congestion, or mental depression, but these are 
probably not the direct result of the disease, but arise indirectly in a way to be 
easily imagined. 

General Course of the Disease. — Arthritis deformans is an extremely chronic 
trouble. It may last even ten or twenty years, or more. Sometimes there is an 
apparent arrest of the process extending over months, or even longer. Sometimes 
the progress of the disease is marked by remissions and exacerbations, affecting 
either the general or the local manifestations. In general, however, the disease 
continually advances. 

The prognosis is therefore unfavorable. Recovery, if it ever occurs, is extremely 
rare, and is possible only in the early stages. For the encouragement of the 
patient, it may be said that under proper care and treatment the disease often runs 
so gradual a course that the general condition remains at least bearable for a very 
long while, although there may be considerable local disturbance. The disease is 
not directly dangerous to life. The eventual fatal termination ensues either from 
general debility, or because of some intercurrent disease. 

The prognosis is somewhat more favorable in the milder cases of "chronic 
articular rheumatism," where the anatomical changes are less severe, and are 
completely limited to the synovial membrane. Even here, however, recovery is 



862 



DISEASES OF THE ORGANS OF LOCOMOTION. 



by no means frequent, and it is always to be feared that grave deformities of tbe 
joints will gradually be developed. 

Treatment. — With regard to regimen, it is requisite in tbe first place to avoid 
all unfavorable external influences. If possible y tbe dwelling should be dry and 
warm ; and it may often seem advisable to make a change of climate. The patient 
must dress warmly, without, however, undermining his powers of resistance too 
much, as he will be in danger of doing. The diet must be abundant and nutritious. 

Internal remedies may be tried, with the hope of modifying the disease, but our 
chief reliance must be upon local treatment of the joints. Among internal reme- 
dies, the most important are iodine and arsenic. Iodine may be given in the form 
of tincture (a few drops in mucilage several times a day), or a better form is in 
combination with potassium. As yet, we ourselves have not seen any great benefit 
from iodine, but we have in repeated instances witnessed a quite striking result from 
the use of arsenic. It is best administered in pills containing one thirtieth to one 
fifteenth of a grain (grm. 0*002-0 "004) of arsenious acid, one pill two or three times 
a day. If this remedy proves beneficial, it must be continued for at least months, 
perhaps with occasional brief intermissions. Salicylic acid has no permanent 
effect, and is useful only when there is an acute exacerbation of the disease. The 
preparations of colchicum may be tried, but will seldom be found efficient. Iron, 
quinine, and cod-liver oil are sometimes indicated by the general condition. 

First among local methods of treatment comes massage, although the good it 
accomplishes is, of course, apt to be evanescent. It will, however, do much to 
hasten the absorption of inflammatory exudations, and also to loosen up the 
joints, invigorate the muscles, and improve the general health. The Swedish 
movement cure will be found of great benefit in all cases if begun early and 
methodically persevered in. It preserves the mobility of the joints as long as 
anything can. Electricity also has a palliative influence. The galvanic cur- 
rent is applied to the affected joints, and the faradic current to the atrophied 
muscles. 

Baths are universally employed in chronic arthritis. Their value should not be 
overestimated, but it is, notwithstanding, undeniable in many cases. Simple warm 
baths, or salt baths (five to ten pounds of salt for each bath), are practicable in 
almost any household. As health-resorts in arthritis deformans, experience shows 
the following to be most desirable : The indifferent warm baths, such as Teplitz, 
Wildbad, Ragaz, and Baden in Switzerland ; the warm chloride-of -sodium baths 
in Wiesbaden ; the acidulated baths of Oeynhausen and Nauheim ; and the mud 
baths of Elster, Marienbad, Franzensbad, and Schmiedeberg. Steam baths are 
admissible only in the early stages of the disease, and for patients whose general 
condition is still vigorous. Even then they should be employed cautiously. 

[The mineral springs within the limits of our own country chiefly to be recom- 
mended are Sharon and Richfield, in New York State, the Sulphur Springs of 
Virginia, and the Hot Springs of Arkansas. At the two former, particularly, 
there is every provision for comfort as well as for the use of the waters.] 

We have repeatedly seen quite excellent results follow the employment of hot 
sand-baths. These also can be easily used at home, particularly if applied merely 
to the hands or feet. They are employed more elaborately in Kostritz and Blase- 
witz. These hot sand-baths seem to do good, not only from the temperature, 
but also from the uniform and persistent compression which they exert. 

Stimulating or narcotic remedies may be rubbed into the joints, but they are 
beneficial only because of the massage which accompanies their employment. In 
practice it is not always possible to omit their use. The application of tincture of 
iodine is usually entirely without effect. As to morphine and other narcotics, the 
disease is so chronic that it is desirable to employ them as little as possible. A 



ACUTE AND CHEONIC MUSCULAR RHEUMATISM. 863 



considerable number of those who suffer from chronic arthritis become opium- 
eaters. 

We may say, therefore, that the use of the various remedies which have been 
suggested will enable us to oppose some obstacles to the progress of the dis- 
ease. Persistent treatment will, in many cases, be rewarded by at least tempo- 
rary improvement. 



CHAPTER III. 

ACUTE AND CHRONIC MUSCULAR RHEUMATISM. 

(Myositis, or Myalgia, Rheumatica.) 

Definition and iEtiology. — Certain acute affections may originate primarily in 
the muscles. These are to all appearance inflammatory in their character, and not 
infrequently result from taking cold or other causes similar to those which pro- 
duce acute articular rheumatism. These affections are classed as " acute muscu- 
lar rheumatism," or rheumatic myositis. It is possible that this disease is also an 
infectious one ; but the question remains entirely undecided. The analogy which 
this trouble bears to acute articular rheumatism is not complete. It is seldom 
that the two processes are seen in combination ; and, furthermore, acute myositis 
is not " poly-muscular," but is usually confined to one muscle, or to a single group 
of muscles ; and it is never followed by acute endocarditis. The two diseases, 
therefore, are alike only in certain symptoms (pain and impairment of motion), 
and in the fact that they are often, although not always, ascribable to wet or 
cold, and the like. There are many cases where pain suddenly occurs in the mus- 
cles ("myalgia") without any attendant objective change. These cases can not 
be called genuine acute myositis. Indeed, it is sometimes difficult to know how 
to regard them. In practice they are often termed muscular rheumatism, espe- 
cially when they are referable to exposure ; and it is possible that many such 
cases are really a very mild form of the genuine inflammatory disease. On the 
other hand, however, there must often be some different process going on. Thus, 
traumatic pain in the muscles is the result of some excessive strain, and in many 
instances is apparently due to laceration of some of the muscular fibers. This is 
generally occasioned by too violent muscular exertion. Any physician who sees 
many patients from the laboring classes meets with an abundance of cases of this 
sort. 

The limitations of acute muscular rheumatism are obscure ; but still more so 
are those of " chronic muscular rheumatism." This disease is also a frequent one, 
and only imperfectly understood. It does not bear a close analogy to chronic 
articular rheumatism, except in this point, that chronic muscular rheumatism 
seems to be quite often occasioned by meteorological influences. While the ana- 
tomical changes in chronic articular rheumatism are almost always striking, 
similar lesions are very exceptional in chronic muscular rheumatism. On the 
contrary, the name is usually applied to cases where there is pain in various mus- 
cles all over the body, but where there is no discoverable objective disturbance. 
Older authorities used to speak of " rheumatic induration " of the muscles, but 
this or any other actual anatomical change is very exceptional. 

These facts justify a doubt as to whether all cases of chronic muscular rheu- 
matism actually deserve their name. It is certainly quite appropriate in those not 
infrequent cases which are due to " rheumatogenous influences," and which are so 
evidently aggravated upon every exposure to cold, or every period of bad weather, 



864: 



DISEASES OF THE ORGANS OF LOCOMOTION. 



that the patient often asserts that he carries in his legs the best of thermometers. 
Such is the " old rheumatism " of those who have passed a large part of their lives 
in the open air, regardless of wind or weather. There are other cases, the charac- 
ter of which is different. In them the muscular pain is associated with a general 
neurasthenic condition, or with corpulence (when it is, perhaps, the result of cir- 
culatory disturbance), or possibly with chronic poisoning. An important instance 
is the " rheumatic pain," sometimes complained of by topers, which we are inclined 
to ascribe, not to changes in the muscles, but to nutritive disturbances of the nerves. 
For these and similar disorders there are no special names, and the practicing phy- 
sician often terms them all " muscular rheumatism," a diagnosis with which the 
patient is usually quite contented. 

Clinical History. — Genuine acute muscular rheumatism is usually, as has been 
said, limited to some one definite group of muscles. The affected muscles often 
seem somewhat swollen and infiltrated, are very sensitive to pressure, and, if not 
quite useless, are nearly so, greatly impairing the motion of the corresponding 
member of the body. All these symptoms are best illustrated in acute myositis of 
the deltoid (omalgia). The whole shoulder is swollen, the muscle is very painful, 
and the upper arm is almost incapable of voluntary motion, although, if caution 
is exercised, passive movement can be made without causing any pain. 

The various forms of acute muscular rheumatism have received names descrip- 
tive of the locality of the affection. We have : 

1. Omalgia, as already mentioned. 

2. Acute rheumatic myositis of the cervical muscles, myalgia cervicalis, or 
rheumatic torticollis. Here the muscles of the back of the neck and throat are 
very painful. The head is usually held to one side, and, in severe cases, is almost 
perfectly immovable. 

3. Lumbago, or myalgia lumbalis. — This is the most frequent form of acute 
muscular rheumatism. The common people in Germany have termed it " witch's 
shot " (Hexenschuss), on account of its sudden onset. The entire lumbar region 
is very sensitive ; and any motion of the trunk, such as stooping or turning, is 
extremely difficult and painful. The disease is more frequent in men than in 
women. Certain persons seem to be especially predisposed to it. It should also 
be stated that lumbago is not always of a rheumatic character, but of traumatic 
origin, as from lifting a heavy weight, or from sudden stooping. 

4. Rheumatism of the thoracic muscles, and particularly of the intercostals. 
This may cause great discomfort, as it renders breathing, coughing, and sneezing 
very painful. It is comparatively rare ; and caution should be exercised in diag- 
nosticating it to avoid confusion with pleurisy and periostitis of the ribs. Very 
. often, also, thoracic disturbance is regarded as rheumatic when it is really trau- 
matic, being the result of stretching or laceration of the fibers of the pectoral or 
other muscles. 

5. Rheumatism of the head also, probably, belongs in this category, although 
the affection is seldom confined to the muscles of the scalp, but involves also the 
fasciae, and may even be almost confined to them. It is not infrequently excited 
by exposure to cold. The pain is quite violent, and greatly increased by any 
movement of the scalp. Of course the diagnosis requires the previous exclusion 
of the various forms of headache described on pages 499 and 556. 

The duration of acute muscular rheumatism is brief. Usually the pain abates 
in a few days ; but a tendency to relapse persists for some time. In chronic mus- 
cular rheumatism there are usually no objective changes to be detected. The pain 
is seldom located permanently in any one place, but it is felt first here and then 
there. It is usually increased during bad weather, and is less severe when the 
weather is warm. The pains are often described as "wandering." Motion is sel- 



ACUTE AND CHEONIC MUSCULAR RHEUMATISM. 



865 



dom much impaired. Sometimes, however, there may be a certain stiffness of the 
muscles, most marked after a period of rest. 

The diagnosis of chronic muscular rheumatism rests, therefore, mainly upon 
the rational signs. Hence it is often impossible to avoid the suspicion of malin- 
gering, particularly where certain applicants for hospital care are concerned. We 
should not, however, be too uncharitable, since without doubt there are cases 
where quite severe pain is felt, now in one set of muscles and now in another, 
without any anatomical basis for such pain being discoverable. Nor should we 
ever forget that other diseases may have pain for their first symptom. It is not 
at all exceptional for the lancinating pains of locomotor ataxia to be for a long 
time regarded as "lumbago." Lumbago may be confounded with insidiously 
developing diseases of the vertebrae, or with various hypogastric disorders (par- 
ticularly in women). We should, therefore, never omit to make a careful phys- 
ical examination. 

Treatment. — Acute muscular rheumatism has this in common with acute 
articular rheumatism : that it is usually very favorably affected by salicylic acid. 
In cases of genuine acute rheumatic myositis the employment of this remedy in 
the manner already described, for twelve to twenty-four hours, will often give 
surprising relief. Local treatment of the affected muscles may also be followed 
by great and speedy improvement. Massage is particularly valuable. It is not 
infrequently the case that a single, properly conducted massage will cause a vio- 
lent lumbago or omalgia to disappear almost completely, and like favorable 
results are witnessed where there is traumatic pain of the muscles. Most of the 
external applications which are so frequently prescribed for rheumatism — such as 
spirits of camphor or chloroform liniment — accomplish less through the cutane- 
ous irritation they produce than by the massage incident to their employment. 
Next in value comes electricity. Both the constant and the faradic current may 
be employed. Simple counter-irritation by means of mustard poultices or hot 
compresses will often prove palliative, but it is less effective than the remedies pre- 
viously mentioned. Great benefit often follows excessive perspiration. The best 
means to this end is a steam bath. This is so favorite a remedy that patients often 
take it of their own accord. 

In chronic muscular rheumatism the benefit of salicylic acid is merely tempo- 
rary, and therefore is to be sought, if at all, only when there is an acute exacerba- 
tion. Massage and electricity are more effective, and, if persevered in for some 
time, will often accomplish good results, even in obstinate cases. Treatment by 
baths is often prescribed with advantage. Steam baths are often beneficial, but 
their use requires great caution where the patient is corpulent and has a tendency 
to congestion or cardiac failure. There is also value in mud baths, pine-needle 
baths, and in the baths given at Teplitz, Wiesbaden, and other places. 

In many cases of chronic muscular rheumatism constitutional treatment is of 
great importance. Particularly where the patient is over-fed, and intemperate in 
the use of alcohol, much benefit will often be accomplished by a proper regulation 
of the ingesta and the prescription of a sufficient amount of muscular exercise. 
Such patients may also be helped by a cautiously conducted cold-water treatment. 

[In acute cases with localized pain I have found a thick flaxseed poultice, 
applied as hot as it can be borne, renewed once or twice, and followed by the 
application of a thick layer of cotton, useful. 

A dry cup or two is also often productive of great relief. In chronic cases, 
plasters and the iodide of potash are often of benefit. 

Muscular rheumatism is a common and often very troublesome affection in 
those whose occupation calls for decided muscular exertion. A muscle is strained, 
pain settles in and is apt to recur in the part ; and, while the general health is suf- 
55 



866 



DISEASES OF THE ORGANS OF LOCOMOTION. 



ficiently good, the man is compelled to remain idle. Quack advertisements dwell 
so much upon pain in the back as a symptom of Bright's disease that we are fre- 
quently consulted by those who, suffering from muscular pain and soreness, think 
themselves the subject of serious disease of the kidneys.] 



CHAPTER IV. 

RACHITIS. 

{Rickets.) 

iEtiology. — The first accurate description and the now universal name of 
"rachitis" (from pdxis, the spinal column) is to be ascribed to the Englishman 
Glisson, who published a comprehensive monograph upon this disease in 1650. It 
was his opinion that it first appeared in England in the beginning of the seven- 
teenth century ; and for this reason rachitis is still often called by Germans " the 
English disease. " 

Although the clinical and anatomical phenomena of rachitis have been often 
and accurately investigated since that time, its true cause still remains entirely 
unknown. It is certain only that its development is promoted by all unfavorable 
externa] circumstances affecting the nourishment and health of the child. It is 
therefore more frequent among the poor than the wealthy, in the damp and 
crowded quarters of large cities than in the country, and among artificially fed, 
and therefore weakly and anaemic, children than such as receive the mother's 
milk. Nevertheless, the essential cause of the disease is not to be sought among 
these various influences, for rickets undoubtedly does occur, although rarely, in 
children whose circumstances seem in every respect most favorable. 

Guerin, Friedleben, E. Voit, Wagner, Baginsky, and many others have made 
very exhaustive experimental researches, with regard to the development of 
rachitis. It has been found possible to produce certain changes in the bones of 
growing animals by giving them as little lime as possible in their ingesta, or by 
administering very large amounts of lactic acid, with the purpose of dissolving 
the calcium salts, or by giving small quantities of phosphorus. The changes thus 
caused have been, with more or less correctness, regarded as analogous to those 
of rachitis. These investigations are of great interest with regard to the physiol- 
ogy of bony structures in general, but, in our opinion, they throw Httle light upon 
the clinical question which here concerns us. It is indeed natural enough to sup- 
pose that rachitis in childhood may be due to an insufficient proportion of lime in 
the food ; or to a defective absorption of the lime-salts, on account of intestinal 
catarrh ; or to an abnormally abundant production of lactic acid, or even of car- 
bonic acid, in the system ; but every one of these theories is contradicted by the 
facts of experience. Everything seems to indicate that some special, specific, aeti- 
ological factor is requisite for the development of rachitis. This factor, however, 
is as yet entirely unknown to us. The thought had occurred to many that the 
disease bears some relation to congenital syphilis ; but this assumption has long 
since been proved to be entirely without foundation. Lately, Oppenheimer has 
propounded an hypothesis which seems at the first glance rather startling, 
namely, that rachitis is a peculiar form of malaria. This supposition does not 
seem to us to rest upon sufficient grounds. The clinical facts, however, which 
Oppenheimer brings forward, are interesting and important ; and we shall refer 
to them later. Many authorities have stated that heredity plays an important 



RACHITIS. 



867 



part in rachitis. The proof of this is lacking". It is, however, noteworthy that 
quite often several children of the same family are attacked by the disease. 

Rickets is most common in children of two or three years old. In a few rare 
instances it has been congenital (foetal rachitis), while in other exceptional 
instances the disease has developed in children eight to twelve years old, and even 
after puberty (so-called late rachitis). Sex exercises no great influence upon the 
occurrence of the disease. 

Pathology. — Rachitis consists in a disturbance of the normal processes con- 
nected with the growth of the bones. It is not that they become soft, but that 
they remain soft. The bones are therefore abnormally flexible, and can be cut 
with comparative ease. 

Upon minute examination, we find both the periosteum and the marrow much 
reddened and congested. If we try to detach the thickened periosteum from the 
bone, not infrequently a few bits of bone adhere to the membrane. The most 
striking changes, however, are exposed upon making a longitudinal section of the 
bone. They are located at the base of the epiphyses, because here is the place 
where the normal, and therefore the abnormal, processes of ossification are most 
active. Under normal circumstances, the epiphyseal cartilage of the bones in child- 
hood is separated from the main shaft by two narrow layers: first, an outer one, 
nearest the end of the bone, of a bluish color, and one or two millimetres thick ; 
this is the proliferative layer, or hyperplastic zone, where the cartilage-cells 
become divided and arrange themselves in rows. Secondly, an inner, dull yellow 
layer, only about half a millimetre thick, known as the ossific layer, or zone 
of calcification, in which the real process of ossification takes place. That is, 
blood-vessels grow into it, osteoblasts develop, lime is deposited, and medullary 
spaces are hollowed out. In healthy bone, these two layers are parallel to each 
other, and are limited by perfectly straight lines. # In rachitic bone, on the other 
hand, they are both much enlarged, and their naturally sharp boundaries are 
replaced by an irregular serrated edge, so that the two zones encroach mutually 
upon each other. These changes affect both layers, but are most marked in the 
proliferative layer. Upon microscopical examination, the details of which can 
not be given here, we can see most plainly the complete confusion, if we may be 
permitted to use the expression, into which the growth of the bone has fallen. 
The proliferation of the cartilage-cells has increased beyond all bounds, and the 
scanty matrix of the cartilage displays a fibrous character. In the midst of the 
cartilaginous structure are seen irregularly scattered foci, which are already 
undergoing calcification, or marrow formation. There is also an extremely active 
new growth of vessels, which form lacunae in the structure, and are often sur- 
rounded by a fibrous connective tissue, said to originate from the cartilage-cells. 

The periosteum presents analogous changes. The innermost osteoblastic layer 
of the periosteum is thickened ; but the newly formed tissue does not become 
completely calcified, but remains in large part soft and spongy. These various 
processes furnish a direct explanation of the macroscopic changes presented by 
rachitic bones. The proliferative process causes marked swelling of the epiphyses 
of the long bones, and thickening of the flat bones of the skull. The abnormal 
flexibility of the bones is due to their insufficient calcification, and it in turn 
causes various deformities, which are, for the most part, very characteristic {vide 
infra). If recovery takes place, the whole bone becomes firm at last, but often 
remains permanently deformed. 

The deficient development of rachitic bones can also be recognized upon chem- 
ical examination. While normal bones in a dry state contain about sixty-three 
or sixty-five per cent, of lime, rachitic bones have only about twenty to thirty per 
cent. 



868 



DISEASES OF THE ORGANS OF LOCOMOTION. 



Clinical History. — Rachitis often begins so insidiously that it can hardly be 
detected. Attention is not called to the disease until the deformity of the bones 
becomes very obvious, or it is noticed that the child does not learn to walk as 
early as other children, or, having already learned, is no longer able to do so. 
Now at last the anxiety of the parents is excited ; and, on seeking medical advice, 
they find their fears only too well grounded. 

In other cases, certain prodromata precede the development of the characteris- 
tic changes in the bones. It is these premonitory symptoms which are especially 
emphasized by Oppenheimer, and which led him to form the above-mentioned 
hypothesis, that rachitis is of malarial origin. There is often a peculiar form of 
diarrhoea, which is said to occur only in the first half of the day, being entirely 
absent at other times. The discharges are scanty and almost colorless. Not 
infrequently the diarrhoea is attended by fever, and it is said that the spleen is 
almost invariably swollen. The children are pale, but not emaciated. The first 
characteristic changes in the cartilages of the ribs and elsewhere are said to appear 
within two or three weeks of these first symptoms. In other cases, Oppenheimer 
observed that the development of rachitis was preceded by attacks of screaming at 
night, likewise associated with intermittent elevations of temperature, and splenic 
tumor ; or, again, there were simple febrile attacks at night, which passed away in 
the morning with profuse perspiration. 

These facts indicate that the entire organism is considerably affected by rachi- 
tis. It would seem reasonable to suppose that the disorder is caused by some spe- 
cific infection. That this infection is malarial is, however, by no means proved. 
The endemic distribution of malaria does not seem to correspond at all with that 
of rachitis. Here in Leipsic, rachitis is extremely common in many districts, 
although we very seldom observe a case of intermittent fever. Furthermore, if 
there is any such relation between the two as has been suggested, why does not 
Oppenheimer report any favorable effects from the administration of quinine in 
rickets ? Further observations in other places are necessary also before we can 
decide as to the frequency of the premonitory symptoms above mentioned. 

The diagnosis of rachitis can not be definitely established until the character- 
istic changes in the bones have been developed. These anomalies vary, of course, 
in their severity and extent in different cases. We append a list of the most 
important : 

The head is often noticeable for its great size and somewhat square shape ; the 
f ontanelles remain open until the second or third year of life ; their edges seem 
soft and yielding; the thinness and softness of the occiput is sometimes very 
striking, so that it can be pressed in like parchment. This phenomenon (the 
craniotahes of Elsasser) appears to be due to the pressure exerted upon the occiput 
when the child is lying on its back. There is often a peculiar change in the shape 
of the jaws, particularly of the lower jaw. This is not rounded, but angular, 
being sharply bent in the neighborhood of the canine teeth ; so that the incisors 
stand in a perfectly straight line, beside being somewhat inclined inward. 
Fleischmann was the first to describe this condition, and referred it to the action 
of the mylohyoid and masseter muscles upon the soft bone. Dentition in rachitic 
children is usually tardy and tedious. 

The thorax presents, even in the mildest cases, very characteristic and notice- 
able changes. There is a swelling at the junction of the cartilages with the ribs, 
which can be felt and seen through the skin, and produces what is called the 
"rosary of rickets." In severe cases the lateral portions of the thorax are often 
drawn inward, particularly at the parts which correspond with the insertion of 
the diaphragm. This change is due mainly to the action of the diaphragm during 
inspiration upon the abnormally soft and therefore yielding ribs. The changes 



RACHITIS. 



869 



are greatest when the respiratory efforts, and particularly abdominal respiration, 
are exaggerated because of bronchitis, pneumonia, or some other disease of the 
air-passages. In such cases the entrance of air into the lungs is impeded, so that 
it is possible that the external atmospheric pressure also contributes to produce 
the deformity of the thorax. Deep hollows may finally be developed on each side 
of the chest, while the sternum becomes unusually prominent, giving the whole 
chest that shape which has been termed pigeon-breast, or pectus carinatum. 
When once this deformity has been developed, of course it in turn contributes to 
render respiration difficult. 

The clavicles are sometimes distorted, and may even be partially fractured 
ividz infra). The spinal column is usually unaffected if the child remains quiet 
in bed ; but if it sits up, or is carried about, or tries to walk, the traction and 
pressure thus exerted often produce curvature of the spinal column (rachitic scoli- 
osis and kyphosis). These deformities may become extreme. Changes in the 
bones of the pelvis are of no special clinical importance at this period of the 
patient's life ; but in later life the consequent shortening of the antero-posterior 
diameter of the pelvis may, as is well known, prove a great obstacle to childbirth. 

The extremities not only present swelling of the epiphyses, but are liable to 
curvature. This latter change is most marked in the lower limbs, inasmuch as 
they have to support the weight of the body. The swelling is especially well 
developed at the lower ends of the bones of the forearm and of the tibia and fibula. 
The curvature is almost invariably greatest, and therefore most easily recognized, 
in the tibia, which becomes convex outward, giving the rachitic child its u bow- 
legs. 1 ' Similar curvature of the femur is less often seen, although it may be 
obvious enough in severe cases. The same is true of the humerus. The deformity 
of the lower limbs causes that waddling gait which can be so often seen on the 
streets of any large city. Sometimes the limbs present a sharp bend, the result of 
partial fracture. These " green-stick fractures of rachitis " are invariably referable 
to some slight traumatism, and are most often seen in the lower third of the tibia, 
although sometimes visible in the clavicles, ribs, and bones of the lower arm. The 
infraction usually takes place upon one — generally the concave — side, so that it 
is often compared to the partial fracture of a quill or an osier rod. 

Symptoms in Other Parts of the Body. — Apart from the changes in the bones, 
a rachitic child may seem to be perfectly well. Even the general nutrition may 
be unimpaired. As a rule, however, rickets is associated with anaemia and 
impaired nutrition. The child seems pale, thin, and feeble, and may present 
swollen lymph-glands and other " scrofulous " symptoms. Sometimes there is a 
tendency to profuse perspiration, especially from the scalp. Yery frequently there 
is chronic intestinal catarrh, and sometimes there is chronic bronchitis or lobular 
pneumonia. The liver and spleen are often, but not invariably, enlarged. It 
should also be stated that spasm of the glottis is frequently observed in rachitic 
children. Possibly it is due to the effect of the disease upon the skull. 

The faeces and urine have been repeatedly subjected to careful chemical exam- 
ination, in the hope of gaining some information as to the pathogenesis of the dis- 
ease. The results have thus far been rather contradictory. Much emphasis has 
been laid upon the fact that the faeces contain a comparatively large amount of 
lime. This has been ascribed to a deficient absorption of the lime-salts from the 
intestinal canal. The amount of lime in the urine, on the other hand, seems to 
be diminished rather than increased. 

The disease almost invariably runs a chronic course. Usually months, or even 
years, pass before the process ends. Its termination is to be recognized by closure 
of the fontanelles, increase in the length of the bones, and, above all, in the fact 
that the patient becomes stronger and makes attempts to walk. Unfortunately, 



870 



DISEASES OF THE OROANS OF LOCOMOTION. 



many results of the disease persist through life. The legs are crooked, the thorax 
deformed, the spinal column curved, and the pelvis narrowed. Even in the most 
favorable cases persons who have once had rachitis usually remain somewhat 
smaller than those who are perfectly healthy. 

Some authorities describe an " acute rachitis," in which painful swelling of the 
epiphyses is said to be developed in the course of a few weeks. At the same time 
the child becomes emaciated, and may also suffer from diarrhoea or ulcerative 
stomatitis. Recovery takes place in a few months. How far cases of this sort are 
related to genuine rickets has not yet been determined. 

Rachitis does not involve direct danger to life, although many rachitic chil- 
dren fall victims to the attendant intestinal catarrh, or to such complications as 
catarrhal pneumonia or tuberculosis. The prognosis is, therefore, not unfavorable 
where the outward circumstances of the child permit of good care and nourish- 
ment. The remote influences of the thoracic, spinal, and pelvic deformities can 
be readily inferred. 

The diagnosis of rachitis is but seldom difficult if the characteristic changes in 
the bones exist. In case cranial changes exist, we should guard against confound- 
ing rickets with hydrocephalus, but we can usually avoid error. The rachitic 
child holds its head erect, and is free from mental or other functional nervous 
disturbances. 

Treatment. — The most experienced specialists agree that the first aim in treat- 
ing most cases of rachitis is to improve the general nutrition. It is often possible 
to bring about recovery simply by means of proper diet (milk, the yolk of eggs, 
and, perhaps, meat), good air (in the country), and baths (brine, malt, and medi- 
cated baths). Digestive disturbances should be corrected by such remedies as 
hydrochloric acid or tincture of rhubarb ; and iron should be administered if the 
patient is anaemic. 

It is very important that the child should be placed upon a good mattress, and 
should neither attempt to walk too early, nor be needlessly taken up and carried 
about. The best way to avoid the development of deformities in the bones is to 
avoid all such unfavorable mechanical influences. 

Attempts have also been made to check the disease by specific remedies. Upon 
theoretical grounds, lime has been very frequently prescribed, in the form of 
phosphate of calcium, of which fifteen to forty-five grains may be given in powder 
several times a day ; or in the form of lime-water, of which one or two teaspoon- 
f uls are added to the milk which the child drinks. The benefit of these remedies 
is seldom very obvious. Kassowitz has given a fresh impetus to the employment 
of phosphorus. To support his belief he brings forward numerous clinical obser- 
vations as well as facts obtained from experiment. We may either dissolve the 
phosphorus in cod-liver oil (0 -01-100), giving one or two small teaspoonfuls of this 
solution every day, or we may write for the following mixture, which is more 
elegant, but is also more apt to spoil: 

B Phosphori 0 01; 

Olei amygdalae expressi 10 "0. 

Misce, deinde adde : 
Pulv. acaciae, 

Syrupi simplicis aa 5*0; 

Aquae destillatae 80*0. 

M. Sig. : Two to four small teaspoonfuls a day. 
The beneficial effects of phosphorus are said to be evident at the end of a few 
weeks. Certainly the remedy deserves a trial. 

It may be eventually necessary to resort to orthopaedic or surgical treatment 
m order to correct the deformities of the bones. 



OSTEOMALACIA. 



871 



[The comparative rarity of rickets, especially in its extreme degrees, in this 
country strikes all observers who have studied in Germany. With a fairly exten- 
sive experience among the poorer classes of the city, the writer can recall scarcely 
half a dozen cases of craniotabes. The colored race furnishes a large contingent 
of cases of rickets, although, as is shown by Haven, in attention to diet and fresh 
air, its members are superior to the Irish laboring classes, as a rule. The more 
pure the negro blood, the greater does the liability to rickets seem to be in this 
latitude — an indication, perhaps, that a northern climate is unsuitable to the Afri- 
can race.] 



CHAPTER V. 
OSTEOMALACIA. 

JEtiology and Pathology. — As a rule, osteomalacia does not, like rachitis, con- 
sist in a disturbance of development. The growing bones are not prevented from 
ossifying; but, having already undergone normal development and acquired 
normal firmness, they afterward become soft. It is mainly a disease of adults, say 
between thirty and forty years* of age. The female sex is noticeably predis- 
posed to the disease, although occasionally it has been observed in men. 

The true cause of osteomalacia has not yet been ascertained. It is a remarkable 
fact that the disease is much more frequent in certain regions than in others. It 
is very common along the Ehine, and in Westphalia, in eastern Flanders, and 
northern Italy. This suggests that there is some specific cause for the disease, 
endemic in certain localities. Among exciting causes, child-bearing is certainly 
the most important, for both the first signs of osteomalacia, and also fresh 
exacerbations of the disease, usually date from a pregnancy. Another factor said 
to promote the development of the disease is found in unfavorable hygienic sur- 
roundings, such as damp dwellings and the like. 

The anatomical process of osteomalacia consists in a disappearance of the 
earthy salts of the bone, which begins interiorly and spreads outward, and causes 
a corresponding softening of the bony structure. The marrow is at first extremely 
hyperaemic ; and extravasations of blood are not infrequently found here and 
there. The bony substance surrounding the myeloid spaces and the Haversian 
canals becomes transformed into a soft fibrous tissue, while the irregularly 
arranged bone-corpuscles are either destroyed or lose their characteristic shape. 
The softening process gradually extends over the spongy substances outward to the 
cortex. The central cavity grows larger and larger, so that finally the cortical 
substance is as thin as paper, and the whole bone like an " inflated and dried coil 
of intestine." At this stage the original hyperemia of the marrow has vanished. 
The marrow acquires a yellow color, and may finally be entirely transformed into 
a yellow, viscid fluid. The affected bones are now flexible and soft, can be easily 
cut, and are of less specific gravity than normal. The periosteum is also at first 
thickened and hyperaemic, as if inflamed. When it is removed, the surface of the 
bone beneath it is found to be rough and uneven. The attendant alterations in 
the shape of the bones will be mentioned below. 

Upon chemical examination of the bones in osteomalacia, we naturally find a 
marked diminution in the proportion of lime-salts. It is also stated that lactic 
acid has been discovered in the bones. This is an interesting fact, as it may be 
that the acid plays an important chemical part in the process of decalcification. 



* Kehn maintains that genuine osteomalacia may occur in children ; but his statement has not yet 
been fully corroborated. 



872 



DISEASES OF THE ORGANS OF LOCOMOTION. 



Clinical History. — Osteomalacia begins very gradually in most cases. Usually 
the first thing noticed is an ill-defined, deep-seated pain, most often felt in the 
sacral region, the nape of the neck, and the back and thighs. The affected parts 
are also sensitive upon pressure. 

The pain is persistent. While it still keeps on, motion becomes gradually 
impaired. The patient experiences more and more difficulty in walking, partly 
because of the pain and partly because of muscular weakness. The gait is either 
uncertain and tottering, or characterized by short painful steps, the lower limb 
and the pelvis being jerked forward as if in one piece. Sooner or later it becomes 
impossible to walk, and the patient is permanently bedridden. Even now the 
pains usually persist in great severity. They are not actually spontaneous, but 
the mere pressure of the mattress and the bedclothes is sufficient to excite them. 

In the meanwhile many of the bones will probably have become distorted. 
Usually the deformity of the spinal column is the first change which attracts 
attention. This is generally kyphotic ; less often the curvature is in the opposite 
direction. At the same time the head approaches the sternum more and more, 
and the patient is thus made to appear much shorter than she really is. In most 
cases, also, the thorax is much distorted. It is compressed laterally, while the 
sternum becomes very prominent, and is sharply bent. The change in the shape 
of the pelvis in osteomalacia is less obvious externally, but it can be detected on 
internal examination. It is, of course, of great importance from an obstetrical 
point of view. The pelvis, like the chest, is compressed laterally, while the sym- 
physis is made to project forward like a beak. The sacrum and its promontory 
are also pushed forward, and the superior strait thus acquires somewhat of a heart 
shape. 

The extremities are less often distorted, particularly if the patient becomes bed- 
ridden at an early period. Manifold changes are, however, possible. Sometimes 
there is also fracture. In a few reported cases the softness of the bones of the 
extremities was so extreme that one could bend the limbs at will, like wax, and 
give them the most extraordinary positions. In cases so far advanced as these, 
the pain in the bones seems finally to cease. 

The bones of the head and face seldom undergo noticeable change. In the 
muscles, several observers have noticed trembling and fibrillary contractions. It 
is also said that sometimes even a slight irritation of the skin suffices to excite 
painful contractions of the underlying muscles. These phenomena have not yet 
been thoroughly investigated. 

The general condition of the patient is often unimpaired for a long while, 
except for the pain and the impairment of motion. The internal organs perform 
their functions in a normal manner, and the appetite is good. Fever is observed 
only when the disease is undergoing some temporary exacerbation. With regard 
to changes in the urine, there have been a good many statements made, but their 
significance is extremely doubtful. It is said that the amount of phosphoric acid 
excreted is diminished. With regard to the amount of lime, no definite statement 
can be made. Lactic acid has been repeatedly detected in the urine, as has also 
albumen. Concretions of lime have been found in the bladder and the kidneys. 

The disease runs a chronic course, occupying seldom less than two or three 
years, and sometimes even five or ten. Apparent arrest of the disease is not infre- 
quently observed, but this is followed by fresh exacerbations. The most frequent 
termination is in death. This results either from general debility, or, more often 
still, from the dyspnoea caused by the compression of the lung, or by some such 
disease as lobular pneumonia. Recovery is exceptional, although not impossible. 

Diagnosis. — In well-developed cases it is not difficult to recognize the disease, 
but at first a correct diagnosis is often impossible, unless the endemic frequency 



OSTEOMALACIA. 



873 



of osteomalacia suggests it. As the disease is almost entirely confined to adults, 
we are seldom in danger of confounding it with rachitis. Besides, osteomalacia 
does not produce swelling of the epiphyses, nor changes in the bones of the skull. 
It is said that osteomalacia is occasionally confounded with diffuse carcinosis of 
the bones, as this may produce similar symptoms and deformities. 

Treatment. — As has been already implied, therapeutic efforts have thus far 
proved almost unavailing in this disease. We must therefore, in many instances, 
content ourselves with the administration of tonics (iron, cod-liver oil), baths, and 
narcotics. The internal use of lime does not seem to have any great effect, but it 
would be well to try phosphorus in the manner above described {vide page 870), 
as in some cases it has apparently proved beneficial. 

The changes in the bony pelvis produced by osteomalacia may eventually 
demand obstetrical interference, but we need not discuss such procedures here. 
We should invariably warn women who suffer from the disease of the dangers of 
becoming pregnant. 



DISEASES AFFECTING THE BLOOD AND TISSUE- 
METAMORPHOSIS. 



{CONSTITUTIONAL DISEASES.) 



CHAPTER I. 
ANZEMIA AND CHLOROSIS. 

Definition and iEtiology. — The word " anaemia " might properly be taken to 
signify diminution of the total volume of the blood, such as, for example, is 
directly brought about by a severe haemorrhage. Usually, however, the word is 
employed to signify not so much diminution in quantity as deterioration in qual- 
ity. The total volume of the blood is not liable to nearly so great variation as is 
the number of its most important constituents — the red corpuscles — inasmuch as 
the total volume is dependent merely upon the amount of watery constituents, 
and even after large haemorrhages the water is quite rapidly replaced by absorp- 
tion. This is undoubtedly the case in most instances of sudden loss of blood. 
Even in chronic anaemia there is usually no reason to assume that the total 
amount of blood is diminished, although it may be where there is general emacia- 
ation, or diminished supply of liquids (persistent vomiting, dysphagia), or large 
watery discharges (as in cholera). The essential element in anaemia is, therefore, 
a diminution in the number of the red blood-corpuscles, or so-called oligocy- 
thaemia. Changes in the character of the red blood-corpuscles, however impor- 
tant, are not taken into consideration here; nor is there usually any stress laid 
upon any incidental variations in the proportion of albumen, especially as oligo- 
cythaemia is not invariably accompanied by a diminution in the amount of serum 
albumen (" hypalbuminosis "). 

The circumstances under which anaemia is observed are manifold. They 
admit, however, of our distinguishing the two great classes of anaemia — primary 
and secondary. Primary anaemia is developed as an apparently primary and 
idiopathic disease in people previously healthy, while secondary anaemia is merely 
a symptom of some already existing disease. However simple this theoretical 
distinction, yet in actual practice it is often quite difficult to determine whether 
the particular case before us should be regarded as primary or secondary. A sec- 
ondary anaemia may occur where the true primary cause can not be at all readily 
determined. There are, nevertheless, quite a large number of cases which would 
seem to deserve the name of primary or essential, in which we feel compelled to 
assume that some pathogenetic influence acts directly upon the blood and the 
haematopoietic processes. 

In the first place, we would class as primary, cases which may best be described 



ANEMIA AND CHLOKOSIS, 



875 



as "simple constitutional anaemia." These often stand close to the borderland 
between health and disease. There are not a few individuals who present a strik- 
ing pallor for a large part, if not all, of their lives. These persons may feel so 
well and vigorous that we scarcely have a right to regard the existent anaemia as 
an actual disease. Sometimes, however, such individuals do betray some diminu- 
tion of energy, are easily fatigued, and are subject to headache. We may then 
certainly regard the condition as pathological. In many instances the cause of 
this simple ansemia is found in the general hygienic surroundings of the patient, 
for such cases are most often met with among the poorer classes. Deficient nutri- 
tion, bad air, unhealthy occupation in factories or the like, not only affect the 
general health, but more especially interfere with the processes of normal blood- 
making. Other cases of constitutional anaemia, apparently primary, occur in 
individuals who are entirely beyond the reach of such influences as have just been 
mentioned, in whom the anaemia has developed and persists despite the best of 
food and air. Here we are forced to the conclusion that the organs engaged in 
the manufacture of the blood are in some way prevented from performing their 
proper functions. The trouble often seems to be congenital, for such individuals 
may present the symptoms of anaemia in their earliest infancy. There are persons 
who have always been pale and feeble. Or, again, anaemia does not develop until 
later on, in which case it not infrequently associates itself with certain phases of 
physiological development, as when growth is particularly rapid, or when adoles- 
cence occurs. Virchow has directed attention to another factor, which he regards 
as potent in many of these cases of congenital anaemia. He has found that the 
arteries may be congenitally small, or that the whole arterial system may be 
imperfectly developed. The condition may be associated with a congenitally weak 
and small heart. The importance of this factor has not yet been fully determined. 
Possibly the condition of the circulatory system just mentioned may be the result 
rather than the cause of the anaemia. 

A second division of primary anaemia includes cases which present a far more 
definite and distinct group of symptoms. They quite often appear in persons pre- 
viously healthy, last for a certain length of time, and then end in complete recov- 
ery. The typical form of this variety is chlorosis (xXoopo? = greenish yellow), or 
"greensickness." This well-known disease is especially frequent in young girls 
fourteen to twenty years of age — that is, at puberty. It often comes on quite rap- 
idly without any ascertainable cause. There are not infrequently predisposing 
influences in the outward circumstances of the patient. Thus it is promoted by 
an unhealthy sedentary mode of life, as in seamstresses; bad air, as in factory 
operatives; mental and physical over-exertion, as in teachers, governesses, and 
students; and, finally, by mental influences. It is, nevertheless, true that chlorosis 
also appears in girls who have lived under the most favorable hygienic conditions 
possible. Sometimes the disease seems to be merely a temporary exacerbation of 
a simple constitutional anaemia which has existed a long while; but it may also 
appear in young women who were previously healthy, and even robust. 

The true cause of chlorosis is unknown. In all probability it is a disease of the 
blood itself, or a process interfering with its normal manufacture. Its pathological 
physiology is, however, as yet entirely beyond our grasp. The old view, that 
chlorosis was referable mainly to sexual derangement, such as disturbance of men- 
struation, or defective development of the genital organs, must be regarded as a 
confusion of cause and effect, although it is true that such disturbances are often 
seen in the disease. Furthermore, cases of marked temporary anaemia, precisely 
like ordinary chlorosis in their symptoms and behavior, occur in men and in 
elderly individuals. 

A third variety of primary essential anaemia is the so-called progressive perni- 



876 



CONSTITUTIONAL DISEASES. 



cious ansemia. This is likewise an idiopathic disease, distinguished from chlorosis 
mainly by its continuous progress and fatal termination. We must confess that 
in our opinion it is not possible, at least from a clinical point of view, to draw a 
sharp dividing line between ''ordinary chlorosis" and "pernicious anaemia." 
Some future investigator may discover aetiological as well as anatomical differ- 
ences between the two diseases, which will separate them widely. In the mean- 
while we have only the clinical phenomena to guide us, and must acknowledge 
our inability to make any sharp distinction. There are " severe cases of chlorosis " 
which resemble " pernicious anaemia " in every respect, except that they finally 
get well ; so that the only point which would enable us to distinguish them from 
the fatal disease is the mode of termination. To take this for a criterion is 
evidently unscientific. . Cases of " severe essential ansemia" also have many points 
in common with certain other diseases, such as pseudo-leukaemia and splenic 
anaemia. These will be discussed later. 

The forms of secondary anaemia offer a contrast to the forms of primary or 
essential anaemia just described in the much greater number of their causes. 
Under this head come cases of anaemia which do not occur idiopathically, but as 
a result of other abnormal processes. The simplest variety is anaemia from 
haemorrhage. This is produced by profuse loss of blood, whether from the 
stomach, lungs, uterus, intestines, kidneys, or some wound. Repeated small 
haemorrhages finally produce the same result as a single large one. Thus the 
most profound anaemia may be observed where there is a very frequent epistaxis 
(haemorrhagic diathesis), or where cancer of the womb gives rise to a constant 
oozing of blood. 

Other cases of secondary anaemia may be divided into two great groups. In 
one class the anaemia is a symptom of impaired nutrition. This is seen in almost 
every severe disease, acute or chronic, and is usually associated with more or less 
emaciation and loss of strength. The bad appetite, the lack of fresh air and exer- 
cise, and perhaps an impairment of digestion, or fever, or some abnormal drain 
upon the system, as in suppuration — these injure the entire body. It is not sur- 
prising that the blood shares in the universal misfortune. This is why most 
chronic invalids seem pale, particularly if they suffer from disease of the stomach, 
kidneys, chest, or nervous system. In the second class, the anaemia is secondary 
to some other disease, but assumes especial prominence as a symptom, independ- 
ently of any general impairment of nutrition. Of course, it is often associated 
with emaciation, but nevertheless its extraordinary intensity offers a striking con- 
trast to the condition of the rest of the body. This " specific secondary anaemia" 
must, like essential anaemia, be due to a special lesion of the blood itself, and is, 
therefore, to be regarded as in a certain sense a special complication or localiza- 
tion of the primary disease. General malnutrition never directly produces 
anaemia of this grade. This fact is illustrated in stenosis of the oesophagus. 
Here the ingestion of food is very greatly, if not completely, impaired, and there 
is the greatest emaciation, with a subnormal temperature and slow pulse. Of 
course, such a patient appears pale and wretched, but he does not present that 
peculiar waxy pallor which is the infallible sign of genuine anaemia. 

The exact mode of origin of specific secondary anaemia is often obscure. We 
have already reported, in a preceding chapter, a very instructive example. In 
cancer of the stomach we find usually emaciation and pallor. This is natural 
enough; but sometimes the carcinoma is complicated by an extraordinarily pro- 
found anaemia, comparable only to the pernicious variety. In one such case we 
found, at the autopsy, an extensive secondary carcinosis of the bone-marrow. 
Here, therefore, the anaemia certainly was not the result of the general impair- 
ment of nutrition occasioned by the gastric carcinoma, but of the disease of the 



ANAEMIA AND CHLOROSIS. 



877 



marrow, which tissue undoubtedly plays an important part in the manufacture of 
the blood. 

Some cases of specific secondary anaemia deserve special mention, although it 
is seldom possible to demonstrate their precise cause. In the first place come such 
cases as develop after certain acute diseases, usually of an infectious character. 
For example, there may be great anaemia after typhoid fever, or less often after 
acute articular rheumatism. A peculiar form of anaemia is often observed during 
the secondary stage of syphilis, although nutrition seems to be otherwise well 
maintained. This is known as "syphilitic chlorosis." Tuberculosis, chronic 
malarial poisoning, and other cases of chronic poisoning (lead), as well as 
amyloid disease, may also be attended by anaemia of such intensity as to justify 
the conclusion that there is some special disturbance of secondary origin affect- 
ing the manufacture of the blood or the blood itself. 

We shall now proceed to describe the symptoms common to all forms of 
anaemia. Upon this will follow a sketch of chlorosis. A special chapter is 
assigned to the grave form of essential anaemia known as progressive pernicious 
anaemia ; and in the same connection will be set forth the little that is known 
with regard to the relations of anaemia to pathological changes in the haemato- 
poietic organs. 

Symptomatology of Anaemia.— The first symptom which attracts the attention 
of the physician in any case of anaemia is the altered appearance, the pallor of 
the skin and visible mucous membranes. This is especially striking in the face, 
but it is sufficiently evident everywhere. Special value is usually assigned to pallor 
of the mucous membranes, for example, of the lips and conjunctivae, inasmuch as 
their color is not liable to be interfered with by pigmentation or opacity of the 
epidermis. The degree of pallor of course varies greatly. The whole body may 
present a waxy appearance. Such pallor of course indicates a very decided 
diminution in the number of the red blood-corpuscles, which elements impart to 
the blood its normal color. More information about this and other changes in the 
blood will be found below under chlorosis and pernicious anaemia. 

Beside the alteration in complexion, there is always a group of symptoms 
ultimately referable to an impairment of the normal processes of innervation 
resulting from a lack of arterial blood. First among these phenomena comes 
general weakness of the motor system. The voluntary muscles are easily fatigued, 
and the patient suffers from constant languor. When the anaemia is very great, 
as after severe haemorrhage, this weakness may be so pronounced that the patient 
can neither walk nor stand. 

This diminished nervous energy is also shown by the mental condition. 
There is no intellectual vigor. The patient is incapable of any great mental exer- 
tion, and experiences a constant feeling of weariness and sleepiness. Whether 
the special senses are blunted in anaemia has not yet been determined. It is very 
probable that a careful investigation would reveal an impairment of the percep- 
tive powers, corresponding to the muscular weakness. If the anaemia reaches a 
certain degree, the patient becomes unconscious. This explains the frequent 
fainting attacks (compare page 669), which are referable to a temporary aggrava- 
tion of the cerebral anaemia, and are therefore apt to come on after the patient 
has been standing for some time, or when he rises from a horizontal position. It 
is an extremely interesting fact that a circumscribed portion of the nervous sys- 
tem may alone suffer: thus we may have an anaemic amaurosis after profuse 
haemorrhage. There is no doubt that this blindness is due to anaemia of the 
optical nervous apparatus. The only question is whether the anaemia affects 
chiefly the retina or the central portion of the optic tract (cortex of the occipital 
lobe). 



878 



CONSTITUTIONAL DISEASES. 



If the anaemia is at all marked, many other organs exhibit functional derange- 
ment. In particular, the secretory organs are disturbed. The mouth and tongue 
are frequently dry. This is in part due to the diminished secretion of mucus and 
saliva. Of course, where there is a sudden great loss of blood, the condition is 
also in part a result of the compensatory abstraction of water from the tissues. 
Other and still more important glands belonging to the digestive system are 
affected. Our knowledge in this regard is as yet very far from complete; but 
Manassei'n has called attention to the interesting fact that the amount of hydro- 
chloric acid in the gastric juice is considerably less than normal, and that the dys- 
pepsia so often seen in anaemic patients must in part be referable to this condi- 
tion. Analogous disturbances in the functions of other digestive organs are pre- 
sumably present, but they have not yet been actually proved to exist. We would 
add only that the constipation to which anaemic persons are very liable is usually 
due to diminished energy of peristaltic action. 

The symptoms thus far described are all referable to diminished functional 
activity. On the other hand, anaemia gives rise to certain symptoms of irritation 
in the nervous system. It would, of course, be illogical to say that these symp- 
toms are the direct result of a lack of oxygen-carrying blood. They are, in all 
probability, expressive of the irritation excited in certain portions of the nervous- 
system by the products of abnormal tissue-metamorphosis. It may be that these 
products are themselves the result of a deficiency in the supply of oxygen. 

The symptoms of cerebral irritation observed in anaemia include vertigo, spots 
before the eyes, and tinnitus aurium. This last is an almost constant symptom, if 
the anaemia is at all severe, and may cause the patient great discomfort. It is 
usually aggravated if the patient lies upon his side. Another irritative symptom 
is eructations. We also have anaemic vomiting, and no doubt this is usually of 
central origin. It may be very troublesome. Sometimes violent hiccoughs are 
observed, as well as frequent yawning of a convulsive character. Anaemic head- 
ache may be very severe. It is usually referred either to the entire head or 
the forehead ; there is a painful feeling of pressure, which may attain great 
severity. 

Other important evidences of irritation are to be found in the behavior of the 
pulse and the respiration. The changes here are apparently in part of a compen- 
satory character. The pulse is accelerated in most cases of any severity, reaching 
80-100 beats per minute, or even more. It is also very excitable, so that compara- 
tively slight external influences suffice to increase its rapidity for the time being. 
This increase in frequency would not, of course, necessitate an increase of intra- 
vascular tension, nor of the rapidity of the circulation ; but it may exert a favor- 
able influence in this direction, and so be teleologic. Respiration is also usually 
accelerated in anaemia. In cases of great severity the breathing may be so deep 
and noisy as to justify the term " anaemic dyspnoea." This is the direct expres- 
sion of the body's hunger for oxygen. It is obvious that this increase in the num- 
ber of respirations favors, to a certain extent, the absorption of that gas. 

There are still other symptoms referable to the circulatory system. It has 
been already stated that the total volume of the blood is not diminished in anaemia 
unless, of course, there has just been an actual haemorrhage. This explains why 
the pulse in anaemia is often comparatively full and strong. Quite frequently 
there is a peculiar quickness of the pulse. This seems to be due to a vigorous 
cardiac systole, in conjunction with a low intra-arterial tension. This supposition 
explains the fact, which we have often observed, that there may be in profound 
anaemia a loud sound in the femoral artery similar to that heard in aortic regur- 
gitation. 

It has long been known that anaemia may produce functional cardiac mur- 



ANEMIA AND CHLOROSIS. 



879 



murs, often called " anaemic murmurs. " Their mode of origin is not yet fully 
explained. They are usually heard loudest over the base of the heart, in the 
neighborhood of the pulmonary valves, although sometimes at the apex of the 
heart. As a rule, they are purely systolic in time, but we certainly heard in one 
case of pernicious anaemia a loud diastolic murmur of anaemic origin. The mur- 
murs are of a blowing character. Sometimes they are so rough as to simulate 
pericardial friction-murmurs; it has therefore been suggested that many anaemic 
murmurs are actually due to the rubbing upon each other of the abnormally dry 
folds of the pericardial sac. Another explanation of their occurrence is, that the 
movements of the cardiac valves are interfered with, as a result perhaps of fatty 
degeneration of the myocardium {vide infra). It is also possible that they are 
due in some cases to relative insufficiency, resulting, for instance, from dilatation 
of the heart or imperfect action of the papillary muscles. 

Murmurs in the large veins of the neck are very often heard in anaemia, either 
with or without cardiac murmurs. They are often called bruit de diable. No less 
an authority than A. Weil has maintained that murmurs in the jugular veins are 
just as frequent in healthy persons as in the anaemic ; but our experience obliges 
us to differ from this view : we believe that the loud venous murmurs are more 
frequent in the anaemic than in other persons. We can not claim, however, that 
they are of any great diagnostic value. 

The processes of tissue-metamorphosis in profound anaemia are of great 
interest, but, unfortunately, they have not yet been thoroughly investigated. It 
is extremely probable that the absorption of oxygen in severe anaemia is less than 
normal, and that the body must, therefore, suffer from a diminished supply of 
oxygen. It has been demonstrated by the experiments of A. Frankel that there 
is an increased destruction of albuminoids within the body and a correspondingly 
increased excretion of nitrogen through the kidneys. This experimental deduc- 
tion we were the first to confirm in a case of very severe essential anaemia ; and 
later various observers have in other cases arrived at similar conclusions. Of 
course, the excretion of nitrogen is influenced by many different factors, so that 
the truth of the above statement is not easily established. There can be no doubt, 
however, that in many instances of profound anaemia a larger amount of nitrogen 
is excreted than is ingested. This fact acquires a special significance when taken 
in connection with certain anatomical lesions produced by anaemia: there is 
almost invariably a well-marked fatty degeneration of many organs, particularly 
of the heart and kidneys. This fatty degeneration is the direct result of the 
abnormal destruction of albuminoid structures. The fat represents the non-nitro- 
genous remnants of the decomposed albuminoids. The reason why the fat itself 
does not undergo oxidation is the same that leads to the destruction of the albu- 
minoids — namely, a lack of oxygen. This explains why the panniculus adiposus 
is for a long while preserved in many cases of anaemia. 

It is evident that the fatty degeneration once produced must, in its turn, lead 
to unfavorable results. It has already been suggested that the fatty degeneration 
of the heart may be the cause of certain irregularities in its functional activity ; 
but it should be said that this is not invariably the case, for often the heart 
exhibits a surprising energy despite marked fatty degeneration of its muscular 
tissue. The corresponding changes in the walls of the blood-vessels are, however, 
of great importance, as they frequently occasion disturbance, above all by haemor- 
rhage. In many instances (for example, in leukaemia, vide infra) an actual 
haemorrhagic diathesis is developed, which is probably referable to the diminished 
resistant power of the walls of the blood-vessels, resulting from fatty degeneration 
of the intima. There is also strong evidence in many cases that there is an abnor- 
mal permeability of the vascular walls. From this results the mild grade of 



880 



CONSTITUTIONAL DISEASES. 



oedema frequently seen in anaemic patients, although in some few cases this 
oedema may be ascribed to passive congestion, resulting from the cardiac debility 
{vide supra). The increased permeability of the renal blood-vessels is sometimes 
shown by polyuria. 

The urine is usually rather light-colored, if the anaemia is at all marked. It is 
evident that there is a diminished production of urinary pigment, the material for 
which is the coloring matter of the blood. Another reason for the light color of 
the secretion is the polyuria above mentioned. There may be fifty to seventy 
ounces (1500-2000 c. c), or more, secreted in twenty-four hours. The specific grav- 
ity may, nevertheless, be comparatively high, and higher than one would expect 
from the appearance of the urine, not infrequently ranging between 1015 and 
1021. This indicates, of course, that the amount of solid constituents is compara- 
tively large ; and in fact we find a corresponding amount of urea, say four or five 
hundred grains (25-32 grm.) in twenty-four hours. This is a large figure when 
we consider the amount of ingesta. As to the other constituents of the urine, we 
possess as yet little definite knowledge. The amount of phosphoric acid is some- 
times surprisingly small, compared with the amount of nitrogen. Albuminuria is 
exceptional in cases of simple anaemia. 

The bodily temperature is very often affected in anaemia. An "anaemic fever" 
is very frequently associated with pernicious anaemia, and even with cases of 
profound secondary anaemia, as after a large haemorrhage from the stomach. 
There are irregular elevations of temperature, usually occurring at evening, and 
attaining 101°-102° (38'5°-39° C), or even still higher figures. This phenomenon 
has not yet been explained. The fever is not inflammatory, but is excited directly 
by the anaemia, and may perhaps be caused by disturbances in tissue-metamor- 
phosis. 

Clinical History of Chlorosis— Chlorosis, or "green-sickness," as already ex- 
plained, is a term applied to the mild forms of essential anaemia, such as are most 
often seen in females at the time of puberty. The disease sometimes develops in 
previously healthy girls with considerable rapidity, and may completely vanish 
again at the end of a few weeks or months. In other cases it runs a more tedious 
course, without sharp limits, so that the condition resembles that of constitutional 
anaemia, or it may be described as an habitual chlorosis. In many instances the 
disease may be said to undergo repeated relapses. 

The various symptoms of chlorosis are almost all direct results of the anaemia, 
so that they have already been described. Their intensity and variety are, how- 
ever, very different in different cases. There are mild cases where the patient can 
hardly be called ill. She feels perfectly well, but is "a little pale." From these 
cases there is a gradual and unbroken transition to the other extreme of severity. 

A constant and essential symptom is the greater or less pallor of the face as well 
as of the rest of the surface of the body, and of the mucous membranes so far as visi- 
ble. There is also almost invariably general languor ; the patient is easily fatigued, 
and has neither the desire nor the ability to make any great bodily or mental exer- 
tion. There is also a tendency to headache and vertigo. Other nervous or " hys- 
terical " symptoms, if they occur, are not directly ascribable to the disease itself, 
but are merely complications. Chlorotic patients often complain of dyspepsia. 
The appetite is usually diminished, and there is often a sense of pressure in the 
epigastrium after meals. There may also be severe cardialgia. This is usually of 
a purely nervous origin, but is sometimes produced by a gastric ulcer existing as a 
complication of the chlorosis. There is not infrequently constipation, as might be 
expected from the small amount of food taken, and from the diminished activity of 
intestinal peristalsis. Over the veins in the neck we often hear a loud murmur, 
above referred to, and called bruit de didble. Sometimes the heart is found to be 



ANiEMIA AND CHLOROSIS. 



881 



slightly dilated. This is probably a result of the diminished power of resistance 
of the cardiac tissues. Anaemic cardiac murmurs are not infrequent ; the pulse is 
accelerated and easily excited. Otherwise physical examination does not reveal 
any abnormal condition of the internal organs. It is a very great exception to 
find any indications of disturbance in the spleen or lymph-glands, or the bone- 
marrow. Fever is rare in cases of simple chlorosis. The urine is usually pale, 
but seldom differs greatly, either in amount or constituents, from the normal char- 
acter. It is noteworthy that chlorotic girls are very apt to suffer from disorders of 
menstruation. The menses may not appear until late, or, if they occur, are very 
scanty. It is only in exceptional instances that chlorotic patients have menor- 
rhagia. 

Examinations of the blood have been made, in the hope of gaining a clearer 
insight into the true character of chlorosis. The blood is usually pale. Upon 
microscopic examination, we notice that the red blood-corpuscles do not tend to 
form rouleaux so much as normally, and sometimes we can perceive that the glob- 
ules are comparatively light-colored, and are not all of the same size. There are 
some of the normal dimensions, others are notably small (microcytes), while there 
are a few which are unusually large (macrocytes). Here and there we see corpus- 
cles of irregular shape (poikilocytes). Often there is some increase in the number 
of white blood-corpuscles — that is, there is a slight degree of leucocytosis {vide in- 
fra). In occasional instances there are considerable numbers of " granular bodies " 
in the blood. These are usually regarded as products of the disintegration of white 
blood-corpuscles. Malassez, Hayem, Thoma, and others have endeavored to deter- 
mine the number of blood-corpuscles in chlorosis and allied diseases by means of 
special methods of counting. In general, we may say that in most cases of chlo- 
rosis the number of red blood-corpuscles is decidedly diminished. In a cubic mil- 
limetre of blood we find perhaps only 3,000,000 to 3,500,000 red blood-corpuscles, 
instead of the normal number of 5,000,000. The diminution may be even greater 
than this. On the other hand, it should be noted that Duncan, Hayem, and Laache 
have met with cases where the number of corpuscles was not diminished. Proba- 
bly here the amount of haemoglobin in the blood-corpuscles was diminished. An 
intelligent and satisfactory explanation of all these isolated facts has not yet been 
given. There are certain hypotheses which have been brought forward, and these 
we shall discuss in the following chapter, where also a more extensive description 
will be found of the changes presented by the blood. 

We have already intimated that there is great variety in the general course of 
chlorosis. Many cases which seem severe at first terminate in complete recovery 
by the end of four to six weeks, or a few months. Other cases are much more 
obstinate, resist all modes of treatment, and undergo frequent relapses. The prog- 
nosis may therefore be regarded as favorable on the whole, but it should always be 
given with a certain degree of reserve. It is true that ordinary chlorosis never 
involves direct danger to life. We shall, however, find that there is no sharp 
dividing-line between " simple chlorosis " and " pernicious anaemia " ; and in any 
individual case it may not at first be possible to decide which variety of anaemia 
is before us. 

Diagnosis.— The diagnosis of chlorosis may be regarded, therefore, either as 
extremely easy or extremely difficult to make, according to the point of view. It 
is easy in that we can readily perceive the characteristic symptoms of pallor and 
the like ; but it is difficult in that the term chlorosis should be applied to those 
cases only where the anaemia is primary and essential. We, therefore, have 
no right to declare the diagnosis of chlorosis until we have made a careful 
and thorough physical examination, and have found that no factors are present 
which might produce a secondary anaemia. We should, above all, bear in mind 
56 



882 



CONSTITUTIONAL DISEASES. 



the possibility of incipient tuberculosis, and examine the lungs, the expectoration, 
and the general condition of the patient, and also consider hereditary and other pre- 
disposing influences. We should also bear in mind the possibility of some organic 
disease of the stomach, such as ulcer, catarrh, or dilatation, or chronic renal dis- 
ease, or possibly constitutional syphilis, giving rise to the syphilitic chlorosis 
before mentioned. In many cases it is easy to exclude all these secondary forms 
of anaemia, but occasionally the task is a very difficult one. 

Treatment of Anaemia and Chlorosis.— The first indication in treating chlorosis, 
as well as every other form of anaemia, is to promote the regeneration of the blood. 
There are two ways in which we can endeavor to fulfill this indication : first, by 
general hygienic and dietetic measures, and, secondly, by employing certain 
internal remedies. 

First among general measures comes a care for pure air and proper food. 
Many a pale city girl regains her ruddy cheeks after a few weeks spent either in 
the country, or on the mountains, or at the sea-shore. The choice of a place must, 
of course, depend mainly upon the circumstances of the patient. In many 
instances, boarding in any suitable country place answers as well as a long and 
expensive journey. If the sea-shore be chosen, some bathing resort on the North 
Sea will usually be preferable. There are other places where the patient can 
combine the advantages of pure forest-air and ferruginous mineral- water ; these 
will be mentioned below. 

The diet of anaemic patients should be easily digestible and rich in albumen ; 
carbo-hydrates and fat should be • given in but limited amounts to patients in 
whom the panniculus adiposus is already well developed. Lean patients, on the 
other hand, require such ingredients in their diet, and should be recommended to 
take simple puddings, extract of malt, butter, and cod-liver oil. If milk is well 
borne it is an excellent article of diet for the anaemic; but what is called the 
" milk cure " — that is, an almost exclusively milk diet — is not advisable, as we 
have already had occasion to observe {vide supra). Some authors ascribe an 
exaggerated value to alcoholic beverages. They may be allowed in moderate 
amount if the patient asks for them and finds the appetite improve under their 
use. The best to choose for an emaciated patient are porter and other varieties of 
beer rich in extractive principles. 

Many physicians also insist upon " abundant exercise in the open air." This 
can, however, be carried too far. A chlorotic girl is often made to take long 
walks in spite of her own reluctance to do so, with the result of becoming more 
languid and exhausted than she was before. We even believe that a case of pro- 
found anaemia will be benefited by a certain degree of bodily rest. Thus any 
needless tax upon the muscles is avoided. The most brilliant results we have 
ever observed in the treatment of chlorosis have been within the hospital. The 
patients, who are usually factory operatives and shop-girls, are often kept in bed 
for the first week. We admit that pure country air may be very beneficial, but we 
would strongly advise moderation in bodily exercise. If the patient begins to feel 
more vigorous, she will of herself take more exercise, and may safely indulge in 
long walks or extended excursions on foot. 

Of internal remedies, the preparations of iron have long occupied the first 
place in the treatment of all varieties of anaemia. The manner in which their 
good effects are exerted was, until recently, unknown, for careful investigation 
had established the fact that the salts of iron are not absorbed from the intestinal 
canal. Bunge has recently enabled us to understand why iron possesses thera- 
peutic value. He has shown that the iron contained in ordinary food does not 
exist in an inorganic form, but in a very complex organic combination, to which 
he has given the name of haematogen. The inorganic salts of iron given as a 



ANEMIA AND CHLOROSIS. 



883 



medicine protect the haematogen from being decomposed, a danger to which it is 
liable, from the sulphides which are generated in the intestinal canal. 

Numerous preparations of iron have been recommended. We can name here 
only those most often used. It may be taken as a general rule to give not too 
small doses, and to give these two or three times a day, directly after meals. Fer- 
rum reductum is perfectly pure iron, in a state of very fine subdivision, and may 
be given either as a powder or in pills, several times a day, in the dose of one to 
three grains (grm. 0 '05-0 '20). A very good preparation for children consists of 
pastilles made of chocolate containing reduced iron. Two other powders are con- 
tained in the list of the German pharmacopoeia — namely, ferrum carbonicum sac- 
charatum, and ferrum oxy datum saccharatum, the dose of each being half a tea- 
spoonful to a teaspoonful in water three times a day. The second of these prepa- 
rations, ferrum oxydatum, has the advantage of not blackening the teeth. An 
easily digestible preparation is ferri lactas, which may be given either as a powder 
or in pills, the dose being five to twelve grains (grm. 0 '30-0*75). Finally, the 
sulphate of iron should be mentioned. This is one constituent of the well-known 
Blaud's pills (ferri sulphatis exsiccat., potassii carbonat., aa grm. 15; pulv. traga- 
canth, q. s. Misce et div. in pil. No. 6. S. : Three to five pills three times a day). 
The German pharmacopoeia contains three tinctures of iron — viz., tinctura ferri 
acetici aetherea, tinctura ferri chlorati aetherea [resembling tinctura ferri chloridi, 
U. S. P.], and tinctura ferri pomata. Often iron is given in combination with other 
remedies, of which quinine is chief. This is said not only to increase the tonic 
action, but to lessen the headaches to which anaemic patients are subject. 
Stomachic tonics, such as gentian, or laxatives, such as aloes, are also combined 
with iron. 

Exceptionally iron is not well borne, and causes digestive disturbances or diar- 
rhoea. We must then try another preparation or diminish the dose. It is com- 
mon to forbid the ingestion of sour articles of diet while taking iron, but the 
injunction is due mainly to prejudice. 

The use of mineral 'waters containing iron is quite common. Of those arti- 
ficially produced, that which contains the pyrophosphate of iron is the best, and 
does not irritate even a delicate stomach. The natural chalybeate waters are also 
bottled and sent to distant places. They are often more effective if drunk upon 
the spot, but merely because, in that case, the general hygienic surroundings of 
the patient are better than they would be at home. The best-known and most 
popular ferruginous springs in Germany and Switzerland are situated at Cudowa, 
Rippoldsau, Homburg, Elster, Schwalbach, Pyrmont, Driburg, Liebenstein, St. 
Moritz, and Tarasp. " Steel baths " are also much employed ; but the effect is not 
due to the iron contained in the water, but to the temperature of the water and 
the carbonic-acid gas it contains. 

No other remedies for chlorosis approach to iron in popularity. Arsenic is the 
only one which needs to be mentioned. Its effects are often very beneficial, and 
it deserves a trial, especially in severe cases. It may be given alone or in combi- 
nation with iron. 

Of course, there may be various symptoms demanding special treatment. Epi- 
gastric distress, and other digestive disturbances, are often benefited by the admin- 
istration of dilute hydrochloric acid, of which six to eight drops may be given in 
water at meal-time. If there is constipation, it is desirable to remedy it rather by 
suitable diet than by laxatives. Thus we may prescribe fruit, Graham bread, and 
other foods which promote peristaltic action by the mechanical irritation which 
they exert. 



884 



CONSTITUTIONAL DISEASES. 



CHAPTER II. 

PROGRESSIVE PERNICIOUS ANEMIA. 

{Grave Form of Essential Ancemia.) 

Definition and iEtiology. — There is no sharp dividing-line in practice between 
the milder forms of essential anaemia, which have been thus far described, and the 
grave "pernicious" anaemia. It is, nevertheless, desirable to discuss these two 
classes separately, inasmuch as the transitional forms are comparatively rare, so 
that individual cases can usually be readily assigned to one or the other category, 
although we are sometimes left in doubt until the termination of the disease as to 
which form is before us. A case which at first is regarded as " pernicious " may 
finally terminate favorably, and earn the name of " profound chlorosis " ; while, 
on the other hand, as already stated, an apparently simple case of chlorosis may 
finally assume a pernicious character. 

We would, therefore, define pernicious anaemia as that variety of essential 
anaemia which does not, like chlorosis, terminate in recovery, or maintain a low 
degree of severity, but which goes on uninterruptedly from bad to worse, in many 
instances leading to a degree of anaemia which, of itself, proves the immediate 
cause of death. The word " essential " is here used to signify that the anaemia is a 
primary one, the result of some pathogenetic cause acting upon the blood itself, 
or the haematopoietic system. We must hold fast to this conception of the disease, 
especially as the attempt has been repeatedly made of late to degrade pernicious 
anaemia from the rank of an idiopathic disease, and regard it as merely a grave 
form of secondary anaemia which may result from any one of the most various 
causes. 

Of course, the diagnosis of primary anaemia may be wrongly made in cases 
where a more careful search will detect some special cause for the condition. Such 
a mistake may become evident at the autopsy. Thus, in repeated instances, cases 
which have been during life regarded as " pernicious anaemia " have been shown 
to be cancer of the stomach {vide page 364). In other cases, however, it is much 
more difficult to discover the primary cause of the anaemia. Thus the profound 
anaemia which attacked the men at work upon the St. Gothard Tunnel was at first 
regarded as idiopathic, but more careful investigation showed that the disease was 
really due to anchylostoma {vide page 419), the ravages of which parasite have in 
other cases also been confounded with the symptoms of pernicious anaemia. Of 
late there have been a number of cases reported where the post-mortem exami- 
nation showed that the progressive marasmus and anaemia of the patient had 
resulted from an extensive atrophy of the coats of the stomach and intestine, asso- 
ciated in some instances with well-marked lesions of the sympathetic plexus. 
These cases are very interesting, but have nothing whatever to do with pernicious 
anaemia, except in so far as the changes are of a secondary nature, analogous to 
the fatty degeneration seen in other organs {vide infra). Often the symptoms 
even during life differ not a little from those of pernicious anaemia, so that we 
can not think it right to establish what is called a " gastro-intestinal variety of 
pernicious anaemia." It is proper to group and classify the forms of secondary 
anaemia according to their various causes, but not the cases of idiopathic anaemia, 
which are all essentially alike. 

The credit of having been the first to study pernicious anaemia as a special 
form of disease belongs to Biermer (1868), although occasional instances of the 
disease had long before been noticed. Its occurrence during pregnancy was first 
pointed out by Gusserow. 



PROGRESSIVE PERNICIOUS ANEMIA. 



885 



With regard to the special aetiology of progressive pernicious anaemia, it must 
be confessed that we have as little definite information as about the aetiology of 
chlorosis. Klebs, and more lately Frankenhauser, have discovered micro-organ- 
isms in the blood, to which they have given the names " cercomonas globulus V 
and "cercomonas navicula" ; and they ascribe to them a pathogenetic influence. 
These discoveries, however, have not yet been satisfactorily confirmed. It is a 
noteworthy fact that pernicious anaemia is much more frequent in some countries 
than in others ; thus, it is seen far more frequently in Switzerland than in North 
Germany. This would be one argument for assuming that the disease is an infec- 
tious one. Here, in Leipsic, pernicious anaemia was comparatively frequent 
several years ago, while of late it seems to have become decidedly less common. 
There do not usually seem to be any special exciting causes. It has been main- 
tained that unfavorable hygienic surroundings and insufficient nourishment pro- 
mote the development of the disease ; and this would apply perhaps to some cases, 
but certainly it does not to all. We are inclined to regard it as characteristic of 
this disease, as well as of chlorosis, that the anaemia may develop despite the most 
favorable outward circumstances. There is, however, one factor which seems to 
have a decided influence, and that is the condition associated with pregnancy and 
childbirth. The first symptoms of pernicious anaemia in women are very apt to 
date from this period. It is a very interesting, but somewhat puzzling fact, that 
the disease may appear as a sequel to a great loss of blood, whether from one or 
several haemorrhages. It seems as if the body were sometimes unable to recover 
from the effects of large haemorrhages of this sort, so that the acute merges into a 
chronic and progressive anaemia, which, despite nursing and treatment, advances 
to a fatal termination. It is quite doubtful, however, whether such cases should 
be classed as genuine pernicious anaemia. 

Most of the cases occur during middle life, between twenty-five and forty 
years of age. Both sexes are equally liable to the disease, except for those cases 
already referred to which seem to be especially connected with the sexual func- 
tions. 

Pathology. — Pernicious anaemia so often terminates fatally that there has been 
abundant opportunity to make accurate anatomical investigations of the lesions it 
produces. We shall not here discuss the changes in the blood itself, inasmuch 
as they will more properly be described among the clinical phenomena. The 
changes in the interna] organs are divisible into two groups : First, such as are 
secondary and the result of the anaemia ; and, secondly, such as may perhaps be 
primary and pathognomouic. All the internal organs are, of course, anaemic. 
Another striking change is fatty degeneration. This is usually best marked in 
the heart, but it also affects the kidneys, liver, and the walls of the stomach and 
intestines, as well as the intima of the blood-vessels (compare page 879). We have 
already pointed out that this fatty change is to be regarded as the direct result of 
the anaemia, or more particularly of the diminished supply of oxygen in the tis- 
sues ; and we have also explained that the destruction of albuminoids indicated by 
this fatty degeneration maintains a direct ratio to the increase of nitrogen in the 
urinary secretion. 

There are frequent haemorrhages, usually small, but occasionally large ; these 
are found in all sorts of locations. They are very likely due to the fatty degen- 
eration of the intima of the blood-vessels, and are therefore to be classed as one of 
the results of the anaemia. The most important of these haemorrhages are into 
the retina, because they can be demonstrated by means of the ophthalmoscope 
during life. They are very frequent. We may also find minute haemorrhages in 
the serous membranes, such as the pleura or pericardium, in the brain and in the 
mucous membranes. Cutaneous ecchymoses are also occasionally found. 



886 



CONSTITUTIONAL DISEASES. 



Still another secondary symptom is an abundant deposit of iron in the cells of 
many organs. This can usually be determined only by the aid of the microscope 
or micro-chemical tests. It is most abundant in the peripheral zone of the hepatic 
lobules, but it also occurs in the kidneys, pancreas, and other organs. Quincke has 
studied this point very carefully, and finds that the total amount of iron contained 
in the liver in pernicious anaemia is much larger than normal. The most natural 
and most probable interpretation of this fact is that the iron originates from the 
destruction of large numbers of red blood-corpuscles. 

We now come to certain changes which differ from those thus far mentioned in 
not being a result of the anaemia, and which, therefore, are common to all cases of 
profound anaemia, whether primary or secondary. On the contrary, the changes 
now to be discussed might perhaps be regarded as the anatomical basis of the dis- 
ease. Of the blood we shall speak later. The solid structures which would natu- 
rally attract attention are those which are believed to be mainly concerned in the 
manufacture of the blood — that is, the lymph-glands, the spleen, and, above all, the 
marrow of the bones. The lymph-glands do not usually present any changes in 
pernicious anaemia. If they are much altered, it is probable that the disease is quite 
a different one, which we shall later have an opportunity to study (vide pseudo- 
leukaemia). The spleen is in many cases normal. In exceptional instances, how- 
ever, it is decidedly enlarged, although never enormous. Even when the organ is 
enlarged there are no important histological changes to be detected. Cases of 
pernicious anaemia with marked splenic tumor are often termed splenic anaemia 
(vide infra), but we do not ourselves see how such cases differ essentially from 
others in which the spleen is not enlarged. The changes in the bone-marrow are 
by far the most constant. This structure plays a much more important part in 
the formation of the blood than does the spleen. C. Wood, and after him Cohn- 
heim, called attention to the fact that the bone-marrow is almost invariably 
affected in pernicious anaemia. Instead of its normal yellow color, it has a red- 
dish-purple appearance. This is due mainly to the fact that the numerous fat- 
cells of the marrow are all, or nearly all, destroyed. This is the more surprising 
as the fatty tissues in other parts of the body are often very little affected in per- 
nicious anaemia. The specific cellular elements of the marrow also exhibit cer- 
tain changes. There is a decided hyperplasia, and often, although not always, 
there are found large numbers of nucleated red blood-corpuscles. Cohnheim is 
inclined to regard the disease of the bone-marrow as specific and primary, but it 
must be confessed that there are many reasons which strongly oppose this view 
and suggest the possibility of this change in the marrow being merely a secondary 
phenomenon, a sign of the extremely active formation and regeneration of the 
red blood-corpuscles. Neumann's investigations would lead to the belief that the 
nucleated red blood-corpuscles are young blood-cells in the process of develop- 
ment. Furthermore, these vigorous processes of regeneration, and the correspond- 
ing changes in the bone-marrow, are often found in cases of profound anaemia 
which are, beyond a doubt, of secondary origin. 

We can not, therefore, feel certain that the lesion of the bone-marrow is the 
primary anatomical disturbance, and we are, therefore, obliged to assume that 
essential anaemia may be a disease of the blood itself— that is, some process which 
does direct injury to the red blood-corpuscles, possibly of an infectious char- 
acter (?). 

Symptoms— As already stated, the symptoms of pernicious anaemia usually 
begin, independently of any demonstrable cause, in individuals previously healthy, 
and develop so slowly and gradually that it is hardly ever possible to determine 
the precise date of the commencement of the disease. This is still more likely to 
be the case if the trouble occurs, as indeed it may, in individuals who were pre- 



PROGRESSIVE PERNICIOUS ANJEMIA. 



887 



viously feeble and pale without being actually ill. Occasionally a more acute 
onset is observed in pregnant women. 

The first symptoms are almost invariably traceable to the incipient anaemia. 
They include the subjective disturbances and the objective changes which are seen 
in ordinary chlorosis. The patient feels languid and is easily fatigued, is liable to 
headache, vertigo, palpitation, and tinnitus aurium ; there are anorexia, frequent 
nausea, and, above all, a striking pallor of the skin and mucous membranes. 
While these symptoms, however, usually remain of slight or moderate severity in 
chlorosis, they attain, in pernicious anaemia, the greatest conceivable intensity. 
Of course, it would be impossible to describe all the stages through which the 
patient passes, but we append a sketch of those symptoms which are almost sure 
to be present, in greater or less completeness, in any well-marked case of per- 
nicious anaemia. 

If the anaemia is profound, the patient may be so weak as to be confined to the 
bed. If he sits up for any length of time, symptoms of increasing cerebral anaemia 
develop, and he is apt to faint. Usually the patient lies upon his back, with ly's 
head rather low, and presents a countenance of waxy pallor. Very frequently a 
slight but distinct yellowish hue may be detected. Occasionally there are cutane- 
ous ecchymoses, but those are exceptional. The mucous membrane of the lips, 
the gums, and the conjunctivae are likewise pale and colorless. The intellect is 
unimpaired, but all answers to questions are slow, apathetic, and delivered in a 
low and feeble tone of voice. The patient is usually incapable of any great men- 
tal exertion. If the body be moved, and especially if an upright position be sub- 
stituted for a horizontal one, there is great liability to syncope, as already men- 
tioned. This may result from other slight physical exertions, and is often 
accompanied by a peculiar spasmodic rigidity of the body. The main subjective 
symptoms are weakness and, more especially, intense headache; this often assumes 
a pulsating character, and is located mainly in the temples or forehead. There is 
also an annoying ringing in the ears, described as a rushing or roaring sound. 
There are certain other subjective sensations, namely, nausea, a sense of thoracic 
oppression, and pain in the bones, which will be further considered below. 

If we now proceed to a systematic physical examination, we are struck, in the 
first place, by the condition of the eyes. The pupils are often somewhat enlarged, 
but react in a normal manner. Vision is often disturbed by spots before the eyes. 
The anaemic amaurosis seen after a sudden large haemorrhage has not yet been 
observed in pernicious anaemia. The ophthalmoscopic examination of the fundus 
has very great diagnostic importance. We find in a majority of cases, although 
not in all, retinal haemorrhage. There may be either one or many haemorrhages. 
If they are extensive enough to involve the macula lutea or the disk, they may 
disturb vision greatly. Retinal haemorrhages invariably signify that the anaemia 
is profound, and are, with considerable justice, regarded as distinguishing perni- 
cious anaemia from chlorosis. 

Respiratory Symptoms. — Breathing is usually accelerated, and, in the most 
advanced cases, is often remarkably deep and noisy (anaemic dyspnoea, vide 
supra). Sometimes there is a very annoying and almost painful sense of thoracic 
oppression, which is evidently connected with the dyspnoea. There is a " hunger 
for air." Physical examination of the lungs gives negative results. Sometimes 
there is a little cough, and there may be suflicient haemorrhage into the mucous 
membrane of the air-passages to give rise to a slight haemoptysis. Even in this 
case no anatomical changes can be detected during life. We may also mention 
in this connection that epistaxis is not very infrequent. 

Phenomena referable to the circulatory system are of still greater clinical 
importance. The area of cardiac dullness is usually normal, although sometimes 



888 



CONSTITUTIONAL DISEASES. 



slightly increased. Upon palpation, we often find that the heart's action is exag- 
gerated, and that its beat is felt over a larger area than normal. The pulse is usu- 
ally decidedly rapid (100-120), but it is regular, and by no means invariably small. 
It is often surprisingly strong. The loud " anaemic murmurs " are very charac- 
teristic. They can be appreciated at the apex of the heart, but are usually still 
better heard at its base. We generally hear a loud bruit de diable in the veins of 
the neck. 

Digestive Organs— The tongue is usually pale, smooth, and dry. The appe- 
tite is often very poor. The most prominent disturbances, however, are not due 
directly to the condition of the stomach, but they result from the cerebral anaemia 
— that is, they are symptoms of the irritation of the nervous centers. We refer to 
eructations and vomiting, which may be very frequent and distressing. There is 
usually a tendency to constipation. Occasionally there is diarrhoea. 

The liver is usually normal ; as is also the spleen in many instances, while in 
others it is shown by percussion and palpation to be enlarged. It is sometimes 
possible, as we can ourselves bear witness, to observe an enlargement of the spleen 
increasing as the anaemia grows more profound, and again decreasing if improve- 
ment occurs (vide infra). On ordinary examination, the urine does not usually 
differ essentially from normal. With few exceptions, it is free from albumen, 
and it never contains sugar. As already set forth, however, accurate quantitative 
analysis often furnishes important evidence of changes in tissue-metamorphosis 
resultant upon the anaemia (cf. page 879). We will merely mention once more 
the comparative increase in the amount of urea excreted, and the occasional 
excess of uric acid. Sometimes the urine gives an unusually vivid reaction for 
indican. 

In regard to what has already been said about the bones, it is an inter- 
esting fact that they are very sensitive to pressure in many cases of pernicious 
anaemia. The sternum in particular is painful upon light percussion ; and some- 
times pressure will cause pain in the 
„ , bones of the extremities. In rare in- 

stances swelling of the knee and other 

j joints has been observed. 

The blood has been made the sub- 
%J A ^ fi| i ec ^ °f numerous and careful investi- 

^^JP gations ; nevertheless, no characteris- 

a tic change has been discovered. The 



Wf0 



w a ^1% changes presented in pernicious anaemia 
*© ^JP r m likewise occur in cases of profound see- 
s' # _ ^ ^ W g c ondary anaemia. This seems the more 



|Bj m ~ readily intelligible to us because of the 



view which we have already expressed 

j | © c on page 876 with regard to the origin 

of secondary anaemia. To the naked 
eye the blood seems extremely pale and 
watery. The number of red blood-cor- 
J £ puscles is sometimes so diminished that 

fig. no. -Changes in the red blood-corpuscles in it seems incredible that life should per- 

pernicious anaemia. (From Quincke.) a. Nor- s i s t # Jt i s not at all unusual, in the last 
mal blood-corpuscles, b. Macrocytes. c. Mi- , , 

crocytes. d. Poikiiocytes. stages of the disease, to nna less man 

500,000 red blood-corpuscles per cubic 
millimetre— that is, about one tenth of the normal amount. The red blood-cor- 
puscles are found to present striking varieties in size and form (vide Fig. 110). 
While some corpuscles have a normal appearance, others may be of an unusually 



PROGRESSIVE PERNICIOUS ANAEMIA. 



889 



large size (macrocytes). These "giant corpuscles" appear normal except in 
dimensions, and some observers have thought that they were even possessed of 
an unusual amount of haemoglobin. It is therefore surmised that they represent 
an effort on the part of nature toward compensation. In contrast with these 
large cells are found a varying number of minute red cells of a spherical shape ; 
these were first described by Vanlair and Masius, and called microcytes. Their 
mode of origin and significance are not known. Finally, there are numerous 
red blood-corpuscles of abnormal shape. These Quincke was the first to notice. 
They present remarkable forms, being biscuit-shaped, hammer-shaped, or anvil- 
shaped, and so on, as illustrated in the accompanying cut. These " poikilocytes 
are found in perfectly fresh undiluted blood, so that there is no reason to suppose 
that they are artificial products. Both the microcytes and poikilocytes are at 
present generally regarded as blood-corpuscles which have undergone imperfect 
or abnormal development, or suffered changes due to disease. Nucleated red 
blood-corpuscles have also been seen by Ehrlich a number of times during life. 
The white blood-corpuscles are not usually increased in number ; in occasional 
instances, however, a temporary leukocytosis has been found. " Granule-masses " 
are often found in considerable abundance. Chemical examination of the blood 
has not as yet brought to light any facts of great importance. Of course there is 
a great diminution in the total amount of haemoglobin. The amount of albumen 
in the blood-serum remains nearly normal. 

We observe in pernicious anaemia that tendency to fever common to all varie- 
ties of profound anaemia. In many cases the evening temperature will for weeks 
reach 100°-101° (38°-38-5° C), or even higher. Previous to death, however, the 
temperature may become subnormal, falling to 86° (30° C), or even lower. The 
cause of the " anaemic fever " is not known. Perhaps it is due to the derangement 
of tissue-metamorphosis. 

General Course, Duration, and Prognosis of the disease. — As the very name 
"pernicious" indicates, the disease generally terminates unfavorably. Death 
usually seems to be the direct result of the extreme anaemia ; special complica- 
tions are exceptional. The disease often maintains a slow but gradual progress to 
the end. Its duration, reckoning from the appearance of the first symptoms, may 
not exceed three to six months. It may even run its course in a still shorter time. 
The disease seldom lasts more than a year. Sometimes the course of the disease is 
interrupted ; there may be an arrest of the process, or improvement, or even 
apparent recovery. Usually, however, there are fresh relapses. In a certain 
class of cases the disease lasts two or three years, and is marked by a number of 
" attacks of anaemia," so intense that the subsequent improvement of the patient 
seems simply marvelous. It is in cases of this sort that splenic tumor has been 
made out at the time the anaemia was at its height ; yet we do not perceive the 
necessity of establishing " splenic anaemia " as an essentially different disease from 
progressive pernicious anaemia. It is merely a clinical variety of the disease 
under discussion. Apparently, it likewise has an invariably fatal termination. 

Permanent recovery may occur in cases of idiopathic anaemia so profound that 
we are at first inclined to regard them as pernicious. These cases are unfortu- 
nately very rare, and even where there is a marked improvement the danger of a 
relapse is to be borne in mind. The prognosis is, therefore, always very grave, 
if not absolutely unfavorable. Of course, general hygienic surroundings and 
good care may exert some influence upon the course of the disease. It is note- 
worthy that if pregnancy be complicated by profound anaemia there is a great 
liability to premature delivery, after which there is often a rapid change for the 
worse. There are exceptions to this rule. 

Diagnosis. — It is seldom difficult to make out the existence of a profound 



890 



CONSTITUTIONAL DISEASES. 



anaemia, or to determine the degree of danger which, the consequent symptoms 
indicate. We have, however, the same difficulty here as in chlorosis in proving 
that the anaemia is primary and idiopathic. The factors essential to this diag- 
nosis have been already indicated. We should bear in mind the possibility of 
incipient tuberculosis, organic diseases of the stomach, or such parasites as the 
anchylostoma. It is not necessary to enumerate again the different symptoms 
which need to be considered. 

Treatment. — For treating progressive pernicious anaemia, we have only the 
same remedies as for the benign variety of anaemia. Abundant and suitable 
nourishment is requisite, and all hygienic influences should be carefully regu- 
lated. Internally, our main reliance is to be put upon the preparations of iron. 
With us a favorite remedy in pernicious anaemia is the tinctura ferri chlorati 
aetherea (analogous to tinctura ferri chloridi, XL S. P.), of which ten drops in 
sweetened water may be given several times a day. It would also be extremely 
advisable to try the effect of arsenic. This remedy sometimes accomplishes strik- 
ing results in the whole group of blood diseases, including leukaemia and pseudo- 
leukaemia as well as anaemia. It is much better administered in pill form than in 
Fowler's solution. Iron may be given at the same time with arsenic. Some 
authorities recommend phosphorus. 

If the case is not too far advanced, baths may prove useful adjuvants to the 
internal treatment. Salt baths, or artificial carbonic-acid baths, may be employed. 
Symptomatic treatment is often indicated : the dyspepsia may call for dilute 
hydrochloric acid, or the troublesome vomiting may require bits of ice, bromide 
of potassim, or opium. 

The transfusion of blood has been employed in pernicious anaemia. Some- 
times the effect seems to be favorable. Experience, thus far, however, would not 
lead one to expect very great benefit from it. 



CHAPTEE ni. * 

LEUKiEMIA. 

(Leucocythcemia.) 

Definition and iEtiology.— Virchow, in 1845, was the first to obtain an insight 
into the disease leukaemia ( u white blood"). He detected the great increase of 
white corpuscles occasioned by it ; and from this time these constituents of the 
blood were subjected to observation in all sorts of diseases. It was soon found 
that there may be a temporary increase of the white corpuscles in various primary 
diseases, and that in certain instances this increase may actually constitute the 
essential symptom. In this latter case the increase is due to a depraved condition 
of certain internal organs. In the temporary cases, where the increase of white 
blood-corpuscles is usually not very great, we find one white corpuscle to one 
hundred red, or even one to fifty— the normal ratio being one to three hundred. 
This is usually termed leukocytosis, in distinction from leukaemia proper. 
Leukocytosis is most frequent in acute infectious diseases, such as typhoid 
fever, recurrent fever, intermittent fever, and pyaemia, and is also often seen hi 
anaemia. 

Genuine leukaemia is a rather rare disease. Its characteristics are well marked 
in most cases, but of its true nature we remain entirely ignorant. In a majority 
of the cases the change in the blood is associated with marked changes in the 
spleen and the bone-marrow, and often also in the lymph-glands. The organs 



LEUKEMIA. 



891 



just enumerated being concerned in the manufacture of the blood, it is very- 
reasonable to suppose that leukaemia is a disease which primarily affects these 
organs, and that the increase in white corpuscles results from the disturbance 
thus occasioned. The cause of the disease in the organs mentioned is as yet 
unknown. Various authors have suggested that there may be some specific infec- 
tion, but they have not been able, thus far, to produce any evidence of the truth 
of their surmise. In few cases can we discover even any exciting cause. The 
illness seems to develop spontaneously in perfectly healthy persons. In some 
cases, on the other hand, leukaemia does seem to be a sequel of some other disease. 
Thus it is occasionally preceded by a tedious attack of intermittent fever. It has 
also been asserted that syphilis may give rise to leukaemia, but this is not very 
probable. Finally, trauma of the spleen or bones has, in repeated instances, been 
regarded as the occasion of the disease. 

The hygienic surroundings of the patient have also been regarded as causes of 
leukaemia. The disease is more frequent among the poorer classes than among 
the wealthy ; but there are numerous exceptions to this rale. ^Etiological impor- 
tance has also been ascribed to anxiety, trouble, and mental depression in general, 
but with how much justice is doubtful. 

Leukaemia is most common in middle life, between thirty and forty-five years 
of age, but well-marked cases have been observed repeatedly even in childhood, 
as also, though less frequently, in old age. Men are somewhat more liable to 
the disease than women. It has been repeatedly stated that in female patients 
the disease is sometimes referable to sexual derangement, but this has not been 
proved. 

Pathological Anatomy. — The pathognomonic change in leukaemia is an 
increase in the number of white blood-corpuscles; this may be so considerable 
that there may be one white to three red, or even one white to two red corpuscles. 
The characteristics of the blood can be studied during the life of the patient, and 
upon them the diagnosis is mainly based. They will, therefore, be discussed 
under symptomatology, while we shall here confine ourselves to the lesions pre- 
sented by the spleen, bone-marrow, and lymph-glands. 

Of the organs just enumerated, the spleen is the one most frequently affected 
(splenic leukaemia). It is often greatly increased in size, not seldom attaining a 
weight of six to thirteen pounds (3-6 kilogrammes) and a length of a foot (30 
ctm.). There is a true hyperplasia of the whole organ: all the histological' con- 
stituents are increased. The cut surface is usually a rather vivid red in early 
cases, but later on it often has a lighter, yellowish color. The consistence is usually 
diminished, but in the later stages it may be greater than normal. Upon micro- 
scopic examination, we find enlargement of the blood-vessels and a great increase 
in the cells of the pulp and of the follicles. Sometimes the hyperplasia of the 
follicles predominates, giving the spleen a spotted appearance, like marble. In 
such cases the pulp usually presents retrograde metamorphosis, with atrophy and 
fatty degeneration of its cells and deposits of pigment. In advanced cases a con- 
siderable amount of firm connective tissue may be present. There are often 
haemorrhagic infarctions, presenting the appearance of circumscribed spots, dark 
red, or in the later stages brownish yellow, in color. 

Lesions of the bone-marrow are next in frequency to those of the spleen 
(medullary and myelogenous variety of leukaemia). Neumann and a few other 
authorities regard changes in the bone-marrow as an essential lesion, and hold 
that they can be demonstrated in every case of leukaemia. There would certainly 
seem to be exceptions to this last rule, but nevertheless in a majority of cases the 
marrow does present a peculiar yellowish or almost puriform appearance. By 
means of the microscope we can detect a great increase in the lymphoid cells of 



892 



CONSTITUTIONAL DISEASES. 



the marrow and the presence of a considerable number of nucleated red blood- 
corpuscles. 

In many cases the lymph-glands remain perfectly normal ; but in others they 
become considerably enlarged, arid form actual tumors in various parts of the 
body, such as the axilla, neck, and groin. Such cases are examples of lymphatic 
leukaemia. Histologically, the change here is simple hyperplasia of the glandular 
tissue. 

These three forms of leukaemia — splenic, myelogenous, and lymphatic — can not 
be regarded as distinct diseases, inasmuch as cases occur which present all sorts of 
combinations of these different lesions. Purely myelogenous cases are very rare, if 
they occur at all ; and we rarely meet with cases which are purely splenic or 
purely lymphatic. Most cases present lesions of the spleen and marrow con- 
jointly. In less frequent instances splenic disease is associated with that of the 
lymphatic glands. The fact that these combinations exist indicates that there is 
one common cause for the disease, which assails sometimes one, sometimes two or 
all three of the organs named. 

Just what the connection is between the changes in the blood and the lesions 
of these various organs is an unanswered question. A view which seems to us 
very plausible regards the disturbance in the spleen, or marrow, or lymph-glands, 
as the case may be, as the primary one, and the alteration in the blood as a result 
of this primary disturbance ; there is an increase in the number of colorless cor- 
puscles formed, and a consequent increase in the number of them introduced into 
the circulatory fluid. Some authorities have taken for granted that the colorless 
blood-corpuscles normally undergo transformation into red blood-corpuscles, and 
believe that in leukaemia this metamorphosis is hindered; but the assumption 
lacks support. It is, however, true that the number of red blood-corpuscles is 
diminished in leukaemia. This diminution in number might be ascribed either 
to scantiness of supply or to increase in the processes of destruction, but which 
factor is in reality the important one must remain undetermined. 

Changes in other Organs. — Leukaemia sometimes causes new growths of a 
lymphatic character in certain organs other than those already mentioned. The 
growths may either be diffuse or circumscribed and nodular. They are observed 
in the tonsils, Peyer's patches, and the intestinal follicles. They are also very fre- 
quent in the liver, kidneys, and retina, and more rarely in the lungs and the 
pleura. These various lesions may be regarded as, in a certain sense, analogous to 
the metastatic tumors of cancer or sarcoma, and suggest the possibility of the diffu- 
sion of the pathogenetic poison throughout the whole body. In one or two cases a 
well-marked leukaemia has been found independent of any demonstrable organic 
lesions. It is impossible, at present, to explain such occurrences. Leube and 
Fleischer have reported a case of this sort, and are inclined to believe that the 
blood itself was diseased. There is little known as yet as to changes in the chemi- 
cal characters of the blood and viscera in leukaemia. Xanthine and hypoxanthine 
have been found in the blood, as have also lactic acid and formic acid. It is also 
noteworthy that octahedral crystals are often found after death in the blood, 
spleen, and marrow, and in other parts. These are known as Charcot's crystals, 
and have already been described as occurring in the sputum in certain pulmonary 
diseases (compare page 155). 

Symptoms. — The clinical phenomena of leukaemia are, in many respects, similar 
to those of progressive pernicious anaemia, and need not be enumerated again 
here. In leukaemia, however, we have, in addition, symptoms referable to the 
spleen, or lymph-glands, or bone-marrow (as the case may be), and also the char- 
acteristic alterations in the blood. The blood-changes, being pathognomonic, 
demand a full description. 



LEUKEMIA. 



893 



The pallor and watery character of the blood in leukaemia are noticeable even 
to the naked eye in advanced stages of the disease. They can not, however, be 
distinguished from the changes present in grave anaemia without the aid of the 
microscope (vide Fig. 111). Looking through that instrument, we frequently per- 
ceive at once an enormous increase in the number of the white blood-corpuscles. 
As already stated, there may be almost as many white as red corpuscles. The size 
of the white corpuscles varies in different cases, and also in the same case. Virchow 
has called attention to the fact that the smaller cells originate mainly in the lymph- 
glands, and are therefore especially numerous where the leukaemia is of a lym- 
phatic type. The larger cells are 
referred mainly to the spleen and 
the marrow. The marrow is also 
said to contribute certain extremely 
large nucleated cells, the dimensions 
of which considerably exceed those 
of the normal white blood-corpus- 
cles. It is not always possible to de- 
termine the origin of the white cells 
from their size. Ehrlich has suc- 
ceeded in making out various forms 
of white corpuscles by staining. 
What are called " eosinophilous 
cells " are especially increased in the 
blood of leukaemia. These are color- 
less cells, the granules of which take 
a deep stain with acid pigments, but 

not with basic. Coincident with this FlG . m.—Ansemic blood. (From Funke.) a. White 

increase in the white cells in leukae- blood-corpuscles, b. Red blood-corpuscles, 
mia, there is almost invariably a con- 
siderable diminution in the number of red blood-corpuscles. We also find an 
occasional nucleated red blood-corpuscle in leukaemic blood, and sometimes also 
microcytes, poikilocytes, and almost always a large number of " granule-masses " 
interspersed between the blood-corpuscles. 

Splenic tumor is the most frequent and important of the organic lesions pro- 
duced by leukaemia. It is rarely possible to observe its development. In most 
instauces the spleen is already large when the patient first comes under observa- 
tion. It projects from under the ribs as a firm, hard mass, the lower and anterior 
extremity of which often extends to the median line of the body. The inner edge 
of the tumor is somewhat characteristic; it is rather sharp, and presents one or 
two notches. At first there is little subjective disturbance or pain referred to the 
spleen. Where the enlargement is very great there is often an annoying, or even 
distressing, feeling of distention and fullness in the abdomen. Respiration may 
also be interfered with by the crowding up of the diaphragm. 

The lesion of the bone-marrow can never be determined absolutely during life. 
The only symptom which renders its existence probable is pain in the bones, but 
even this is not an infallible symptom. There is seldom pain except upon pressure. 
It is usually brought out by percussion of the sternum, but there may be well- 
marked disease of the marrow without this " sternal pain." 

As already stated, the lymph-glands often remain perfectly normal. If they 
are affected, the disturbance is betrayed by their increase in size. Not only may 
the glands in the neck, axilla, and groin be enlarged, but occasionally also those 
of the mesentery and retroperitoneum, as can be demonstrated upon palpation of 
the abdomen. The enlarged lymph-glands rarely cause severe pain, if any at all. 




894 



CONSTITUTIONAL DISEASES. 



We have already referred to leukaemic new growths in other internal organs. 
These possess, for the most part, merely a scientific interest, as they cause no spe- 
cial symptoms. Sometimes hepatic enlargement occurs, as the result of a diffuse 
leukaemic infiltration. The changes in the retina associated with leukaemia are of 
importance, as they can be detected by means of the ophthalmoscope. The retina 
presents white spots or stripes running parallel with the blood-vessels. They are 
due to collections of lymphoid cells, or to actual lymphoid growths. These lesions 
have been inappropriately called leukaemic retinitis. Eetinal haemorrhages occur 
also in leukaemia, as in grave cases of idiopathic anaemia. 

All the other clinical phenomena of leukaemia result from the abnormal con- 
dition of the blood, meaning thereby the anaemia. The ability of the blood to 
perform its normal functions is impaired mainly through the loss of red blood- 
corpuscles ; the resulting symptoms are, therefore, precisely the same as in essen- 
tial anaemia, and we do not need to describe them again. They usually are the 
most prominent symptoms of the disease, and include noticeable pallor of the 
skin, equal to that sometimes seen in anaemia; anaemic murmurs over the heart 
and the veins of the neck ; general debility ; anorexia, and digestive disturbances ; 
palpitation and dyspnoea; and, finally, the whole group of the "cerebral symp- 
toms of anaemia," that is, headache, vertigo, syncope, and tinnitus aurium. Some- 
times there is a troublesome pruritus. We would also call attention once more to 
the frequent haemorrhages. These must be due to impaired nutrition of the 
vascular walls, and sometimes justify our speaking of a " haemorrhagic diathesis." 
Obstinate epistaxis is particularly frequent. Less often we ha^e haemorrhage from 
the intestine, stomach, kidneys, or into the skin. We may have cerebral haemor- 
rhage, with hemiplegia, or sometimes immediate death, consequent upon it. Severe 
cases may present a slight oedema of the skin and serous effusions into the various 
cavities of the body. 

The urine in leukaemia is essentially like that excreted in pernicious anaemia. 
Fleischer and Penzoldt have shown that in leukaemia as well as in pernicious 
anaemia there is increased destruction of albuminoids, and a consequent increase 
in the excretion of nitrogen. There is often also a considerable increase of uric 
acid. 

The temperature is apt to undergo slight elevations, as in severe cases of anae- 
mia. In advanced stages there may be quite high fever of an intermittent char- 
acter, reaching 103°-104° (39 ^-iO 0 C). The fever is sometimes accompanied by 
chills, and when the temperature falls there is often a profuse and debilitating 
perspiration. 

Complications are, on the whole, rare. Sometimes we observe pulmonary 
tuberculosis, or some acute intercurrent disease like pneumonia. 

Clinical History. — Leukaemia is almost always chronic in its course. The dis- 
ease begins insidiously and progresses gradually; the patient grows pale, feels lan- 
guid, and has slight and apparently insignificant symptoms, which gradually 
give place to alarming phenomena. The patient may himself notice the organic 
lesions incident to the disease. If the leukaemia is of the lymphatic type, he is apt 
to be struck by the swelling of the lymph-glands, while in splenic leukaemia his 
attention is attracted by the feeling of tension and pressure in the abdomen, the 
increasing prominence of the left side, and the unusual sense of resistance present 
in that part of the abdomen. Sometimes it is obstinate epistaxis, or haemorrhage 
from some other source, which first attracts attention and leads to a careful exam- 
ination of the blood and spleen. 

The disease usually lasts several years. Many cases are rather mild and grad- 
ual in their progress, while in others there is a rapid development of all the symp- 
toms. Some cases go on so rapidly, occupying but a few months, that they might 



LEUKAEMIA. 



895 



almost be termed "acute leukaemia." Instances of this form are most frequently 
seen in children. Apparent arrest of the disease is frequent, as is also temporary 
improvement, followed by fresh exacerbations. The final termination is almost 
invariably unfavorable. Death is usually preceded by symptoms of the most pro- 
found anaemia, and is caused directly by the general debility. It is sometimes hast- 
ened by the occurrence of haemorrhages, for instance, obstinate epistaxis or cerebral 
haemorrhage. 

Recovery is not absolutely impossible, but still it is very rare, and it is out of the 
question after the disease has passed its first stages. In an advanced case, there- 
fore, the prognosis must be regarded as hopeless. 

Diagnosis. — Leukaemia can be easily and unmistakably recognized by a micro- 
scopic examination of the blood. In a very early stage of the disease the increase 
of white blood-corpuscles may be so slight as to leave room for doubt ; but the 
later developments will afford absolute certainty in any typical case. 

We can not fail to recognize a case of leukaemia if the blood is examined. 
Such an examination is therefore demanded in every case of obstinate anaemia, 
and, above all, in such patients as have a chronic enlargement of the spleen, or 
swelling of the lymph-glands in various parts of the body. The enlarged lymph- 
glands are readily recognizable. The splenic tumor can usually be diagnosticated 
from its characteristic position and shape, and especially from its internal edge, 
with the notches already spoken of. It may be simulated by hydronephrosis and 
other diseases causing enlargement of the kidneys, and in women by ovarian 
tumors. In cases of doubt the blood should be examined, and, if the result is a 
positive one, we may feel certain of our diagnosis. If there is a chronic enlarge- 
ment of the spleen without a leukaemic change in the blood, we must consider all 
the possible causes of such an enlargement ; thus, there may be a passive conges- 
tion of the spleen, with enlargement, as the result of hepatic disease, portal 
thrombosis, or disease of the heart, or a splenic tumor from malarial poisoning. 
Again, there are cases where we have the signs of a gradually progressive anae- 
mia, apparently idiopathic, and a chronic enlargement of the spleen, or still more 
frequently enlargement of the lymph-glands in various parts of the body, without 
increase in the number of white blood-corpuscles. Such cases are termed pseudo- 
leukaemia and are described in the next chapter. 

Treatment. — Nearly the same remedies are employed in leukaemia as in idio- 
pathic anaemia. Of course the greatest attention should be paid to general nutri- 
tion. Of internal remedies, the preparations of iron have been mainly employed. 
They seldom produce any brilliant or permanent effects. We have much more 
confidence in the administration of arsenic, and this remedy should certainly be 
tried in large doses. It may be given either in the shape of pills, or possibly with 
still more advantage subcutaneously. Of course no permanent benefit is to be 
hoped for even from this, except in the early stages of the disease. 

What are called " splenic remedies " have been often employed, but do not 
seem very effectual in leukaemia. Mosler obtained good results from the long- 
continued use of quinine (5-8 grains = 0 •30-0* 50 grm., or more, in twenty-four 
hours). He also recommends a trial of piperin and oil of eucalyptus: 



M. et fiant pilulae no. c. 

S. Three to five pills three times a day. 
Local treatment of the spleen has also been attempted. If an ice-bag be con- 
stantly kept on the splenic region, it will sometimes diminish the size of the tumor, 



5 Olei eucalypti 
Piperini, 
Cerae albae. . . . 
Pulv. altheae. 



aa 3 j (grm. 4'0) ; 
3 ij (grm. 7*5). 



gtt. 100; 



896 



CONSTITUTIONAL DISEASES. 



and may also relieve pain. Botkin has recommended faradization of the spleen, 
but we can scarcely expect any great benefit from such a procedure. Injections 
of quinine, arsenic, and other remedies, have been made into the substance of the 
spleen. We do not believe that this is advisable. The splenic tumor of leukaemia 
has actually been extirpated surgically ; but the proceeding is so ineffectual and so 
fatal that it is now universally abandoned. The transfusion of healthy human 
blood has also been tried, but without satisfactory results. 

Many other particulars of treatment have been mentioned under anaemia. 



CHAPTER IV. 

PSEUDO-LEUKEMIA. 

(Hodgkbi's Disease. Adenia. Malignant Lymphosarcoma. Pseudo leucocythcemia.) 

It was mentioned in the preceding chapter that there are cases in which the 
organic lesions are apparently the same as in genuine leukaemia, and yet there is 
little if any increase in the number of white corpuscles in the blood. There is 
usually, however, a diminution in the number of red corpuscles. These cases 
usually receive the name which Cohnheim gave them of pseudo-leukaemia. It is 
nevertheless doubtful whether they are to be regarded as a special form of dis- 
ease, and there are various facts which indicate that they are at least very closely 
allied to genuine leukaemia. There is a great similarity in most of the symptoms 
of the two diseases and in their general course, as well as in the organic changes 
they produce. Furthermore, a case of pseudo-leukaemia may finally assume the 
character of genuine leukaemia, with its characteristic blood changes. 

The purely splenic type of pseudo-leukaemia is the least frequent one. As yet 
very few such cases have been reported. There is a gradually increasing anaemia 
with the usual symptoms, and associated with these, increasing enlargement of 
the spleen. It is impossible to draw any sharp dividing-line between such cases 
and cases of pernicious anaemia attended with moderate enlargement of the same 
organ (splenic anaemia). It may be said to be a matter of taste which name the 
physician shall give to a case of this sort. The bone-marrow seems to present the 
same characteristics in splenic pseudo-leukaemia as in pernicious anaemia. 

Pseudo-leukaemia Lymphatica.— Pseudo-leukaemia of a lymphatic type is a 
much more frequent and well-defined disease. It was first described in 1832 by the 
Englishman Hodgkin, and is sometimes called Hodgkin's disease. Wunderlich 
was the first in Germany to study the disease thoroughly; he described it in 1858 
under the name of " progressive multiple hypertrophy of the lymph-glands " ; and 
later Billroth termed it " multiple malignant lymphoma." Trousseau gave it the 
name of "adenia." 

Little is known about the aetiology of lymphatic pseudo-leukaemia. It is said 
to be connected with malarial poisoning, syphilis, and some other diseases; but 
such statements are without a satisfactory basis. The tendency of late is to assign 
adenia to the group of infectious tumors, although the reasons for this belief are, 
as yet, purely theoretical. Pseudo-leukaemia is most common in young and mid- 
dle-aged people, and is apparently rather more frequent in men than in women. 

Pathological Anatomy. — The hyperplasia of the lymph-glands may be very 
great, producing large tumors of varying consistency. These have been called 
lymph omata, lymph adenomata, and lymph osarcomata. On section, the tumors 
display a white or grayish-red surface, and are seen to be made up of a number 
of swollen glands fused into nodular masses. Upon microscopic examination, we 



PSEUDO-LEUKAEMIA. 



897 



find a very abundant proliferation of lymph-cells, sufficient to obscure the reticu- 
lum of the gland completely. The new growth may even escape beyond the 
capsule of the gland and invade surrounding structures. Inflammatory adhesions 
often take place between the tumor and the overlying skin. There does not seem 
to be any essential difference between the harder and the softer varieties of these 
tumors. 

These changes in the lymph-glands are often, though not invariably, associated 
with a swelling of the spleen. Its increase in size is usually slight. Lymphomata 
may also develop in the tonsils, the intestinal lymphatics, liver, kidneys, and other 
organs. Whether there are changes in the bone-marrow has not yet been deter- 
mined. 

The symptoms are very gradually developed. It is almost invariably the 
swelling of the lymph-glands which first attracts the attention of the patient or 
his physician. The glands upon one or both sides of the neck are usually the 
first to be enlarged, and they may finally grow to tumors the size of the fist, or 
even larger, producing great disfigurement. To the changes in the neck succeed 
swelling of the axillary, inguinal, and perhaps also the internal lymph-glands. 
The changes are gradual, and vary in their rapidity and extent. 

At first the general health is hardly at all affected, but as the disease progresses 
its constitutional effects become more and more marked. The patient grows pale 
and languid, and finally presents all the symptoms of profound ansemia. We 
may also have certain symptoms due to mechanical compression occasioned by 
the growth of the lymphomata. The tumors in the neck may cause dysphagia, 
from compression of the pharynx and oesophagus ; dyspnoea, from compression of 
the larynx and trachea; and perhaps alarming cardiac disturbance, from inter- 
ference with the vagus. Hypertrophy of the bronchial glands sometimes occa- 
sions great difficulty in respiration ; enlargement of the abdominal glands may 
produce ascites or jaundice; and enlargement of the glands in the groin may give 
rise to oedema in the lower extremities. In advanced stages we may have " cere- 
bral symptoms of ansemia " precisely similar to those seen in genuine leukaemia or 
in pernicious anaemia. There may be a tendency to haemorrhage and pruritus, 
and the urinary secretion and temperature may be abnormal. For particulars the 
reader is referred to the preceding chapters. 

Upon examination of the blood, there are usually found the changes charac- 
teristic of ordinary ansemia, without increase in the number of white blood- 
corpuscles. Sometimes, however, there may be a slight leukocytosis ; and some- 
times, as already said, lymphatic pseudo-leukaemia may merge into genuine 
leukaemia. The examination of the blood must therefore be repeated from time 
to time. The spleen should also be examined. It is usually somewhat enlarged, 
and in some cases the enlargement may be considerable. Such cases might be 
properly denominated splenic-lymphatic pseudo-leukaemia. We may also discover 
a tenderness of the sternum or other bones. 

The disease often lasts but a few months ; it may, in rare instances, extend over 
two or three years or more. Eecovery is not absolutely impossible in the early 
stages of the disease (vide infra), but at a later period the prognosis is absolutely 
unfavorable. The fatal termination results either from increasing debility and 
anaemia, or from the effects of mechanical compression, or from haemorrhage, or 
from some intercurrent disease. 

The diagnosis of pseudo-leukaemia is usually easy. It is to be based upon the 
objective signs and the condition of the blood. The disease is most apt to be con- 
founded with swelling of the lymph-glands occasioned by tubercular infection; 
but in this latter case the changes are seldom seen in so many parts of the body, 
and the patient usually presents other indubitable evidence of tuberculosis. 
57 



898 



CONSTITUTIONAL DISEASES. 



Treatment. — We possess only one remedy capable of promoting absorption of 
the lymphomata, namely, arsenic. We have ourselves, in common with a great 
number of observers, had the most convincing evidence of the favorable influence 
of arsenic. It must, however, be given in sufficient doses : for example, a pill con- 
taining one fifteenth of a grain (0*004 grm.), or even a larger amount of arsenious 
acid, three times a day; and its use must be persisted in for a long time. It 
might also be tried subcutaneously. We have also seen apparent benefit from 
associating with the arsenic inunctions of iodoform (iodoform one part, vaseline 
fifteen parts) over the tumors. 

In early stages decided benefit may be expected from this mode of treatment. 
At a later period we may obtain a decrease in the size of the tumors, but we can 
hardly hope for any permanent improvement. Operative interference is out of 
the question, except at the very beginning of the disease. Later on, it would be 
perfectly useless, and could seldom be carried out. 

Other suggestions with regard to treatment may be obtained from the chapters 
on anaemia and leukaemia. 



CHAPTER V. 
H2EMOGLOBINJEMIA AND HEMOGLOBINURIA. 

Definition and General .Etiological Considerations— If any cause produces a 
solution of the red blood-corpuscles in the blood-serum, haemoglobin is excreted 
through the kidneys. The haemoglobinaemia — the presence of free haemoglobin 
in solution in the blood — excites haemoglobinuria, i. e., the excretion of haemo- 
globin in the urine. The causes of haemoglobinaemia and its correlative haemo- 
globinuria are manifold. In the first place, there are a whole series of poisons 
which, if introduced into the blood in sufficient amount, exercise a directly de- 
structive influence upon the red blood-corpuscles, and thus excite haemoglobinuria. 
To this list belong chlorate of potash (Marchand), pyrogallic acid and naphthol 
(Neisser), arseniuretted hydrogen, hydrochloric acid, and many other substances. 
Distilled water is also in this sense a poison. Bostrom has discovered a fact of 
practical importance which deserves mention in this connection. It is that a cer- 
tain kind of mushroom (Helvetia esculenta), when fresh, contains a poison which 
is capable of producing intense haemoglobinuria, and such grave symptoms as 
jaundice, delirium, drowsiness, and tetanic convulsions, with perhaps a fatal ter- 
mination. This poison is, however, so evanescent and so readily soluble in hot 
water that the mushroom becomes perfectly harmless if thoroughly soaked and 
then boiled, or if it has been dried. 

Secondly, haemoglobinuria may be developed in connection with infectious 
diseases. In this case, also, it may be referable to the action of poisons created 
within the system. Thus haemoglobinuria has been observed in the course of a 
severe attack of scarlet fever or typhoid fever. Possibly malarial poisoning and 
syphilis may give rise to paroxysmal haemoglobinuria. This question will be dis- 
cussed later on. 

There is a third mode of origin which also possesses practical importance. If 
blood from one animal be injected into another of a different species, haemoglo- 
binuria is almost sure to result. Not only do the injected blood-corpuscles undergo 
solution, but also the injected serum acts as a poison upon the original blood-cor- 
puscles, destroying and dissolving them. This transfusion-haemoglobinuria has 
been described by Prevost, Dumas, Ponfick, and Landois. It can be produced in 
human beings, as there was only too good opportunity to observe during the brief 



HiEMOGrLOBINiEMIA AND HEMOGLOBINURIA. 



899 



period wlien the transfusion of lamb's blood was in vogue. The practical deduc- 
tion is evident, that we should not use for injection into the circulatory system of 
a patient anything but an unirritating salt solution, or human blood. 

A fourth and very important aetiological factor is exposure to extremes of 
temperature. Haemoglobin uria is a very frequent result of severe burns. The 
blood-corpuscles in that region of the periphery exposed to the heat are destroyed. 
Cold is capable of producing precisely analogous results. This is particularly 
evident in the cases of so-called paroxysmal hsemoglobinuria described by Wick- 
ham Legg, Lichtein, and Kiissner. The peculiar symptoms of this condition will 
be presented below. 

Pathology and Symptoms of Haemoglobinsemia, particularly the Paroxysmal 
Variety. — In most of the cases above enumerated, hsemoglobinuria is the result of 
an obvious or easily demonstrable cause. There is, however, another variety 
which appears paroxysmally in individuals who are otherwise perfectly well. Its 
symptoms are extremely characteristic. Although not a very frequent disease, 
there has been abundant opportunity to study it. 

As just intimated, the disease is paroxysmal. Yery often an attack is ushered 
in by frequent and persistent yawning. To this symptom are soon added pain in 
the limbs, headache, nausea, vomiting, and coolness of the periphery. The tempera- 
toe speedily rises to 102° (39° C.) or more. With this is often associated a decided 
chill. Sometimes there is a violent, cramp-like pain in the hepatic region.. Then 
the temperature falls again, perspiration appears, and the patient, although lan- 
guid and depressed, soon recovers. A slight icteric hue can almost invariably be 
detected toward the end of the attack, the ordinary duration of which is from two 
to twelve hours. An eruption of urticaria is noticeably frequent in connection 
with the attacks. 

The most interesting phenomenon of all remains to be described. We refer to 
the condition of the urine during and directly after the paroxysm. This secretion 
presents a dark brownish-red color resembling blood ; it may even appear almost 
black. Its reaction is almost invariably acid ; its specific gravity is usually 
rather low, say 1008-1012. On boiling the urine, the haemoglobin is decomposed, 
and a brown coagulum of albumen formed. If the excretion be examined 
through a spectroscope, we find the stripes characteristic of haemoglobin, and 
sometimes also the narrow stripes indicative of methaemoglobin. It is therefore 
impossible to doubt the existence of haemoglobin in the urine ; and yet, upon 
microscopic examination, we find no red blood-corpuscles in the urine ; or, in 
other words, no " haematuria. " Frequently there are great numbers of opaque 
red granules in the urine, the shape of which is extremely irregular. These are, 
doubtless, granules of haemoglobin. Some of them are free in the urine, some 
are attached to casts : of the latter, we find hyaline and a few epithelial casts 
present. Sometimes masses of haemoglobin assume the appearance of casts. The 
sediment may also contain a few cells of renal epithelium. The presence of this 
and of hyaline casts indicates that the kidneys have been slightly irritated by the 
excretion of haemoglobin. 

If now we examine the blood during a paroxysm, we shall find that haemoglo- 
binaemia is associated with hemoglobinuria of the paroxysmal type, as well as 
with that occasioned by the action of various poisons. Kiissner obtained blood 
from a patient during a paroxysm, and found that its serum had a ruby-red color, 
and contained haemoglobin in solution. This proves that the destruction of blood- 
corpuscles takes place within the circulatory system. Indubitable tokens of this 
destructive process are to be seen upon microscopic examination of the blood 
during a paroxysm, especially when the paroxysm has been produced artificially 
in the manner described below. The red blood-corpuscles have little tendency to 



900 



CONSTITUTIONAL DISEASES. 



form rouleaux. They are pale, and many of them are irregular in shape (poikilo- 
cytes). Irregularly shaped flakes of haemoglobin are also present, and often large 
numbers of decolorized red blood-corpuscles are to be seen. To these latter Pon- 
fick has given the name of " shadows." 

In many cases, the exciting cause of each separate paroxysm is perfectly 
evident. There is a cooling off of peripheral portions of the body, that is, the 
temperature of the blood in those parts is lowered, and this leads to a destruction 
of red corpuscles. Patients are free from attacks unless they have been out in 
cold or stormy weather, or have been wet through in a cold rain. As we might 
expect, the paroxysms are extremely rare in summer ; they may, however, as 
Eosenbach showed by experiment, be artificially produced at any time, by expos- 
ing the surface of the body to severe cold, as by giving the patient foot-baths of 
ice-cold water. Ehrlich and Boas have both performed experiments which show 
that the action of cold is a purely local one. They have separated a finger of the 
patient from the general circulation by means of an elastic ligature, and then 
immersed it for a quarter of an hour in iced water. Blood taken from this finger 
invariably exhibited the above-mentioned changes, while the condition of the rest 
of the blood in the patient's body remained almost perfectly normal. 

There can, therefore, be no doubt that in certain cases cold affects any por- 
tion of the peripheral circulation exposed to it in such a way as to excite a 
paroxysm of haamoglobinuria. The paroxysms cause headache, fever, nausea, 
and other symptoms, the immediate origin of which is not perfectly understood. 
Several authorities believe that these phenomena are uraemic ; and it has indeed 
been proved, both from the post-mortem appearances in such patients as have, 
from some coincidence, come to autopsy, and from experiments upon animals, 
that the kidneys may be plugged up with granules of haemoglobin in sufficient 
amount to give them a dark-brown hue. The granules collect chiefly in the 
straight tubules, and also in the convoluted tubes and the glomeruli. Such a con- 
dition may present a considerable obstacle to the excretion of the urine, and more 
especially to the elimination of its solid constituents. In point of fact, the urine 
is usually of low specific gravity. This retention of urinary constituents in the 
blood certainly might produce some of the symptoms observed ; but the present 
views are based more upon theory than upon fact. 

No explanation has yet been offered for the liability of certain unfortunate 
individuals to paroxysms of this sort, from which most men are exempt.* As yet 
not even a conjectural solution has been offered. It may be mentioned that most 
patients have had a syphilitic history. Whether there is some essential connec- 
tion here, and if so, what, we do not know. English physicians have thought 
that paroxysmal hemoglobinuria is associated with previous exposure to malarial 
poisoning. The correctness of this view is very doubtful. In conclusion, certain 
pathological facts should be mentioned. The kidneys are not the only receptacles 
of the debris resulting from the destruction and solution of the blood-corpuscles. 
Ponfick has been led by the result of certain experiments to believe that the 
spleen and liver are also affected. The spleen appropriates the undissolved 
remnants of the corpuscles, and, as a consequence, may undergo considerable 
enlargement. The liver absorbs a large part of that portion of the haemoglobin 
which has undergone solution, and converts it into bile. As a result, there seems 
to be an increased secretion of bile. A part of the dissolved haemoglobin becomes 
transformed into bile pigment while still mixed with the blood. This pigment is 



* It must be added that, in individual instances, other influences than that of cold appear capable 
of producing a paroxysm of hsemoglobinuria. Chief among these are great physical exertion, excessive 
walking, etc. 



SCURVY. 



901 



deposited in the skin, and gives rise to the slight degree of (purely hematogenous) 
jaundice already mentioned. 

Prognosis. — When hemoglobinuria is merely a symptom of other abnormal 
processes, caused by poisoning or by some specific infection, the future of the 
patient depends entirely upon the severity of the primary disease. An attack of 
paroxysmal hemoglobinuria would not seem to involve any direct danger to 
life. Recurrence of the paroxysms is always to be feared if the patient is 
exposed to those influences which produce it. There are no certain means of 
decreasing the patient's liability to attacks. In a few cases, however, where there 
had been syphilis, the paroxysms are said to have been permanently banished by 
mercurial inunctions. Likewise, if we suspect malarial influences, quinine 
should be tried. 

No special treatment is required during the paroxysm itself. The patient 
must escape as soon as possible from the exciting cause ; it is then advisable for 
him to lie quietly in bed, and to drink a large amount of fluid, so as to wash out 
the masses of hemoglobin from the kidneys. 



CHAPTER VI. 

SCURVY. 

(Scorbutus.) 

Prefatory Remarks. — Scurvy is one of a group of diseases which may be 
termed " hemorrhagic. " They all have one predominant symptom — namely, a 
decided hemorrhagic diathesis, respectively associated in the different diseases 
with various other more or less pronounced disturbances. This tendency to spon- 
taneous hemorrhage is in many cases, particularly the milder ones, more or less 
exclusively confined to the skin, but in numerous other instances hemorrhage 
also takes place into the underlying tissues, such as the muscles or joints, as well 
as into the mucous membranes. 

The distinctions between these various diseases are founded upon the manner in 
which the hemorrhages occur, and the symptoms which attend them. We may 
mention scorbutus, purpura simplex, purpura hemorrhagica, and peliosis. It 
should, however, be stated that, although it is possible to distinguish several 
varieties of disease, each one of which presents a tolerably characteristic picture, 
there are innumerable transitional forms. It may, indeed, be almost a matter of 
taste in any particular case what name shall be applied to it. The existence of so 
many intermediate forms renders it evident that the various members of this 
group of diseases are at least closely related if not actually identical. We shall 
even find, upon careful consideration, that certain other diseases not usually 
regarded as hemorrhagic are nearly akin to the group now under consideration. 
We refer to certain skin diseases, which are characterized mainly by inflamma- 
tory and exudative lesions of the skin. Chief among these should be mentioned 
erythema exsudativum multiforme, which not very infrequently exhibits some 
tendency to hemorrhages, and thus presents external appearances closely simulat- 
ing the forms of purpura. 

In order to understand the underlying connection between these various dis- 
orders, a precise knowledge of their etiology is requisite. Already considerable 
evidence has been gathered pointing to the importance of infectious influences in 
their production (vide infra), but no absolute proof has yet been obtained. In the 
meanwhile, we must be guided mainly by the purely clinical phenomena. These, 



902 



CONSTITUTIONAL DISEASES. 



again, indicate that sharp distinctions between the various hemorrhagic diseases 
would be purely artificial. In this and the following chapters we shall discuss 
the two main types of hemorrhagic disease. 

-Etiology of Scurvy. — Scurvy is sometimes sporadic, and sometimes epidemic 
and endemic in its occurrence. There were formerly very extensive and fatal 
epidemics of the disease, at a time when the laws of health with regard to large 
aggregations of human beings were little regarded. The disease was prone to 
attack armies, or the inhabitants of besieged cities, or, above all, seamen. It was, 
and to a certain extent is still, one of the diseases most dreaded by the mariner. 
It has often swept away an entire ship's crew. To-day endemics of scurvy are by 
no means infrequent, although not so extensive as formerly. They are most apt 
to occur in prisons and similar institutions, or barracks. 

These facts, under the light of our present views in regard to such matters, 
would almost force us to seek some organic infectious poison as the origin of the 
disease. Formerly men were inclined to direct their sole attention to such cir- 
cumstances as the character of the food, the dwelling, the climate, and similar 
conditions. Nor can it indeed be denied that these hygienic factors do exert a 
decided influence upon the spread of the disease. It is, however, evident that they 
can not be its proper cause, for, beyond a doubt, scurvy may occur independently 
of any of the factors usually regarded as essential to its development. These 
causes must therefore be regarded as simply predisposing influences. 

Great etiological importance has long been ascribed to certain errors in diet. 
These include the use of bad or insufficient food, the undue predominance of 
certain kinds of food, and in particular of the salt meats so much employed on 
shipboard ; or, again, the deficiency of certain varieties of food, in particular the 
lack of vegetable food, and still more of fresh vegetables. Much industry and 
acuteness have been expended in defending the theory that the lack of vege- 
table food is injurious because of the deficient supply of potassium salts under 
such circumstances (Garrod). Nevertheless, this view does not reach the heart of 
the matter, for in numerous epidemics of scurvy there has been no such lack of 
vegetable nourishment ; and in some instances the diet employed has contained an 
unusual abundance of potassium compounds. 

A like predisposing but not specific influence is exerted by the other factors to 
which etiological importance has been assigned. They are indeed often present 
in epidemic as well as in sporadic cases, but, as previously stated, they may not 
exist at all. To this class belong damp and unfavorable quarters, cold, moisture, 
persistent heat, and excessive muscular exertion. 

Age and sex exert no great influence upon the disease. Weakly persons seem 
to be somewhat more liable to be attacked than are the vigorous. The possibility 
of contagion has been maintained repeatedly, but contagion has not been proved 
to exist, and unprejudiced observation would incline one to doubt its existence. 

[It seems probable that the dietetic causes of scurvy lie rather in a want of 
variety in the food than in the absence of any one class or order of foods. Wales 
says (Pepper, " System of Medicine ") : " No single natural order contains plants 
that supply all the elements essential to the nutrition of the body and the right 
composition of the blood. The graminaceous and leguminous articles of food, for 
instance, are numerous, but not various ; they all afford the same or analogous 
albuminous elements, which have about the same nutrient value as the corre- 
sponding substances in animal food, and hence health and vigor can not be sus- 
tained on a diet of flesh, combined with wheat, rice, and oatmeal, or with beans 
and peas, or with all of them together. Outbreaks of scurvy have occurred on 
shipboard where the ration is made up principally of these articles — as in Anson's 
ship when supplied with an abundance of fresh animal, farinaceous, and legumin- 



SCUEYY. 903 

ous foods. It is clear, therefore, that, in order to obtain a variety of materials 
required in nutrition, we must resort to several of the natural groups, those par- 
ticularly which comprise the succulent vegetables and fruits." 

It is certain that scurvy is a disease which we can produce artificially, and that 
it is preventable in the vast majority of cases. It is now as rare among seamen as 
it was formerly common, a change which is the result chiefly of care to vary the 
diet, especially on long voyages. The United States law requires that lime- or 
lemon-juice, sugar, and vinegar shall be carried by all sailing-vessels bound on 
ocean voyages or engaged in the fisheries, specifies the circumstances and mini- 
mum doses under which the antiscorbutics are to be given, and provides penal- 
ties for violation or neglect.] 

Clinical History. — The disease does not usually begin suddenly. There is a 
gradual onset, marked by certain constitutional symptoms. The chief of these 
are languor and debility, a sense of thoracic oppression, palpitation, and usually 
a " rheumatic, dragging pain " in the loins and extremities, especially in the lower 
extremities. The patient is obliged to take to his bed if the case is at all severe ; 
he is very sensitive to cold, and often is drowsy and apathetic. These somewhat 
indefinite premonitory symptoms last for a few days or a week, when other and 
more characteristic phenomena appear. 

Among these new appearances are spontaneous haemorrhages, occurring chiefly 
in the lower extremities. There are cutaneous haemorrhages, producing dark-red 
macules of varying size, most of them with a hair-follicle in their center, and 
there are almost invariably haemorrhages into the deeper tissues also. The sub- 
cutaneous connective tissue and muscles, and sometimes the periosteum, are 
affected. These deeper extravasations are a peculiarity of scurvy. They can 
sometimes be felt as hard, painful swellings in the parts affected, and are some- 
times discernible from the discoloration of the skin, which soon results from the 
solution and diffusion of the blood-pigment. The patches present a diffuse bluish 
color, merging into greenish or yellowish at the periphery, and they are often 
quite large. They have a precisely similar appearance to " black-and-biue " spots 
resulting from injury. Of course, the more abundant and the more superficial 
the extravasation, the more extensive and darker is the macule. Similar appear- 
ances may sometimes be observed in the upper extremities and trunk, mainly in 
severe cases. The face and scalp rarely present ecchymoses. 

Sometimes a haemorrhage results in the necrosis and sloughing away of a por- 
tion of the skin. The necrosis is succeeded by ulceration (" scorbutic ulcers "). 
Under unfavorable hygienic influences this process may assume a grave signifi- 
cance. It should also be stated that we may observe other cutaneous disturbances, 
such as erythema, wheals, vesicles (the contents of which may be tinged with 
blood — " scorbutic pemphigus "), papules, and pustules. These eruptions are more 
frequent in some epidemics than in others ; they may either be associated with or 
replace the cutaneous ecchymoses. 

In the ordinary sporadic cases of scurvy which occur among us, haemorrhages 
into the mucous membrane, except of the gums, are very rarely seen. The same 
is true of haemorrhages from the stomach and other internal organs. In severe 
cases, during epidemics and under bad hygienic surroundings, it is otherwise; 
haemorrhage may take place from the nose, stomach, intestines, bronchi, and kid- 
neys, and blood may be effused into the serous membranes. 

Next in importance to haemorrhage is another peculiar symptom, presented by 
the mucous membrane of the mouth, and particularly that of the gums. In order 
to establish a diagnosis of scurvy in sporadic cases, we must demonstrate the exist- 
ence of these two main symptoms — namely, the haemorrhage into the skin or mus- 
cles, and the changes in the gums now to be described. 



904 



CONSTITUTIONAL DISEASES. 



The scorbutic changes in the gums usually appear quite early in the course of 
the disease, being, in many cases, simultaneous with the haemorrhages, although 
they may either precede or follow the latter. The gums assume a bluish hue, 
become swollen and spongy, are painful, and have a tendency to Weed. The 
changes are usually most pronounced in the salient parts of the gums between 
the teeth. It is a remarkable fact that they are hardly visible at all at places 
where there are no teeth; and the gums of very young children and of aged 
patients remain almost intact. In severe cases the gums are not only swollen but 
necrosed ; the change is first a superficial one, but may extend inward and pro- 
duce dirty-looking ulcers. Other parts of the mouth are liable to become involved 
in the ulceration, producing a diffuse ulcerative stomatitis, and giving the breath 
a most offensive odor. 

Certain other local and constitutional phenomena are not infrequent, though 
less characteristic than the haemorrhages and the alterations in the gums. Chief 
among the general disturbances is scorbutic anaemia. This is often in part refera- 
ble to the unfavorable hygienic influences surrounding the patient, but the disease 
seems itself to impair the general nutrition. The patient looks pale, has a dry skin, 
and loses flesh rapidly. The temperature is often normal. Sometimes there may 
be an occasional rise of temperature, either in the beginning or in the further 
course of the disease. If complications occur, they are not infrequently accom- 
panied by considerable fever. 

Among more localized symptoms should be mentioned the premonitory sore 
throat which sometimes occurs. It is usually of the ordinary catarrhal variety, 
but it may assume a haemorrhagic character. Bronchitis may also occur. Lobular 
pneumonia and genuine lobar pneumonia have been repeatedly seen in severe 
cases. Pleurisy, pericarditis, and inflammations of other serous membranes occa- 
sionally complicate the disease. They may likewise display a haemorrhagic ten- 
dency in the exudations to which they give rise. Disturbances in the joints are 
sometimes seen, and are characterized by an effusion of liquid into the articular 
cavities, which effusion may be either serous or haemorrhagic. This is a favora- 
ble opportunity to call attention to a peculiarity common to all the haemorrhagic 
diseases and allied affections (vide supra) — they are apt to be associated with 
articular swelling. 

The pulse may be somewhat accelerated, or may be slower than normal. It is 
usually small and compressible. Endocarditis may occur, but it is very exceptional. 
The blood does not present any constant and characteristic alterations in scurvy. 
The spleen may be decidedly enlarged, particularly in severe cases. Albuminuria 
has been repeatedly observed, but it is almost wholly confined to severe cases, in 
which, indeed, a typical acute nephritis may be developed. 

Varieties of Scurvy. Prognosis.— The sporadic cases usually met with in this 
region almost invariably pursue a favorable course. The symptoms are mainly 
confined to constitutional disturbance, ecchymoses in the lower extremities, and 
the affection of the gums, the grave complications above mentioned being rarely 
met with. The average duration of the disease is, nevertheless, some weeks. 
Recovery is deferred in proportion as the hygienic surroundings are unfavorable, 
but even then the termination is almost sure to be favorable. 

The prognosis in grave cases, occurring under unfavorable hygienic influ- 
ences, and aggravated by the lack of proper food and attention, is far otherwise. 
Here death is not infrequent, sometimes as a result of progressive cachexia, some- 
times because of pneumonia, pericarditis, or a similar intercurrent disease. 

Anomalous or rudimentary cases of scorbutus may occur. They are most apt 
to be seen when the disease is epidemic or endemic. As a rule, the symptoms are 
mild- We find, for example, a scorbutic gingivitis and stomatitis without haemor- 



SCUKVY. 



905 



rhage, or, on the other hand, haemorrhage into the skin and mucous membranes 
unattended by alteration in the gums. There have even been cases reported of 
simple scorbutic anaemia without any local symptoms. 

[The experience of army surgeons during our late civil war deserves mention in 
this connection. Hammond, Woodward, and others state that' many cases 
classed in the sick reports as " general debility " were cases of incipient or imper- 
fectly developed scurvy, haemorrhage from mucous membranes or into the skin 
being absent.] 

Diagnosis. — The diagnosis of scorbutus is almost self-evident when the two 
chief symptoms of haemorrhage and alteration in the gums are both present. If, 
however, one or the other of these symptoms is suppressed or imperfectly devel- 
oped, it may be difficult to determine what disease we have before us, or to exclude 
ordinary stomatitis, rheumatic peliosis, and similar diseases. If we remember the 
statements made at the beginning of this chapter, and bear in mind that these 
various diseases are probably aetiologically related to one another, we shall be 
less disturbed by these uncertainties. It may be mentioned, in conclusion, that 
various septic disorders, and also acute ulcerative endocarditis, may occasion the 
appearance of numerous haemorrhages, and thus simulate scurvy. 

Treatment. — The essential requisites in the treatment of scurvy are proper 
hygiene and diet. Fresh air, suitable nourishment, and good nursing, if 
promptly supplied, are usually of themselves sufficient to induce recovery, while 
the physician possesses no remedies which compensate for their absence. 

The belief that a main cause of scurvy lies in a deficiency of fresh vegetables has 
given rise to a practice, still in vogue, of prescribing a great abundance of fresh 
vegetables, such as lettuce, spinach, and sorrel, fruit, lemonade, and other drinks 
prepared from fruit syrups. There is no reason to deviate from a course to which 
experience has given its sanction, although we have repeatedly had opportunity 
to see that the administration of fresh vegetables is by no means essential to rapid 
recovery. Patients supplied with any other proper nourishment thrive equally 
well. Certain varieties of plants have attained a special reputation as " anti- 
scorbutics," such as the spoon wort (Cochlearia officinalis), so frequently mentioned 
in accounts of early polar expeditions. None of these plants, however, possess the 
specific properties assigned to them. The administration of vegetable acids and 
the salts of potassium (bitartrate and nitrate of potassium), in a chemically pure 
form, has also been repeatedly tried, but it has not gained popularity. 

The drugs most employed are the bitters and tonics. They have no specific 
value, but are perhaps as good remedies to prescribe as any. We may give a 
decoction, of cinchona, to which may be added a small amount of dilute sulphuric 
acid and syrup, or some preparation of gentian or a similar bitter. It was once 
believed that the internal administration of the mineral acids exerted a specially 
favorable influence upon the haemorrhagic diathesis ; but this is very doubtful. 

Certain symptoms may demand attention; in particular, the affection of the 
mouth and gums. It is of great importance to cleanse the mouth frequently with 
disinfectants and mild astringents, such as chlorate of potassium or sage tea. It 
is also advisable to paint the inflamed and spongy gums at short intervals with 
tincture of myrrh or tincture of rhatany. The absorption of the ecchymoses in 
the lower extremities will be promoted by cautious massage. Inunctions of lini- 
mentum chloroformi and the like give great relief from the pain caused by the 
extravasations into the deeper tissues. In severe cases stimulants are often de- 
manded, such as camphor, ether, and alcohol. Such complications as appear may 
also demand special treatment. 

Convalescence is promoted by continued attention to diet, bathing, and the 
administration of iron and quinine. 



906 



CONSTITUTIONAL DISEASES. 



CHAPTER VII. 
PURPURA. MORBUS MACULOSUS WERLHOFII. PELIOSIS. 

As already stated in the preceding chapter, the various " hemorrhagic dis- 
eases " are so intimately related to one another that it is quite impossible to make a 
rigid categorical division of them. The numerous names which have been intro- 
duced into the literature of this subject certainly contribute more to obscure than 
to elucidate the attendant phenomena. 

From a clinical standpoint this fact is the all -important one — namely, that 
there are cases in which the foremost symptom is the spontaneous occurrence of 
haemorrhage. There are cutaneous ecchymoses, and there may be at the same time 
haemorrhages in the internal organs and into the mucous membranes. In the 
milder cases of this sort these haemorrhages constitute almost the only symptom 
of disease ; but they may be associated with considerable general disturbance, indi- 
cated by fever and weakness, or with certain local complications. The true cause 
of these diseases has not yet been discovered. There is seldom any evidence of an 
exciting cause, and the disorder may attack either the well-nourished or the poorly 
nourished, the old or the young, men or women. There is, however, an indisput- 
able relationship between these diseases and certain others — namely, scurvy, 
erythema exsudativum, and perhaps acute rheumatism and endocarditis. This 
similarity indicates that the process is of an infectious character. Such an assump- 
tion promotes greatly a proper understanding of the phenomena under consider- 
ation. In some few cases the weight of evidence would seem, however, to point to 
an antecedent impairment of nutrition in the walls of the blood-vessels. A good 
example of this is seen where cutaneous ecchymoses occur in old and marantic 
individuals (peliosis senilis). There is some doubt whether these exceptional 
cases belong with the others. 

The mildest forms of the diseases under discussion are termed purpura. The 
haemorrhages are seen mainly in the skin of the lower extremities, and are apt to 
take place into the follicles. There may also be ecchymoses upon the trunk and 
upper extremities, but the mucous membranes and the deeper tissues remain intact. 
A means of distinguishing purpura from scorbutus lies in the fact that in purpura 
there are no haemorrhages into the muscles or lesions of the gums, although it 
should be confessed that transitional forms between the two occur. The disorder 
is called purpura simplex if the cutaneous ecchymoses constitute the only symp- 
tom, or, at any rate, the only important one. These cases almost invariably ter- 
minate in recovery, and are over at the end of ten days or three weeks. Some- 
times elevations of the skin are formed resembling wheals, and haemorrhages take 
place here and there into them. This sub- variety has been called by some pur- 
pura urticans. It forms a connecting link between purpura simplex and those 
cases of erythema exsudativum which are associated with haemorrhage. Further 
particulars may be found in special works upon dermatology. 

Quite often the haemorrhages are attended by " dragging rheumatic pains " : 
such cases are termed purpura rheumatica or rheumatic peliosis (Schonlein). 
There may also be constitutional disturbance, slight fever, anorexia, and indis- 
position to either bodily or mental exertion. There may sometimes be actual 
arthritis, with an inflammatory efPusion into the joints. The knee and other joints 
of the lower extremities are most apt to suffer in this way. The gums are usually 
normal; nor is there, as a rule, haemorrhage into the mucous membranes or the 
viscera. These cases may last but two or three weeks. Often, however, they are 



HAEMOPHILIA. 



907 



more tedious, being marked by the recurrence of the ecchymoses and articular 
pain. Most of them get well at last. 

No sharp dividing line can be drawn between the forms of purpura thus far 
described and certain graver cases. These latter are most of them grouped under 
the name of purpura hcemorrhagica, or its preferable, because more distinctive 
synonym — every purpura being hemorrhagic — morbus macnlosus Werlhofii. The 
cutaneous ecchymoses in this class of cases are usually extensive ; and, further- 
more, we have haemorrhages into the mucous membranes of the nose, mouth, soft 
palate, stomach, and intestinal canal, as well into internal organs (the brain and 
kidneys), and also into the serous membranes. The constitutional disturbance is 
apt to be severe. The condition maybe distinctly a typhoidal." Fever maybe 
entirely absent, even in grave cases, although sometimes there is a considerable 
rise in temperature. 

There are usually no local symptoms beyond those already mentioned. In 
typical cases the gums remain intact. Swelling of one or more joints has been 
repeatedly observed, as have also endocarditis and acute haemorrhagic nephritis. 
If marked cerebral symptoms are developed, suggesting an apoplectic shock, we 
may surmise that a cerebral haemorrhage has taken place. It should also be stated 
that marked gastro-intestinal disturbance may occur. Cases of this sort have been 
observed by Henoch in children. They may also occur in adults. In rare in- 
stances there may be intestinal ulceration, with perforation and consequent peri- 
tonitis. The spleen may undergo acute enlargement. 

The prognosis in purpura haemorrhagica should always be a guarded one; the 
patient is in danger both from the general depression and anaemia, and from 
certain special lesions. Even a severe case may, however, recover. The disease 
sometimes proves very tedious ; it may occupy several months. 

Treatment. — The general regimen to be prescribed is similar to that directed in 
scurvy. The physician must strive to support his patient's strength by means of 
proper nourishment. A great many internal remedies have been recommended, 
most of them on purely theoretic grounds. It is difficult to say whether they 
actually exert a favorable influence upon the course of the disease. The following 
drugs are chiefly employed : Ergotine, perchloride of iron, dilute sulphuric acid, 
and cinchona. If there were swelling of the joints or endocarditis, we should 
advise a trial of salicylic acid. Such special symptoms as demand attention should 
be treated according to general principles. 



CHAPTEK VIII. 
HEMOPHILIA. 

Definition and JEtiology. — Haemophilia is the term used to denote a peculiar 
constitutional anomaly, exhibited in a remarkable tendency to spontaneous and 
traumatic haemorrhage. The condition is probably in every instance congenital, 
and is usually hereditary ; the existence of families of "bleeders " has long been 
known. Generation after generation displays frequent cases of haemophilia, both 
among the direct descendants and the lateral branches. Bleeders are very apt to 
have a numerous progeny. Not all of the children, however, fall victims to the 
disease. Grandidier has pointed out two facts which are of interest in this con- 
nection, as they might aid in deciding as to the marriageability of certain persons. 
If a man belonging to a family of bleeders marries a healthy woman, neither a 
bleeder herself nor inheriting a predisposition to haemophilia, his children are 



908 



CONSTITUTIONAL DISEASES. 



almost certain to be healthy, even though the father himself is a bleeder. On the 
other hand, a woman belonging to a family of bleeders, even though she herself 
is healthy, will almost always have some children who are subject to haemophilia. 
In other words, hereditary predisposition is transmitted much oftener through the 
female than through the male members of the family. Haemophilia itself is, on 
the contrary, much more frequent in the male sex than in the female ; at least 
this is true of the pronounced cases. It is doubtful whether race and place of resi- 
dence are of aetiological importance. So far as is known, haemophilia appears to 
occur in all countries, although it is fortunately rare anywhere. 

[A similar transmission through the females, who themselves usually escape, is 
seen in color-blindness and in pseudo-hypertrophic paralysis.] 

The real causes of haemophilia are entirely unknown to us. We can make one 
or two steps toward the source of the haemorrhage, but we are unable to proceed 
further. It would seem that the bleeding must depend, in the first place-, upon an 
abnormal delicacy of the walls of the vessels predisposing them to rupture, and, 
secondly, upon deficient coagulability of the blood. This latter abnormality is 
evident from the fact that in haemophilia it is difficult to check even the most 
insignificant haemorrhage. Thus far all attempts to discover any anatomical or 
chemical explanation of this imperfect coagulability have been vain. It has not 
been possible to detect any variation in the saline constituents of the blood, or in 
the amount of albuminoids, such as fibrinogen, that it contains, or in its morpho- 
logical elements. And likewise no anatomical change in the vascular walls or the 
heart has yet been reported which throws light upon the character of the disease. 
Various authorities have laid stress upon the small diameter of the arteries and 
the thinness of the intima, but these conditions may occur independently of haemo- 
philia. Fatty degeneration of the intima is, to be sure, often found in connec- 
tion with this disease, but it is doubtless rather a result of the coincident anaemia 
than the cause of the haemophilia. The observations with regard to the heart are 
very contradictory, sometimes it is found to be very small, sometimes of normal 
size, and again actually hypertrophied. 

The subjects of haemophilia do not present any distinctive constitutional pecul- 
iarities. It has been stated that they are very apt to be blondes with a delicate 
white skin, and superficial and abnormally distended cutaneous veins ; but the 
exceptions to this rule are not a few. 

Clinical History. — Haemophilia does not display equal malignity in all cases. 
If we have opportunity to obtain thorough information with regard to families of 
bleeders, we shall find that quite often rudimentary varieties occur, side by side 
with typical and severe cases. There is, to be sure, a striking tendency to haemor- 
rhage even in them ; but the haemorrhage never assumes threatening proportions. 
By perseverance and industry it is possible to collect an almost unbroken series 
of cases, varying in degree from extreme mildness to extreme severity. The fol- 
lowing sketch applies mainly to typical and severe cases. 

That haemophilia is a hereditary constitutional disease is shown by the fact 
that it sometimes appears in earliest infancy. Many cases of umbilical haemor- 
rhage in the new-born are referable to haemophilia. Of course this does not 
apply to all cases. In Jewish children the disease may betray itself for the first 
time when the rite of circumcision is performed. In many cases the disease does 
not betray itself at so early a period ; but this is no proof that the disease is not 
already developed, inasmuch as the young child is not much exposed to trauma- 
tism and other causes which naturally occasion haemorrhage. 

The most striking symptom in a fully developed case of haemophilia is the 
occurrence of severe haemorrhage as a result of the most insignificant causes. A 
slight blow produces a " black-and-blue spot" such as is ordinarily seen only after a 



HAEMOPHILIA. 



909 



very violent injury. The prick of a pin, or a slight cut on the finger, or the extrac- 
tion of a tooth, may give rise in haemophilia to an obstinate and alarming haemor- 
rhage. Epistaxis may be caused by blowing the nose, and haemorrhage from the 
gums by brushing the teeth, and so on. Whether there is ever a perfectly spon- 
taneous haemorrhage is uncertain. It is true that in severe cases haemorrhages 
take place independently of any visible cause. This may be seen in the skin and 
mucous membranes (nose and gums) ; and in rare instances we may even have 
free haemorrhage from the stomach, intestines, or urinary passages. Yet it may 
be doubted whether these occurrences are not the result of comparatively insig- 
nificant mechanical injuries which escape our notice. At any rate, we scarcely 
ever find haemorrhage taking place into the parenchyma of the viscera, in places 
where injury from external sources is entirely out of the question. This fact con- 
stitutes an important point of distinction between haemophilia and the acquired 
haemorrhagic diathesis. 

The second important symptom of haemophilia has been already referred to : 
it is extremely difficult, and may even be impossible, to check by artificial means 
any free haemorrhage which may occur. It is this which makes the disease so 
dangerous, and prevents most patients from reaching old age. It has frequently 
happened that an apparently trifling wound of the skin, or some insignificant 
operation, or a leech-bite, or in women childbirth, has started up a haemorrhage, 
which eventually became fatal. In other cases the haemorrhage is finally checked, 
but not until it has caused profound anaemia. Bleeders are apt to recover with 
remarkable rapidity from the effects of excessive haemorrhage; yet continually 
repeated haemorrhages may lead to a persistent and profound anaemia, attended 
by all the symptoms described in preceding chapters. 

We see, therefore, that the general condition in haemophilia varies with the 
severity of the individual case, and with the more or less fortuitous circumstances 
which develop its dormant characteristics. If no special accident occurs, the 
patient may maintain the appearance of perfect health for years. In the worst 
cases, however, such a state is very temporary, if it exists at all, because the haem- 
orrhages can be so easily excited. As a consequence, the skin almost always pre- 
sents a greater or less number of ecchymoses, while haemorrhages from the internal 
organs contribute from time to time to the general debility and anaemia. Certain 
complications may occur in haemophilia, but they are little characteristic. There 
is a noticeable tendency to " rheumatic " inflammation of the muscles and swelling 
of the joints, wherein is seen a striking analogy to the "haemorrhagic diseases." 
Often there is an actual effusion of blood into the joints. This may cause consid- 
erable functional disturbance of the joints, and even f uate in anchylosis. Various 
writers have also called attention to the comparative frequency of neuralgia, espe- 
cially in the trigeminus. 

Prognosis. — In only too many instances the victims of haemophilia die in 
childhood ; in other cases the patient attains an advanced age. A fact of great 
practical importance is that often, although not invariably, haemophilia grows 
gradually milder with advancing years. If, therefore, the patient has survived 
the period of adolescence, we may believe that his prospects are gradually improv- 
ing. The prognosis of haemophilia is obvious. The amount of danger at any 
given time depends upon the severity of the haemorrhage and the consequent 
anaemia. The comparative severity of the case must be judged from its previous 
history ; as has just been said, the prognosis grows more favorable as the patient 
grows older. 

Treatment. — Prophylaxis assumes a very important place in the treatment of 
haemophilia. First, children who inherit a tendency to the disease, or who have 
given evidence of its existence, should be treated with a view to improve their 



910 



CONSTITUTIONAL DISEASES. 



general constitutional condition, so as to check the development of the disease as 
far as possible. The means to this end need not be described at length. They 
comprise good nourishment, fresh air, cautious endeavors to harden the system, 
baths, and tonics. Secondly, when haemophilia already exists, the patient should 
be guarded as much as possible from any mechanical injury, such as might excite 
haemorrhage. Thus caution is demanded in performing vaccination and other 
apparently trifling operations. 

As regards direct treatment of the disease, no effectual remedy is known. The 
general tonic treatment already referred to should not be neglected; but the 
administration of ergotine, acetate of lead, and similar drugs is indicated, if at all, 
only when haemorrhage is actually taking place, and even then it is very apt to 
fail. The only way to stop the haemorrhage is by surgical methods, and these 
need not be described here. They do not differ essentially from those employed 
when haemorrhage occurs independently of haemophilia. If mechanical efforts 
to check the bleeding fail, we can expect nothing from the remedies above men- 
tioned, nor from sulphate of sodium and the other laxatives which have been 
recommended. For the symptomatic treatment of the anaemia and of its results, 
we may refer to the first chapter of this section. 



CHAPTEE IX. 
DIABETES MELLITUS. 

Definition and ^Etiology. — Under normal circumstances, the blood always con- 
tains a slight amount of sugar ; but this ingredient does not usually pass over in 
appreciable quantities into the urinary excretion. If, however, the amount of 
sugar in the blood exceeds certain limits — that is, if there exists an abnormal 
" glykaemia " — then sugar is excreted in the urine, and we have glycosuria. This 
is seen as a more or less temporary phenomenon under the most varied conditions. 
The amount of sugar in the urine is usually comparatively slight, and it soon dis- 
appears again. Its presence does not imply any persistent abnormal condition. 
This phenomenon has been termed glycosuria or melituria, in contrast with the 
peculiar disease which has for its chief symptom a persistence of sugar in the 
urine, and has therefore received the name of diabetes mellitus. 

The causes of glycosuria need not be discussed here at any length. We will 
briefly state that sugar may appear temporarily in the urine as a result of poison- 
ing from various substances, chief among which are carbonic-acid gas, morphine, 
hydrocyanic acid, mercury, nitrite of amyl, and curare. Temporary glycosuria 
has also been seen in connection with the acute infectious diseases — for example, 
malignant pustule, cholera, typhus or typhoid fever, scarlet fever, diphtheria, and 
malarial poisoning. A far more frequent cause is disturbance of the nervous sys- 
tem. Thus, glycosuria may result from severe concussion of the brain, fracture 
of the skull, cerebral haemorrhage, cerebro-spinal meningitis, and after epileptic 
fits. It is especially apt to occur when there is disease of the medulla ; and we 
need hardly point out how close is the connection between this clinical fact and the 
famous discovery of Claude Bernard, who found by experiment that, when certain 
injuries are inflicted upon the floor of the fourth ventricle, glycosuria inevitably 
follows. It has been thought that diseases of the stomach and liver may occasion 
glycosuria; but this is doubtful. With regard to the theory of diabetes (vide 
infra) it is an interesting fact that extensive disease of the liver — as seen in phos- 



DIABETES MELLITUS. 



911 



phorus poisoning or cirrhosis — occasions no glycosuria, even when the patient's 
diet contains large amounts of sugar (Frerichs). 

Diabetes mellitus is a disease in which a considerable amount of sugar is con- 
stantly present in the blood, and consequently in the urine. The immediate cause 
and the true nature of this strange disease are entirely unknown. It is therefore 
difficult to determine whether all cases of "diabetes mellitus" are essentially 
identical. In most of the typical cases this question may, indeed, be answered 
affirmatively witli little hesitation; but other cases, particularly many of what 
are called the " milder varieties " of diabetes, afford more room for doubt. We 
must not forget that diabetes mellitus is at present known to us only through its 
symptoms, and that the individual cases do not exhibit any uniformity either as 
to causation or as to anatomical changes. 

As has been said, we know practically nothing of the true causes of diabetes. 
All that the physician can do in any particular case is to search for certain excit- 
ing or predisposing causes, the significance of which has been learned from clinical 
experience. It must, however, be borne in mind that in many cases of diabetes, 
and some of them most severe, no cause whatever can be made out ; the disease 
seems to have developed of itself in persons who were previously perfectly well. 
We append a list of such exciting influences as seem to be most frequent and 
important. First, heredity: diabetes has been repeatedly observed to occur in 
several generations of the same family, or in several brothers and sisters. It is 
" noteworthy that the disease may also occur in families where there is a heredi- 
tary predisposition to nervous diseases. Second, improper mode of life : by this 
is meant chiefly unsuitable diet, especially the persistent over-indulgence in starchy 
foods and sugar ; sedentary habits are also considered harmful, especially if asso- 
ciated with over-eating. This is said to be the reason why diabetes is more fre- 
quent among the wealthy classes, and why it is quite common in corpulent persons. 
Third, taking cold and getting wet seem, in occasional rare instances, to determine 
the appearance of diabetes. Fourth, emotional disturbances, excessive mental 
exertion, anxiety, and passion, are sometimes thought to occasion the disease. 
Fifth, it is very remarkable that sometimes the same factors which we have 
already seen to be possible causes of temporary melituria, may also occasion a 
chronic diabetes mellitus ; thus, cases of diabetes have been known to follow 
injuries to the head, and such acute infectious diseases as typhus, typhoid, or 
scarlet fever, cholera, and malarial poisoning. Sixth, certain chronic constitu- 
tional and infectious diseases, particularly gout and syphilis, may perhaps promote 
the development of diabetes. The disease also appears in connection with certain 
organic diseases ; this list includes cerebral diseases, such as haemorrhage, tumor, 
sclerosis, particularly when in the region of the fourth ventricle ; other nervous 
disorders, such as organic disease of the peripheral nerves, and functional dis- 
eases; and, in rare instances, disease of the pancreas, such as suppuration and 
cancer. It is obvious that such cases of diabetes should be regarded as " acci- 
dental," in distinction from the true idiopathic disease. 

Diabetes occurs everywhere, but certain countries and districts seem to be 
particularly liable to it, for example, India, Ceylon, and Italy. In Germany, 
Wiirtemberg and Thuringen are said to present the largest relative number of 
cases. Jews are very liable to the disease. Most cases occur in patients between 
thirty-five and fifty years of age. Next in liability to the disease come younger 
individuals, under thirty-five and over twenty years old. After the fiftieth year 
diabetes is not very exceptional ; but, in the other direction, children under ten 
are very seldom attacked by it, although they are not absolutely exempt. With 
regard to sex, males are much more often attacked than females. 

Clinical History. — With few exceptions, the symptoms of diabetes mellitus come 



912 



CONSTITUTIONAL DISEASES. 



on slowly and gradually. Sometimes the symptoms are merely general and indefi- 
nite, such as languor, emaciation, weakness, and deficient endurance. Sometimes 
we have mild nervous disturbances, including headache, mental depression, wake- 
fulness, and neuralgia, and in still other cases gastro-intestinal symptoms, includ- 
ing nausea, eructations, and irregularity of the bowels. At last the patient's 
attention is called to the altered character of the urine, and particularly to its 
increased amount. He also notices that he is very thirsty, and that, in spite of 
his enormous appetite, he is constantly growing weaker. Sometimes it is quite 
different symptoms which first arouse suspicion of the existence of diabetes; these 
will be mentioned later. In order to make a diagnosis of diabetes mellitus, a 
knowledge of the abnormal character of the urine is indispensable. We shall, 
therefore, proceed to describe the changes produced in the urinary excretion as a 
result of diabetes mellitus. 

1. Character op the Urine. Demonstration of Sugar.— Usually the first 
point that attracts attention is the increased amount. There are often a hundred 
to a hundred and fifty ounces (three to five quarts, 3000-5000 c. c.) excreted in 
twenty-four hours, and sometimes there may even be as much as ten or twelve 
quarts (8000-12,000 c. c). Under suitable treatment and with proper diet the 
amount may, of course, be much smaller. In some cases the polyuria will almost 
cease from time to time (" diabetes decipiens ")• Often the amount of urine 
undergoes diminution, when some intercurrent disease appears, or when death is 
imminent. 

In color the urine is light yellow, corresponding to its amount. It often has 
something of a greenish hue, but a small quantity of it may seem almost as color- 
less as water. Ordinarily the urine is clear and without sediment ; but after it 
has stood for some time it may become cloudy, usually as a result of the develop- 
ment of fermentation spores in great numbers. 

The odor may be somewhat aromatic, suggesting acetone {vide infra). Its 
taste, as determined by earlier observers, may be distinctly sweetish. The reaction 
is acid, and the acidity of the urine may increase on standing, because of the 
alcoholic and lactic-acid fermentation processes which the sugar undergoes. 

The specific gravity is almost invariably greatly increased, as a result of the 
large amount of sugar. If a pale urine is found to have a specific gravity of more 
than 1025, we may feel almost certain that it contains sugar. Specimens often 
have a specific gravity of 1030-1045, and even higher. In exceptional instances 
the specific gravity may fall below 1020 ; this may occur, for instance, where the 
patient is very much debilitated. 

The diagnosis requires that sugar be detected in the urine. The sugar found in 
both the blood and the urine of diabetic patients is grape-sugar (glucose, dextrose), 
The amount of sugar secreted in twenty-four hours often reaches half a pound to 
a pound C200-500 grm.). Of course the amount varies greatly according to the 
diet, mode of life, and treatment of the patient. The greatest amount ever known 
to be produced in twenty-four hours was more than two and one fifth pounds 
(1000 grm.). The percentage of sugar in the urine varies between 0"5-l per cent, 
at the lowest extreme, and 8-10 per cent, as the maximum ; usually it is about 2-4 
per cent. It is noteworthy that in the last weeks, or just before death, the sugar in 
the urine may become greatly diminished in amount, or may absolutely disappear. 

The most important tests for sugar in the urine are, first, Trommer's test : To 
urine in a test-tube sufficient potassic or sodic hydrate is added to make the reac- 
tion strongly alkaline ; then a solution of sulphate of copper (about one part of 
the salt to ten of water) is added, drop by drop. If the urine contains sugar, the 
hydrated cupric oxide, which is at first formed in large amounts, is dissolved, and 
usually the fluid assumes a beautiful deep-blue color. We ought, properly, to go 



DIABETES MELLITUS. 



913 



on adding the sulphate of copper until the hydrated cupric oxide ceases to be dis- 
solved. The urine is then heated, whereupon the cupric oxide is reduced and a 
yellow, or reddish-yellow, precipitate of cuprous oxide, or hydrated cuprous oxide, 
is formed. The application of heat should not be continued long after the precipi- 
tation begins to take place, lest the test be obscured ; the reduction will go on even 
without heat. If the urine contains more than 0*5-1 per cent., this test is perfectly 
reliable. If the reaction is a doubtful one — that is, if there is no precipitate of 
cuprous oxide, although the urine becomes yellow — we should be cautious in mak- 
ing a diagnosis, as the urine may contain other substances than sugar, capable of 
reducing the copper. Second, the bismuth test (Bottger's) : Sodic hydrate or 
sodic carbonate is added to the urine, and then a small pinch of subnitrate of bis- 
muth. Upon boiling, the urine, if it contains sugar, quickly assumes a perfectly 
black color, the oxide being reduced to the metallic state. Third, the potassium 
test (Moore's) : Potassic hydrate is added to the urine in the test-tube and the 
uppermost layer cautiously heated; if it contains sugar, the urine quickly assumes 
a deep-brown color, as a result of the action of the potassium on the sugar; and 
this upper dark-colored layer contrasts strongly with the clear urine below. 

[Fehlings test is justly a favorite in this country, and has the advantage of 
being applicable to the quantitative as well as to the qualitative analysis. The diffi- 
culty of its not keeping well can be met by having separate bottles for the copper 
and tartrate solutions, and making the mixture at the time of using the test. The 
Fehling's-test pellets, put up by chemists, are convenient for the qualitative 
analysis, but, on the whole, they are inferior to the solution.] 

If the above-described tests leave us still in doubt, there can be only a small 
amount of sugar, if any, present. We may, however, attain certainty by employ- 
ing the fermentation test (which causes a decomposition of the sugar into alcohol 
and carbonic dioxide), or circumpolarization (deflection of the plane of polarization 
to the right by the grape-sugar). Further particulars in regard to these and other 
tests, and also in regard to the quantitative estimation of sugar, may be found in 
works on medical chemistry. 

Diabetic urine sometimes contains other varieties of sugar in small amounts — 
namely, levulose, which deflects the plane of polarization toward the left, and 
inosite ; these are, however, of no practical importance. 

The amount of urea is usually somewhat increased {vide infra). Uric acid, on 
the contrary, is excreted in small amounts. The amount of kreatine is normal or 
even increased (Senator). The amount of phosphoric acid and sulphuric acid 
usually corresponds to the amount of urea, or, in other words, to the decomposi- 
tion of albuminoids. Occasionally, according to Teissier, the amount of phos- 
phates is surprisingly great, and may either correspond with the amount of sugar 
simultaneously excreted, or replace the sugar in the urine. This subject has not 
yet been fully investigated. The amount of sodic chloride excreted depends, as in 
health, merely upon the amount ingested. 

Hallervorden has discovered an important fact in regard to the excretion of 
ammonia. In many cases of diabetes, although not in all, it is much increased : 
forty-five to ninety grains (grm. 3'0-6"0), or even more, may be excreted in twenty- 
four hours. Despite this, diabetic urine has an acid reaction ; and, as Stadelmann 
has shown, the basic elements are considerably out of proportion to the acids known 
to us. It is, therefore, evident that diabetic urine, since it contains a large amount 
of ammonium and yet has an acid reaction, must have among its constituents some 
unusual acid. Stadelmann was at first inclined to believe that this was crotonic 
acid. Minkowsky has, however, shown, by his more recent investigations, that 
the acid in question is really oxybutyric acid, or, more accurately, beta-oxybutyric 
acid. This acid is readily decomposed into crotonic acid, which explains Stadel- 
58 



914 



CONSTITUTIONAL DISEASES. 



mann's error. Another interesting fact is that, upon oxidation, oxybutyric acid 
changes to acet-acetic acid, a substance easily decomposed into carbonic-dioxide 
gas and acetone. This suggests the possibility that oxybutyric acid may give rise 
within the system to acetone, a substance which has occupied an important place 
in the literature of diabetes. 

Acetone was first discovered by Petters in diabetic urine. This was regarded 
as an important discovery, because it was believed that the accumulation of this 
substance in the blood produced those grave nervous disturbances (vide infra, dia- 
betic coma) sometimes observed in diabetes. More recent developments have ren- 
dered this view extremely improbable, but it is an established fact that acetone is 
quite often present in the urine of diabetic patients.* Whether it is a primary or 
secondary product remains uncertain. It was formerly believed that acetone was 
formed from ethyldiacetic acid (acet-acetic ether), but of late the tendency is 
rather to regard acet-acetic acid as the source of acetone (Deichmiiller and Tol- 
lens, Jacksch). Acetone is probably the cause of the reaction to which Gerhardt 
has called attention — namely, the development of a Burgundy-red color in the 
urine upon the addition of ferric chloride. This is quite often to be observed in 
the urine of diabetic patients. In speaking of diabetic coma we shall have occa- 
sion to revert to this ferric-chloride reaction. 

Albumen may be found in diabetic urine, as will be seen below under renal 
complications. 

2. Tissue Metamorphosis in Diabetes. Sources of the Sugar, and Vari- 
ations in its Amount occasioned by External Influences.— Inasmuch as the 
presence of sugar in the urine is the most prominent symptom in diabetes, the 
question of its origin is all-important. One fact is indubitable— namely, that the 
secretion of sugar depends in large part upon the amount of potential sugar 
ingested — that is, the proportion of starches in the food. The amount of sugar 
excreted with the urine increases and diminishes with the amount of starchy food 
eaten. If a diabetic patient abstains totally for any length of time from such arti- 
cles of food as contain starch, sugar will, in many instances, entirely disappear 
from the urine. In other words, the system of a diabetic patient is almost, if not 
quite, incapable of oxidizing sugar into carbonic-dioxide gas and water. Voit and 
Pettenkof er have made an experiment, the result of which confirms this statement. 
By means of the great Munich respiration apparatus, they have demonstrated that 
in diabetes the amount of oxygen absorbed from the air, and of carbonic-dioxide 
gas and water given off from the body, is less than in health, the diet being pre- 
cisely the same in both cases. Previously to this many investigators had shown 
that there was a diminution in the amount of the "insensible excreta." 

The oxidation of sugar is not absolutely nil in diabetes. Kiilz has proved by 
numerous experiments that not all the starch is excreted in the form of sugar, and 
he has also found that many varieties of sugar, such as mannite, fruit sugar, and 
inosite, are decomposed even in diabetes, so that their ingestion does not lead to 
an increase of sugar in the urine. 

The disturbances in metamorphosis affect other substances than the carbohy- 
drates. While they escape oxidation, on the other hand, the destruction of albu- 
minoids is increased. We have already stated that diabetic urine contains a large 
amount of urea. Gathgens and others have shown, by means of carefully conducted 
investigations, that this increase in the amount of urea is not merely relative, but 
absolute. The system of the patient destroys a larger amount of albumen than 
does the system of a healthy man, the ingesta in both cases being alike. Whether 



* It should be added that acetone has been found by Kaulich and Von Jacksch to occur frequently 
in the urine during many other diseases, both febrile and non-febrile, and even in normal urine. 



DIABETES MELLITUS. 



915 



this is true in all cases of diabetes is quite doubtful, but the fact is established with 
regard to severe cases. It is also certain that in severe cases a part of the albumen 
is transformed into sugar, escapes oxidation, and is excreted in the urine. The 
proof of this is that in some cases of diabetes sugar continues to be present in the 
urine, although the diet is exclusively nitrogenous. Seegen accordingly divides 
all cases of diabetes into two varieties — a milder form, where sugar ceases to be 
excreted if starchy food is excluded from the diet, and a severer form, where sugar 
persists upon an exclusively meat diet. 

Muscular exertion is one of the external influences which modify the excretion 
of sugar in diabetes. According to our present views, muscular activity wastes 
mainly non-nitrogenous substances, and, accordingly, we find in diabetes that an 
increase of muscular exertion, other things being equal, diminishes the amount of 
sugar excreted. 

Emotional excitement is said to increase the amount of sugar excreted. 

Intercurrent acute febrile diseases may cause a great diminution in the amount 
of sugar, but sometimes there is no essential change. Probably the altered diet 
of the patient plays an important part in this connection, although doubtless the 
special modifications of tissue-metamorphosis occasioned by the high temperature 
or by the disease itself also exert some influence. 

3. Constitutional Symptoms in Diabetes Mellitus. — In many of the milder 
cases there is for a long time little apparent disturbance of the general health. 
The patient is well nourished, and suffers little discomfort, except the incon- 
venience occasioned by the polyuria and the polydipsia. In severer cases the 
system is deeply affected by the drain upon it. The patient becomes emaciated, 
weak, and easily exhausted, and at length there may be profound marasmus. 
Mentally, the patient is apt to be depressed and irritable. The intellectual powers 
are not impaired, but there is indisposition to mental effort. The temperature is 
normal or subnormal. Fever invariably indicates some complication. 

4. Symptoms referable to the Digestive Organs. — We have already men- 
tioned the excessive thirst experienced in diabetes. This may be a source of great 
discomfort, obliging the patient to drink at short intervals, even through the 
night. The interdependence of polyuria and polydipsia is not yet fully under- 
stood. The most natural view seems to be that the increased excretion of water 
by the kidneys is the primary factor, and the increased thirst secondary thereto. 
One cause of the polyuria is the excretion of sugar, in order to dissolve which a 
large amount of water is necessary, but certain nervous factors would also seem 
to be implicated. That they exert some influence is rendered probable by the fact 
that the amount of urine does not always correspond to the amount of sugar 
excreted. A very large amount of urine may be excreted containing little or no 
sugar ; and, on the other hand, there are genuine cases of diabetes mellitus where 
the amount of urine is normal, and the patient feels no unusual thirst {diabetes 
decipiens). It has also been suggested that the sugar may irritate the nerves of 
the mouth and throat, and thus cause thirst. According to this idea, the polyuria 
would be merely the result of the excessive ingestion of liquids. The abnor- 
mally great appetite in diabetes seems in most cases to be due to defective assimi- 
lation of the food. Many patients are never able to eat enough. They have a 
longing, in many cases, for carbohydrates. Occasionally the hunger becomes 
ravenous, and is associated with headache and a general sense of weakness, all 
these symptoms being alleviated when food is taken. This rule has rare excep- 
tions in which the appetite is not unusually great, even though the case is a 
severe one. 

The tongue is frequently dry ; it is broad and thick, with an irregular and fis- 
sured surface, sometimes coated and sometimes red. The gums may be spongy, 



916 



CONSTITUTIONAL DISEASES. 



and may exhibit a tendency to bleed. The teeth frequently decay rapidly. The 
saliva is invariably f omid to give an acid reaction. This is true of the isolated 
secretion of the parotid gland also, and is said to be due to the presence of lactic 
acid. It is only in exceptional instances that sugar can be demonstrated in the 
saliva. Thrush quite often appears on the soft palate. 

There are no marked gastric symptoms. There is usually constipation, but 
sometimes there is a severe, though temporary, diarrhoea. The liver and spleen 
are seldom much affected ; the liver rarely is somewhat enlarged. Jaundice is 
frequently observed, but it is always referable to some complication. As a rule, 
the secretion of the bile goes on as in health. 

5. Symptoms referable to the Respiratory Organs. — In many cases the 
organs of respiration are unimpaired for a long while. It may be mentioned that 
often patients have a decidedly fruity odor to the breath (acetone odor). In the 
later stages of the disease pulmonary complications are very frequent. Almost 
one half of all diabetic patients perish from secondary disease of the lungs. Most 
frequently there is pulmonary tuberculosis ; its course, symptoms, the presence of 
tubercle bacilli, and all other details are the same as in ordinary cases of tuber- 
culosis. Next in point of frequency is pulmonary gangrene. Sometimes there is 
a diffuse gangrenous process, and sometimes there are isolated foci of necrosis, 
which become liquid, and have an acid reaction, but they often have compara- 
tively little odor. The expectoration in these cases may be odorless. Croupous 
pneumonia may also occur. It often terminates unfavorably, and may, as we 
have ourselves observed, result in gangrene. 

6. Symptoms referable to the Circulatory System. — In many instances 
the circulatory apparatus presents no special lesions. The pulse is either of a nor- 
mal rate or a trifle slow. It is usually soft, although exceptionally it may exhibit 
increased tension. There is often distinct evidence of cardiac weakness (Schmitz) ; 
the pulse is small, intermittent, sometimes very slow (50 or even 40 beats per min- 
ute), and sometimes accelerated, 100 to 120 beats per minute. There are shortness 
of breath, fahitness, nausea, and the like. Sometimes sudden and profound car- 
diac disturbance occurs, and may occasion speedy death (vide infra, coma). Not 
very rarely diabetes is combined with general arterio-sclerosis. This is particu- 
larly apt to be the case in patients who have been subject to gout. 

7. Genito-urinary Symptoms. — Despite the great demands made upon them, 
the kidneys usually maintain a normal condition. As we shall see when we come 
to the pathological anatomy of diabetes, the kidneys are often very large. Some- 
times a chronic nephritis is developed as a complication, usually in the later stages 
of the disease. The urine contains albumen, and there are oedema and other 
symptoms of renal disorder. It was formerly a common opinion that the nephri- 
tis results from the irritation of the sugar excreted by the kidneys, but this is not 
very probable, especially as in most cases of nephritis complicating diabetes there 
are usually present at the same time other disorders, to which the nephritis might 
be referable, such as pulmonary consumption or cardiac disease. We have seen 
well-marked suppurative pyelo-nephritis as a complication of diabetes. If the 
amount of albumen in the mine becomes considerable, the excretion of sugar usu- 
ally undergoes marked diminution. 

Saccharine urine is apt, as it decomposes, to cause irritation of the skin. This 
is the explanation of the troublesome pruritus pudendi, which is especially marked 
in women. It may, indeed, be this symptom which first directs attention to the 
disease. Sometimes the external genitals are attacked by eczema or furunculosis. 
Men often suffer from balanitis, with inflammatory phimosis, or paraphimosis. A 
frequent and important symptom in men is impotence. This sometimes occurs 
very early in the disease, but it may afterward undergo improvement. The origin 



DIABETES MELLITUS. 



917 



of it is not determined. Some authorities state that diabetes is apt to occasion 
atrophy of the testicles. 

8. Disturbances of the Organs of Special Sense. — An important and not 
infrequent result of diabetes is cataract. This may occasion almost total blind- 
ness. The cause of cataract in diabetes is not known. It was formerly supposed 
that the sugar in the blood absorbed water from the crystalline lens, and thus 
occasioned its opacity ; but this has not been confirmed. Diabetic patients are also 
subject to disturbances of accommodation. Ketinitis, atrophy of the optic nerve, 
and purulent choroiditis may also occur, but they are very rare, and perhaps are 
merely chance complications. 

Noue of the other special senses are peculiarly affected in diabetes. 

9. Cutaneous Affections. — In most cases the skin is remarkably dry and 
rough. There may, however, be abundant perspiration. Several authorities claim 
to have found sugar in the perspiration, but this statement has not been confirmed 
by later investigators. Sometimes there is a troublesome pruritus. In many cases 
there is a great tendency to furunculosis. This may be the first symptom to sug- 
gest the existence of diabetes. In the later stages there are sometimes extensive 
carbuncles, which may prove fatal. Once we saw an eruption resembling pem- 
phigus appear a short time previously to death. Gangrenous processes have been 
repeatedly observed, and in particular necrosis of one or more toes, or rarely of 
an entire extremity. This gangrene often seems to be due to arterial sclerosis ; in 
other cases its cause is obscure. 

QEdema of the subcutaneous cellular tissue may occur independently of nephri- 
tis. It is then probably occasioned by the cardiac weakness. 

[Another skin affection which deserves mention is eczema. In the neighbor- 
hood of the genitals it is more common in women than in men, and is attributable 
to the irritating properties of sugar contained in the urine acting on a skin the 
nutrition of which is impaired owing to the morbid condition of the blood. Some- 
times the eczema involves other portions of the integument, is generally acute, and 
has an angry appearance.] 

10. Symptoms referable to the Nervous System. — It has already been 
mentioned that there is frequently in diabetes a moderate disturbance of the 
whole nervous system, as indicated by headache, physical and mental hebetude, 
and depression of spirits. Still more characteristic is neuralgia. This is most 
often located in the sciatic nerve, and an obstinate bilateral sciatica may be one of 
the first symptoms of diabetes. Occipital or trigeminal neuralgia or hemicrania, 
and, on the other hand, anaesthesia, have also been repeatedly observed. Bou- 
chard has called attention to the frequent absence of the patellar tendon reflex in 
diabetes. To what this is due, or what relation it bears to the primary disease, is 
not known. Possibly it is caused by degeneration of the peripheral nerves. 

The most important nervous symptom of all is a peculiar disturbance, which 
occurs in a considerable proportion of all cases with more or less suddenness, and 
usually terminates in a surprisingly speedy death. This strange phenomenon 
was first thoroughly investigated by Kussmaul, although known long before. It 
is termed diabetic coma. The condition sometimes develops without any evident 
cause. In other instances it is apparently brought on by violent muscular exer- 
tion, mental excitement, or some trifling illness, such as gastric catarrh, bron- 
chitis, or sore throat. 

Frequently certain mild prodromata herald its onset. There may be nausea, 
headache, a sense of thoracic oppression, and general uneasiness. Soon the con- 
dition becomes aggravated. The patient is seized with a feeling of great anxiety, 
and becomes delirious, sometimes jumping out of bed and growing uncontrolla- 
ble. Gradually, however, the excitement gives place to an ever-increasing 



918 



CONSTITUTIONAL DISEASES. 



drowsiness, usually terminating in the most profound coma. One of the most 
frequent and striking symptoms attending this condition is the peculiar alteration 
in respiration. The breathing becomes remarkably deep and noisy. Its rate may 
remain nearly normal ; or it may be considerably increased, so as to justify the 
term " diabetic dyspnoea. " The patient is sometimes cyanotic. The pulse is usu- 
ally very rapid and small. The temperature gradually sinks, and has in repeated 
instances fallen to 88° (30° C), or even lower. In most instances, also, the 
breath has a very noticeable odor, resembling fruit or chloroform, which may be 
perceived on entering the room. Even the urine may have this same odor ; and 
it almost invariably becomes dark red on the addition of ferric chloride (vide 
supra). 

Diabetic coma does not pursue the same course in all cases ; sometimes the 
patient lingers on for several days before death, while in other instances the 
change is extremely rapid, and death speedy. The early stage of excitement may 
be wanting. The patient becomes somnolent, and then comatose, and never 
regains consciousness. Temporary improvement, and even complete cessation of 
the threatening symptoms, are not impossible, but they are very exceptional. 

We have no certain information as to the cause of diabetic coma. Of course 
the cases where an autopsy discloses some marked organic lesion, such as cerebral 
haemorrhage, capable of producing the nervous symptoms, are not true diabetic 
coma. Nor do the cases of sudden death reported by Frerichs deserve to be 
classed as diabetic coma, where death occurred with the symptoms of acute car- 
diac failure — namely, collapse, coolness of the extremities, small and rapid pulse, 
and unconsciousness. Besides, these patients never have the acetone odor, the 
exaggerated respiration, nor the ferric-chloride reaction, and usually the myocar- 
dium is found to be in an advanced state of degeneration. 

In genuine diabetic coma, on the other hand, everything seems to indicate 
that the system has been poisoned by some noxious product of the abnormal pro- 
cesses of metamorphosis. Great effort has been made to discover what this prod- 
uct is, but in vain. Kussmaul regarded acetone as the injurious substance, and 
therefore called diabetic coma " acetonsemia. " Other investigators believe that 
acet-acetic acid (Jackscb) is the cause of the phenomenon in question, or at least 
regard the coma as a result of poisoning from some of the unusual acids present 
in diabetes (Stadelmann — vide supra). No one view has obtained general accept- 
ance, nor has it been possible to produce diabetic coma in animals by the employ- 
ment of acetone, acet-acetic acid, crotonic acid, or similar substances (Brieger 
and others). It is, nevertheless, extremely probable that these substances do have 
some close connection with "diabetic intoxication" (Frerichs). 

Pathological Anatomy and Histochemistry of Diabetes Mellitus.— The mysteri- 
ous phenomena of diabetes mellitus present a problem the solution of which has 
been most industriously sought post mortem ; but no satisfactory result has been 
reached, even in this way. 

If we exclude the organic diseases, such as pulmonary tuberculosis and nephri- 
tis, which are merely complications, the pathological changes in diabetes are 
trifling, Bernard's discovery, that an injury inflicted in a certain spot on the 
floor of the fourth ventricle produces glycosuria in animals, has directed the 
attention of investigators to the condition of the nervous system in this disease. 
In some instances tumors, sclerosis, or similar troubles have been found in the 
medulla and cerebellum ; but in these cases the diabetes was evidently not idio- 
pathic (vide supra). In idiopathic cases the central nervous system presents no 
striking macroscopic changes. By means of the microscope, Frerichs has found 
lesions of the medulla oblongata in frequent instances. The minute blood-vessels 
are widely dilated ; there are small capillary haemorrhages, some of a more recent 



DIABETES MELLITUS. 



919 



and others of a more remote date ; and occasionally there are microscopic foci of 
myelitis. The nervous elements proper, the nerve-fibers and ganglion-cells, betray 
no alteration. The significance of these changes must be determined by further 
investigation. 

The stomach and intestinal canal present no constant alterations of impor- 
tance. 

The liver has naturally been the object of repeated and careful examinations, 
because of its well-known part in the manufacture of glycogen. Yet this organ 
seldom presents any special abnormality. It is usually of the natural size, and 
may either contain considerable or very little blood. The amount of glycogen in 
the hepatic cells can be demonstrated with iodine by a micro-chemical reaction. 
It appears that, other things being equal, there is less glycogen present than 
normal. It is usually found only in the cells situated upon the periphery of the 
lobules, and in small quantities. In an extremely advanced case of diabetes 
Ehrlich obtained, by means of a hollow needle, small amounts of the hepatic 
parenchyma for examination during life, and found that glycogen was almost 
completely absent. In other cases the liver has been examined as early as possi- 
ble after death, and presented no trace of glycogen. Sometimes, however, 
glycogen has been found. 

The spleen is usually of normal size. Occasionally it is atrophied, or, on the 
other hand, slightly enlarged. No other changes in it have been observed. Many 
cases have presented a striking atrophy of the pancreas (Bouchard). The con- 
nection of this atrophy with the diabetes is unexplained ; nor has it yet been deter- 
mined whether the cceliac plexus is frequently involved in the atrophy. 

The kidneys are often enlarged, from functional hypertrophy. Ehrlich dis- 
covered in them a glycogenic degeneration * of the loops of Henle. This change 
is a constant one. The epithelial cells in the loops are enlarged, and the proto- 
plasm in these cells, although apparently homogeneous, is found, by the addition 
of a solution of iodine in mucilage, to contain glycogen, in flakes and clumps of 
varying size. How important this glycogenic degeneration of the kidneys may be 
has not yet been determined. Perhaps the glycogen represents sugar which has 
been absorbed by the cells. That chronic nephritis may complicate diabetes has 
already been mentioned. 

No thorough investigation of the chemical composition of the blood in diabetes 
has yet been made. One important and constant characteristic is the gradually 
increased proportion of sugar in the blood. There is usuaMy somewhere between 
0'2 and 0*45 per cent, of sugar, while in health the blood rarely contains over O'l 
per cent. The lymph, and such serous effusions as are found, contain sugar, but 
the saliva, perspiration, bile, gastric juice, and other secretions rarely furnish evi- 
dence of its existence. 

Varieties, Course, and Prognosis of the Disease.— The study of a large number 
of cases of diabetes will show great variations in the course and duration of the 
disease. As already stated, we may in practice distinguish mild and severe forms 
of diabetes. In the mild cases, sugar ceases to be excreted if the patient is put 
upon a diet containing no carbohydrates. Sometimes it is even possible for the 
patient to eat a small amount of starchy food without occasioning glycosuria, 
particularly if he takes sufficient exercise {vide supra). In the severe form, sugar 
persists in the urine even upon a purely meat diet ; and upon the ingestion of 
carbohydrates there will be, at the end of half an hour or an hour, a large increase 
of sugar. Most of the other symptoms are alike in both forms of the disease, 
varying only in degree. The moderate form may eventually assume a severe 



Ebstein noticed and described this condition ; but he regarded it as a necrosis of the epithelium. 



920 



CONSTITUTIONAL DISEASES. 



character ; and sometimes, although the secretion of sugar remains permanently 
small, there are finally developed fatal complications, such as tuberculosis of the 
lungs. 

The general course of diabetes varies in different cases, exclusive of the differ- 
ences already referred to. In a few instances the disease occupies only a few 
weeks, and may almost be termed " acute diabetes." Other cases last one or two 
years, and still others ten or twenty years. The patient's condition may vary 
from time to time. We have repeatedly seen the sugar disappear temporarily 
from the urine, and the patient apparently completely recover ; but sooner or later 
the disease breaks out again. These cases have been called " intermittent dia- 
betes." The relapse is often brought about by emotional excitement or some 
grave error in diet. Again, the disease may undergo apparent arrest and the 
patient enjoy comparative comfort for years. As a general rule, it may be said 
that older patients are more apt to have the mild form of diabetes, while in young 
adults and children the disease is wont to pursue a more rapid and unfavorable 
course. 

Different cases also differ in the relative severity of particular symptoms. 
Thus, the clinical picture presented by diabetes may be modified by the general 
constitution of the patient — for instance, his corpulence or emaciation ; by such 
complications as diseases of the lungs, kidneys, or brain, or syphilis and gout ; and 
by many other conditions. We would again call attention to the fact that diabetes 
may exist without polyuria or abnormal thirst, and so be overlooked. It is a very 
interesting fact that diabetes mellitus occasionally undergoes gradual transforma- 
tion into diabetes insipidus (see the next chapter). Frerichs has given some strik- 
ing examples of this change. 

The usual termination of diabetes is death. We have already seen how great 
a difference there may be in the length of time preceding the fatal termination, 
and in what various ways it may be brought about. The most frequent immediate 
causes of death are marasmus, diabetic coma, pulmonary consumption, nephritis, 
furunculosis, or the development of carbuncles. 

There is no doubt that complete recovery may occur ; but this is exceptional, 
and is possible only in the milder cases. It should also be borne in mind that 
apparent recovery does not exclude the possibility of a fresh outbreak of the dis- 
ease. 

[It should be clearly understood that the presence of sugar In the urine does 
not in itself indicate diabetes; and that diabetes is not now considered nearly as 
hopeless a disease as it was. The diagnosis was formerly seldom made unless one 
or all of the cardinal symptoms — increased thirst and appetite, with progressive 
emaciation, and polyuria — were markedly present, a condition of things which 
may be roughly compared to phthisis in the stage of cavity. The prognosis is 
more grave in the young than in those past middle life, in thin than in stout 
people, in those from whose urine the sugar does not disappear under dietetic treat- 
ment alone. If the bodily weight and the strength are well maintained, sugar may 
be excreted for long periods without any obvious ill effects.] 

Theoretical Discussion of the Nature of Diabetes. — We have endeavored to 
give an approximately complete summary of the facts pertaining to diabetes. We 
trust we shall be excused from detailing all the theories and hypotheses which 
have been devised to explain the peculiar phenomena of the disease, particularly 
the glycosuria. It is a better way simply to confess that the true nature of dia- 
betes mellitus as yet remains very obscure. We shall confine ourselves to a few 
remarks upon the present state of the question. 

The essential fact which demands explanation is the excess of sugar in the 
blood. The source of this sugar is probably the same as of the sugar normally 



DIABETES MELLITUS. 



921 



contained in the blood. The largest part of the sugar probably comes from the 
carbohydrates contained in the food. These are, for the most part, converted into 
sugar in the primse viae, which sugar thereupon enters the portal system. It may 
also be assumed that glycogen, so widely diffused throughout the system, is an- 
other source of sugar. The liver is the main seat of the manufacture of glycogen ; 
but it is produced in other parts as well, and in particular in the muscles. The 
question next arises, From what is the glycogen formed ? A part of it is probably 
manufactured from the carbohydrates contained in the food, but another part is 
certainly due to the ingested albuminoids. Again, the transformation of glycogen 
into sugar is not confined to the liver, but may take place wherever glycogen is 
produced. How it takes place is unknown. It is usually assumed that there is 
some ''saccharine ferment." 

It would seem, therefore, that the sources of sugar are the same in diabetes as 
in health. We have next to seek for the reason of its excessive accumulation in 
the blood. Under normal circumstances, the sugar present in that fluid rapidly 
undergoes decomposition into other substances. In health there is no great 
excess of sugar in the blood, even upon a diet extremely rich in starch ; and it is 
possible to eat large amounts of sugar without any glycosuria. We see, there- 
fore, that diabetes can not be explained by assuming that there is an increased 
production of sugar except in so far as corresponds to the increased amount of 
ingesta. On the other hand, everything points toward the conclusion that in 
diabetes the ordinary processes effecting the decomposition and destruction of 
sugar are suspended. The sugar is excreted by the kidneys unaltered, for the rea- 
son that it is not destroyed. It is difficult to conjecture what the circumstances 
may be which thus interfere with the decomposition of the sugar. Perhaps it 
is some special nervous influence, or perhaps some ferment may be wanting in 
diabetes which in health promotes the metamorphosis of the sugar. Another 
point that is difficult to understand is, that in the milder cases of diabetes only 
such sugar as originates from the starch contained in the food is excreted, while 
the sugar manufactured from albumen seems to be completely decomposed. The 
cause of the excretion of sugar can not lie in the disturbed condition of the kid- 
neys, for in diabetes insipidus, as Frerichs shows, no glycosuria is produced, even 
when a very large amount of sugar is ingested. 

Diagnosis. — For the diagnosis of diabetes mellitus it is indispensable that 
sugar should be demonstrated in the urine. We have, furthermore, to decide 
whether the condition is a temporary or a permanent one, or, in other words, 
whether we have to deal with mere glycosuria or genuine diabetes mellitus. This 
point is to be determined by means of the symptoms and general course of the 
disease. 

Diabetes often exists for some time, unsuspected even by the physician. It 
may therefore be well to name over the symptoms which may be the first to 
attract the patient's attention, and which should, therefore, always suggest to a 
physician the possibility of the existence of diabetes. They are : 1, languor and 
debility ; 2, f urunculosis ; 3, pruritus pudendi in women, balanitis in men ; 4, cata- 
ract; 5, sciatica, especially if bilateral; 6, impotence. Of course a complaint of 
polyuria, or excessive thirst, would be still more suggestive. 

If symptoms similar to those just enumerated lead to an examination of the 
urine, and the result of this is ambiguous, it is advisable to have the patient par- 
take of a meal rich in starchy elements, and to examine the urine thereafter. If 
even then no sugar is found, diabetes does not exist. 

[The urine passed three or four hours after a full meal often contains sugar, 
when that passed on rising is quite free from it.] 

Treatment. — Medical science does not possess the power to cure the disease, 



922 



CONSTITUTIONAL DISEASES. 



but it can greatly benefit the patient, both by alleviating his symptoms and by 
shielding him, at least for the time, from many of the secondary effects. 

The first requisite is to institute a proper regimen. All the hygienic circum- 
stances of the patient should be regulated. This is more important than any sort 
of medicinal treatment. We have seen that a large part of the food taken by a 
diabetic patient escapes from the body unutilized, and that, as a result of this, 
certain disturbances are produced in the tissues : thus there is a tendency to 
furunculosis and gangrene and cataract. Furthermore, the sugar contained in 
the urine gives rise to certain secondary symptoms, such as balanitis, and perhaps 
its presence in other secretions has analogous bad effects. "We must therefore 
endeavor, first, to promote the conversion of the non-nitrogenous elements of the 
food ; and, secondly, to furnish the system with a substitute for that portion of 
the food which it can not assimilate, and to obviate the excessive ingestion and 
production of sugar. It would be erroneous to conclude that this last point is the 
only essential one, and that we accomplish our whole duty by reducing the amount 
of sugar contained in the urine to a minimum. The general condition of the 
patient should invariably be taken into consideration. There can be no doubt 
that a diabetic patient whose strength is well maintained is better off than one 
whose urine contains only one per cent, of sugar, but yet is daily growing weaker. 

Mental excitement has been suggested as a possible cause of the disease ; and 
there can be still less doubt that it almost invariably has a bad effect upon its 
course. The physician should therefore endeavor, as far as he is able, to guard 
the patient from excitement, whether incidental to his occupation or to his social 
position. 

A proper diet is of the greatest importance. It has already been stated that in 
many instances the excretion of sugar may be entirely stopped by excluding 
starch from the ingesta ; but such exclusion does not always result in permanent 
benefit to the patient. Cantani, however, believes otherwise, and has laid down a 
very strict dietetic regimen. He states that in not a few cases an almost exclusive 
meat diet may be persisted in for years, and the patient at length experience com- 
plete recovery, or even acquire the ability to partake once more of starchy food 
with impunity. That such favorable results may occur we have no doubt ; but 
we must call attention to the fact that it is frequently impossible to enforce the 
strict regimen of Cantani, and that many patients, while following it, feel worse 
than when they indulge in a moderate amount of carbohydrates. The " cure " 
affords them no relief, but merely distress. At present authorities are generally 
inclined to recommend a diet mainly of flesh or albuminoids, but not absolutely 
devoid of carbohydrates. The amount of starch which can be safely ingested 
varies with the individual. Of course, the best way is to judge of the system's 
power to tolerate starch by means of daily quantitative estimations of the amount 
of sugar excreted. We repeat that, within certain limits, the percentage of sugar 
should not be the only criterion of the suitability of the diet, but that the general 
condition should also be taken into consideration. 

If we consider the most common articles of diet with regard to the proportion 
of carbohydrates they contain, we shall find that they may be classified somewhat 
as subjoined. First, the following articles may be allowed ad libitum : All sorts 
of fresh meat, ham, smoked meat, tongue, fish, crabs, eggs, caviare, sour milk, 
cheese, butter, bacon ; also green vegetables, lettuce, spinach, and cucumbers. 
Secondly, the following may be used moderately : Bread, milk, fruit, rice, turnips, 
beets, asparagus, radishes, cauliflower ; also light beer, claret, and other dry wines. 
Thirdly, if possible, the following should be entirely abandoned : Sweet dishes, 
cake, honey, potatoes, grits, sago, peas, beans, lentils, sweet fruit, sweet wine, and 
liqueurs. 



DIABETES MELLITUS. 



923 



The greatest trial for most patients is to give up bread. Every physician has 
had experience of the cunning which patients exercise in order to satisfy their 
invincible craving for it. Faults of this kind are not so apt to be committed if 
the patient is allowed a limited amount of bread, say two or three ounces a day in 
divided portions. There have also been many attempts to make a bread out of 
such carbohydrates as have been found by experience not to increase the excretion 
of sugar, and thus to furnish a substitute for ordinary bread; but these succedanea 
have not become popular, mainly because of their bad taste. They may, however, 
be tried. We have not space to describe in detail the various kinds of " diabetic 
bread " which have been recommended. The best known are bread made from 
bran flour (Prout), from almonds (Pavy), from inulin and Kchenin (Kiilz). Most 
of these substances contain a considerable amount of starch. 

Since we can not supply the system of a diabetic patient with carbohydrates in 
sufficient amount, it suggests itself that we should endeavor to supply the lack by 
other non-nitrogenous substances, and that the patient should be allowed a large 
proportion of fat in his diet. With regard to this, experience and theory coin- 
cide. Fatty substances are well borne in most cases, and we should not only 
allow, but urge patients who are at all emaciated to use butter, cream, and similar 
articles of diet. Cod-liver oil is also frequently employed, and is even regarded 
by many physicians as having a specific effect. It may be stated in this connec- 
tion that for a time it was believed that glycerine might serve as a substitute for 
sugar (Schultzen) ; two to three ounces may be given in a day ; but, with some 
apparent exceptions, its administration has not proved especially satisfactory. 

Duhring claims that by long-continued boiling the carbohydrates may be so 
modified as to cease to affect the excretion of sugar in diabetes. Duhring gives 
his patients mainly rice and fruit, these substances having previously been soaked 
in water and boiled for several hours. His method also includes certain other 
dietetic and hygienic measures, but it has not yet been satisfactorily tested. 

To quench thirst, we may allow the patient simple water or Seltzer- water, and 
acidulated drinks. If the thirst be very troublesome, the patient may let little 
pieces of ice melt in the mouth. Tea and coffee may be taken with cream, but 
without sugar. In place of sugar, we may make trial of glycerine or mannite. 
Milk does not need to be absolutely banished, but few patients care for it. Alco- 
holic beverages may be allowed in moderation, particularly red wine, such as 
Bordeaux, and light beer. Thirst may also be moderated by weak brandy and 
water. 

[The dietetic treatment of diabetes is so important that it is desirable to go more 
into detail. 

There is some discrepancy between the authorities on this point, a more strict 
diet being laid down by some than by others. Half e's list is as rigid as any, and 
is as follows : 

To avoid milk (except very small quantities for cooking purposes). The liver 
of all animals (as the liver of oysters and all mollusca is large, and abounds in 
glycogen, these animals must be forbidden), so also the interior of crabs, lobsters, 
etc. Bread, biscuits, rusks, toast, farinaceous vegetables, such as potatoes, Jeru- 
salem artichokes, rice, oatmeal, corn-flour, sago, tapioca, arrowroot, etc. Saccha- 
rine vegetables, turnips, carrots, parsnips, green peas, French beans, beet-root, 
asparagus, tomatoes. Blanched vegetables of every sort, as celery, sea-kale, endive, 
radishes ; also the stalks and white parts of such vegetables as cabbage, lettuce, 
broccoli, etc. Fruits of all kinds. Jams, syrups, sugars. Certain condiments, 
such as chutnee and sweet pickles, cocoa, chocolate, liqueurs, sweet wines. 

May take meat, fish, poultry, game, bacon, ham, eggs. Bread and biscuits made 
with prepared gluten, bran, or almond-flour. Green vegetables, summer cabbage, 



924 



CONSTITUTIONAL DISEASES. 



turnip-tops, spinach, broccoli-tops, water-cresses, mustard and cress, laver, sauer- 
kraut, the green parts of lettuce, sorrel, mushrooms. Nuts of various kinds (except 
chestnuts). Cheese. 

Flint's list is more lenient, allowing oysters and a much larger choice of vege- 
tables, such as asparagus, string beans, artichokes, cauliflower, tomatoes, etc. 
("Journal of the American Medical Association," July 12, 1884 ; also "Pepper's 
System of Medicine," vol. ii, page 221). 

Donkin's treatment by skim milk exclusively is highly approved by Tyson. 

Rhenish and similar wines, moderate quantities of spirits, or a malt liquor in 
which the sugar has been entirely converted into carbonic acid and alcohol (Bass's 
ale, for instance), are permitted. 

In the opinion of the writer, it is always well to begin treatment with a very 
stringent dietary, which may be relaxed gradually as circumstances dictate. The 
severity of the case is to be regarded rather than the name of the disease. The 
gluten and other diabetic flours are unreliable; and I agree with Flint that, if 
bread is allowed, it is better to give the crust of a French roll the ingredients of 
which are known.] 

Certain other general directions are important. The patient should take suffi- 
cient exercise. Kiilz has determined by means of accurate experiments that, other 
things being equal, the assimilation of sugar is increased upon increase of muscu- 
lar activity, with a consequent diminution in the excretion of sugar. Practical 
experience also shows that regular exercise is extremely beneficial. A proper dis- 
cretion should be employed, however ; nothing would be more injudicious than to 
force a feeble patient to exhaustive efforts. But if the patient is vigorous and well 
nourished, he should be strongly urged to take a walking-trip in the mountains, 
or to try horse-back riding and the like. 

Proper care of the skin is indispensable. Baths, cold sponging, and douching 
may be employed. Strict attention should also be given to the teeth, lest they 
become carious. Thorough ventilation should be maintained, both day and 
night. 

Of internal remedies, opium should be named first. One good effect of this drug 
is that it lessens the annoying thirst. It sometimes also causes decided diminution 
in the amount of urine and sugar excreted. It is further indicated when there is 
general restlessness or sleeplessness. It is often well borne by diabetic patients, 
even in large doses. A patient sometimes can take four to eight grains (0 •25-0* 50 
grm.), or even more, of opium in twenty-four hours without any bad effects. It is 
noteworthy that the alkaloids of opium, such as morphine and codeia, possess 
much less value than opium itself. 

[If sugar does not disappear from the urine under diet alone, or if a strict diet 
is not tolerated for any reason, opium is indicated. The drug is usually well tol- 
erated, and can be given in divided doses or in one dose at bed-time. If the latter 
course is adopted, one grain can be given and increased until the sugar either dis- 
appears or ceases to diminish in amount ; this dose varies with different individ- 
uals, but, when reached, it can be maintained without increase for a long time. 

The author seems to me hardly to do justice to codeia, or to arsenic, which 
latter, in the form of Clemens's solution— the arsenite of bromine— is often useful 
in doses of three to five minims after meals.] 

Belladonna, cannabis indica, chloral, and bromide of potassium are also given, 
but they are less efficient than opium. Bromide of potassium would probably be 
the best of these, particularly if there were a condition of nervous excitement. 

The alkalies, and still more the alkaline mineral-waters, enjoy a reputation 
second only to that of opium. Hundreds of patients visit Carlsbad, Neuenahr, 
and Vichy every year to return much benefited. Of course it must not be for- 



DIABETES MELLITUS. 



925 



gotten that it is not merely the waters which produce these beneficial changes. 
Other factors are also important, in particular the strict diet, fresh air, and free- 
dom from the cares of the household and business. Why the alkalies should act 
favorably we do not know. Griesinger, and later Kulz, as well as others, have 
made careful comparisons of the amounts of sugar excreted under like circum- 
stances, with and without the ingestion of bicarbonate of soda or of Carlsbad 
water and similar substances, and, for the most part, have not been able to per- 
ceive any benefit from these remedies. Practical experience, however, shows the 
value of these alkaline springs ; and their use is to be recommended, although the 
expectations of the patient should not be wrought to too high a pitch. 

From a theoretical point of view, there is interest in the fact that certain reme- 
dies which are antagonistic to fermentation have been shown by Ebstein and 
Muller to diminish the excretion of sugar in many cases of diabetes. Chief among 
these are carbolic acid and salicylate of sodium. The carbolic acid is given in the 
amount of ten to twenty grains (0'5-l*5 grm.) per diem. The amount of salicy- 
late of sodium is one to two and a half drachms (5-10 grm.) daily. There is no 
doubt that these drugs possess the property ascribed to them ; but they are neither 
of them advantageous to the patient, inasmuch as the general condition is hardly 
ever improved by their use. On the contrary, very unpleasant effects are some- 
times observed. 

There is no need of enumerating all the remedies which have been recom- 
mended in diabetes. All that possess any extended reputation have already been 
mentioned. We have therefore merely to refer to certain drugs which have been 
lately introduced. 

Cantani has suggested the employment of lactic acid in the amount of one to 
two and a half drachms (grm. 5-10) per diem, dissolved in half a pint of water. 
This drug may perhaps serve as a physiological substitute for sugar, as glycerine 
is supposed to do {vide supra), but it has no specific virtues. 

Certain salts of ammonia, such as the carbonate and acetate, are said to dimin- 
ish the excretion of sugar, and have, therefore, been long employed in diabetes, 
but without special benefit. 

Iodoform has been recommended by Moleschott to the amount of three to six 
grains (grm. 0*2-0*4) per diem. It is said not only to diminish the amount of 
sugar in the urine, but also to alleviate other symptoms. Arsenic, tincture of 
iodine, and quinine have also been employed ; and we may mention that even 
electricity has been tried, we need hardly say, in vain. 

It is evident, in brief, that the best mode of treating diabetes, at least according 
to our present knowledge, is by regulating the diet, and that it is well, in addition, 
to recommend the employment for a time of the above-mentioned mineral-waters, 
with opium and other internal remedies to combat special symptoms. The treat- 
ment of such complications as phthisis or cutaneous eruptions need not be 
described here. 

In diabetic coma, camphor or ether, sabcutaneously, should be employed, 
together with lukewarm baths and douching. As it is possible that the coma 
may be due to poisoning from the acids in the blood (vide supra), we should also 
try bicarbonate of sodium in large doses ; but the efficiency of such treatment 
remains to be decided. 



926 



CONSTITUTIONAL DISEASES. 



CHAPTER X. 
DIABETES INSIPIDUS. 

Definition and JEtiology. — In the preceding chapter a distinction was drawn 
between diabetes mellitus and the symptomatic condition termed glycosuria. 
There is a similar distinction to be made between diabetes insipidus and polyuria. 
Polyuria is an increase in the volume of urine, and mainly in the amount of 
water excreted by the kidneys. It is a symptom which may be produced in many 
different ways. In the first place, it is a natural consequence of the ingestion of 
large amounts of water, or of the absorption of serous effusions ; it also occurs in 
certain diseases of the nervous system, especially of the medulla and cerebellum; 
it is also occasionally seen, as we have had opportunity to observe, in chronic 
hydrocephalus, and is a not very infrequent phenomenon in hysteria. Large 
amounts of urine are also secreted in certain renal diseases (interstitial nephritis 
and amyloid degeneration), and often during convalescence from acute diseases, 
such as typhoid fever, or after the ingestion of certain drugs, called diuretics.* 

Diabetes insipidus, on the other hand, is a disease which may develop idio- 
pathically in people otherwise perfectly healthy. Its aetiology is unknown. 
It occasionally seems to be excited by emotional disturbance, concussion or other 
injury of the brain, or some previous acute disease, such as typhoid or typhus 
fever, malarial poisoning, and cerebro-spinal meningitis. The disease sometimes 
appears in the syphilitic, and may, therefore, in many instances, be due to syphilis. 
Patients frequently state that then symptoms began immediately after drinking 
a very large amount of some fluid, as on a very hot day or after a long march. 
In such cases the assumption is a probable one that the primary symptom is not 
polyuria, but an abnormally great thirst (polydipsia), the increase in urinary 
secretion being a result of the large amount of water ingested. Finally, the dis- 
ease may be hereditary {vide infra). The true nature of diabetes insipidus is 
entirely unknown to us. 

The view which seems most probable of any is, that some nervous disturbance 
is its direct cause. In support of this, we have the appearance of a " symptomatic 
diabetes insipidus" in connection with organic disease of the brain {vide supra), 
and the fact that polyuria may be artificially excited by injury to a definite spot 
in the floor of the fourth ventricle or by section of the vagus nerve. Diabetes 
insipidus presents a most striking analogy with diabetes mellitus. This is shown 
both by the similarity in aetiology and symptomatology, and still more by the fact 
that occasionally one disease merges into the other. 

Diabetes insipidus is a disease of very infrequent occurrence, and, at least in 
Germany, is decidedly less often seen than diabetes mellitus. Most patients are in 
young adult or middle life. Males are somewhat more liable to the disease than 
females. 

Clinical History. — Diabetes insipidus may be developed gradually or with con- 
siderable abruptness ; the latter case is especially frequent when there is some defi- 
nite cause, such as the ingestion of a large amount of liquid, or traumatism. 

The essential and characteristic symptom is an increase in the volume of urine. 
This is usually very considerable. Often eight or ten quarts (8000 to 10,000 c. c.) 
are excreted in twenty-four hours, and cases have even been reported where the 
amount reached the almost incredible volume of thirty to forty quarts (litres). If 
a healthy person and a sufferer from diabetes insipidus are each given the same 

* We have repeatedly observed that the use of large doses of salicylate of sodium may be followed 
by the excretion of a very large amount of urine of low specific gravity (1003-1005). 



DIABETES INSIPIDUS. 



927 



amount of water in food and drink, the sick man will excrete more urine than the 
healthy. In color the urine is very pale, and sometimes almost like water. The 
specific gravity is very low, being usually 1004 to 1002, or even 1001. The reaction 
is slightly acid, sometimes almost neutral. 

The percentage of solid constituents in the urine is, of course, trifling. The 
total amount of solids, however, corresponds perfectly with the ingesta, or indeed 
is even somewhat above normal. The amount of urea in particular seems to be 
increased, but it has also been stated that other constituents of the urine have been 
excreted in abnormally large amounts — namely, phosphoric acid, sulphuric acid, 
lime, and kreatinine. Inosite has been found in the urine by Strauss and other 
observers, so that it has even been proposed to give diabetes insipidus the name of 
" diabetes inositus," in distinction from diabetes mellitus. Inosite is not invariably 
present, however, in the urine of diabetes insipidus. In cases of true diabetes 
insipidus, albuminuria is extremely exceptional. 

Another important symptom is the excessive thirst. To make up for the great 
loss of water by way of the kidneys the patient is obliged to drink great quantities 
of liquid, and, indeed, it is always found that the amount of water ingested, in the 
way of drink and solid food, somewhat exceeds the total volume of urine excreted. 
Despite this, the tongue is usually dry, as is also the skin, the insensible perspira- 
tion being considerably below the normal amount. The f urunculosis seen in dia- 
betes mellitus is exceptional in diabetes insipidus. The same is true of pruritus and 
balanitis. Occasionally profuse salivation has been associated with the disease. 

Symptoms referable to the various internal organs are few. Cataract has been 
occasionally observed, but it is much less frequent than in diabetes mellitus. The 
same may be said of pulmonary tuberculosis. In most cases the appetite is not 
excessive. The bowels are regular or slightly constipated. There is seldom much 
gastro-intestinal disturbance, unless from some chance complication. The sexual 
functions are usually unimpaired. 

The general health is considerably affected in cases of any severity. The 
patient becomes emaciated, languid, and feeble, and has no inclination to mental 
or physical exertion. Sleep is often disturbed, the mind depressed. The tempera- 
ture is normal, or even a trifle below normal, probably as a result of the large 
amount of cold water drunk. 

Diabetes insipidus is a very chronic disease. If there is no serious complication 
it may last for decades, yet there are cases that run a more rapid and unfavorable 
course. Sometimes there are considerable vicissitudes in the condition of the 
patient, in part dependent upon external circumstances and in part apparently 
spontaneous. In case some intercurrent acute disease develops there may be, 
during its continuance, a considerable diminution in the amount of urine excreted. 

The termination is usually unfavorable. Recovery is extremely rare. In the 
more fortunate cases the condition finally becomes stationary, and the patient 
attains to advanced years. Sometimes, however, death occurs more prematurely, 
being usually hastened by phthisis or some similar complication. 

Weil has lately contributed to our knowledge of this disease the results of an 
accurate study of its hereditary and apparently congenital variety. Weil narrates 
the history of a family in which marked polyuria and corresponding polydipsia 
appeared in numerous members for several generations. These persons all enjoyed 
excellent health, with this exception; and most of them attained old age. We 
hardly need to emphasize the fact that this form of the disease is radically differ- 
ent from the ordinary acquired variety. Perhaps its true cause is an abnormal 
congenital permeability of the glomeruli, but we have no certain information in 
regard to it. 

Post-mortem Appearances. — Such lesions as have been found in diabetes insipi- 



928 



CONSTITUTIONAL DISEASES. 



dus are usually the result of fortuitous complications, sucli as tuberculosis, carci- 
noma, and pneumonia. There are but very few changes referable directly to the 
disease itself : among these are enlargement of the kidneys and dilatation of the 
ureters. In rare instances a possible cause for the symptoms has been found in 
some lesion of the central nervous system, but these were properly cases of symp- 
tomatic polyuria and not of genuine diabetes insipidus. Instances of this sort are 
seen in connection with tumors or inflammatory changes in the medulla or cere- 
bellum, and exostoses at the base of the skull. 

Diagnosis. — The characteristic urinary phenomena usually render the diagnosis 
of diabetes insipidus an easy matter. It is of course necessary to exclude such dis- 
eases as might occasion symptomatic polyuria (vide supra) ; but this is seldom 
difficult if we make a careful physical examination arid carefully consider all the 
attendant symptoms. The differential diagnosis between diabetes insipidus and 
diabetes mellitus can almost invariably be made by means of the urinometer. If 
the specific gravity is below normal, it is scarcely necessary to test for sugar. 

Treatment. — No special injunctions with regard to diet are required. It would 
of course be a mistake to forbid the patient to assuage his excessive thirst ; but we 
may possibly lessen the amount of water drunk by prescribing bits of ice, or 
lemonade and other acid drinks. Opium sometimes lessens both the thirst and the 
amount of urine excreted. It is also important that the skin should be well cared 
for by means of baths and friction, and every effort should be made to promote 
the general vigor of the patent. He should have nourishing food and good air. 

Numerous internal remedies have been recommended as specific, but few of 
these have won any great reputation. Valerian appears, on the whole, to be the 
most efficient drug, and may be given in powder or infusion to the amount of 
one to two and a half drachms (grm. 5-10) per diem. Ergotine may also be tried. 
Carbolic acid, salicylate of sodium, and nitric acid have been said to prove benefi- 
cial. It is also said that galvanization of the medulla and upper part of the spinal 
cord sometimes accomplishes good results. 

Occasionally we may find an apparent cause for the disease and endeavor to 
remove it. If there is a suspicion of syphilis, mercurial inunctions should be 
tried. Sometimes they have an excellent effect. Of course, where there is 
symptomatic polyuria, the primary disease, such as hysteria, demands treatment. 

[Da Costa and others report very good results as following the administration 
of ergot.] 



CHAPTER XI. 

GOUT. 

(Podagra.) 

iEtiology. — Thomas Sydenham was the first to write a careful clinical descrip- 
tion of gout. He himself suffered from the disease for about forty years, and has 
given a detailed description of his own case in the treatise which he published in 
1683, under the title " Tractatus de podagra et hydrope." It was, however, Wol- 
laston who, in 1797, threw the first light upon the peculiar anomaly of tissue-meta- 
morphosis which exists in this disease. He demonstrated that the gouty deposits 
found in the joints and other parts of the body are mainly uric acid. From his 
time an all-important point with regard to the nature of the disease has been the 
relation between the symptoms of gout and disturbances in the manufacture and 
excretion of uric acid. In 1848 Grarrod showed that in gout the blood contains an 
excess of uric acid, and that the excretion of uric acid by the kidneys is dimin- 



GOUT. 



929 



ished. He was thus in a position to frame a theory consistent with all the clinical 
facts. Numerous investigations have been undertaken since his day ; but we still 
remain with regard to gout in a position analogous to that which we hold toward 
diabetes. We are, it is true, in the possession of a considerable number of well- 
established facts relating to it, but we do not know why the normal chemical pro- 
cesses are disturbed, and are unable to explain the connection between the various 
phenomena observed. 

Clinical experience has taught us certain remote causes of gout, first of which 
comes heredity. About fifty per cent, of all cases occur in patients whose families 
have already suffered from the disease, and it is sometimes possible to trace this 
transmitted taint through many generations. It is decidedly more apt to pass 
down through the male members of the family than through the female. 

Next in importance to hereditary influences is the mode of life. From time 
immemorial this has been regarded as an exciting cause of the disease. It has 
been a matter of universal belief that over-feeding, and especially the ingestion of 
too large a quantity of albuminoids, is strongly provocative of the disease. The 
same opinion has been held with regard to persistent over-indulgence in alco- 
holic beverages. Seneca relates that at the time of the decay of the Eoman 
Empire women practiced such excesses that they were as subject to gout as the 
men, and an old verse runs : " Wine is the father of gout, feasting is its mother, 
and Venus is the midwife. " This view is, however, an exaggerated one. It can 
not be denied that there is some truth in it, but, on the other hand, gout is not 
exclusively an " arthritis of the rich." It occurs also among the poor, who have 
had only too little acquaintance with the pleasures of the table ; and many a bon 
vivant has reached old age without ever experiencing pain in his great toe. 

[Gout is a disease so much more common in England than in Germany or this 
country that English opinions in regard to it are deserving of especial weight. 
The most commonly accepted, though by no means the only, view as to its nature 
is that it depends on defective oxidation, which may be brought about in two 
ways : either by the ingestion of more food than can be properly oxidized, or by 
the presence of such conditions that even a moderate supply of food can not be 
worked up and undergo its proper transformations. This theory will account for 
gout in the poor as well as in the rich. 

There can be no question that the use of malt liquors, especially in the stronger 
forms, consumed so enormously in England, is much more favorable to the devel- 
opment of gout than is the use of distilled spirits ; so also the stronger wines — 
such as port, sherry, Madeira, and the heavy Burgundies — are more dangerous 
than are the lighter and more acid wines of France and Germany. In this 
country gout is becoming more common, a fact which may be fairly explained by 
the accumulation of wealth and the consequent growth of luxury.] 

There is a noteworthy, although mysterious, connection between gout and 
chronic lead-poisoning. The fact is well established that persons who have to do 
with lead, such as type-setters and house-painters, are subject to genuine gout 
with deposits of uric acid in the joints. 

With regard to still other alleged serological factors, confirmatory evidence is 
lacking. Possibly, however, when the foundation for the disease is already laid, 
an attack may be excited by certain determining causes — namely, trauma, taking 
cold, errors in diet, and mental emotion. 

The geographical distribution of gout is remarkably unequal. The disease is 
much more frequent in England than in Germany, although in the latter country 
certain regions appear to be more affected by it than others. Here in Leipsic 
gout is decidedly rare. 

Gout is rarely seen in young persons. It is a disease of advanced life, rarely 
59 



930 



CONSTITUTIONAL DISEASES. 



appearing previously to the fortieth year. Men are much more often attacked 
than are women. 

Clinical History. — Grout may produce symptoms in many different organs; but 
its effect upon the joints is so characteristic that the arthritic disturbance has long 
been termed " normal or regular gout," in contradistinction from " atypical, 
internal gout. " This distinction is of course an artificial one, for the various phe- 
nomena of gout present the most manifold gradations and transitions. It will, 
however, be advantageous, in attempting to gain a practical insight into the vari- 
ous symptoms of the disease, if we first discuss the so-called " typical attack of 
gout," subsequently appending a description of the other manifestations of the dis- 
ease. Furthermore, the regular attack of gout is, in at least a majority of cases 
(vide infra), the first and earliest symptom of the disease. 

L The typical attack of gout is seldom abrupt. It is usually preceded for a 
longer or shorter period by certain premonitory symptoms, the meaning of 
which, though not evident to one who is about to suffer from his first attack, is 
sufficiently clear to more experienced patients, particularly as each individual 
case is apt to present a marked similarity in the prodromata of the separate 
paroxysms. These premonitory symptoms vary in different individuals. Some- 
times they consist in dyspeptic disturbances ; sometimes in a feeling of languor 
and mental depression ; very often in dragging, muscular pains or cramps in the 
calves of the legs ; or again in slight f everishness, with chilliness, sense of heat, 
and perspiration. On the other hand, it must be confessed that a patient may 
feel unusually well just before an attack. 

The attack is noticeably apt to begin in the night-time, or very early in the 
morning. The patient is awakened by a sudden and very violent pain in the 
metatarso-phalangeal joint of one of the great toes ("podagra"). The joint 
becomes swollen, the skin over it red, hot, and tense, the veins in the neighbor- 
hood distended. At the same time there is chilliness and moderate fever. This 
condition persists till morning. Then the pain is almost sure to abate, the fever 
to remit at the same time that sweating begins, and the patient to feel tolerably 
well during the day. The joint, however, remains swollen, with inflammation 
and oedema. The next night the pain begins again, and there is a fresh fever ; 
and these alternations are repeated, as a rule, for three to ten days. Even where 
the attack is more persistent than this, the pain is usually much less severe after 
the first two or three nights. After that time it gradually abates ; and it is com- 
monly said that an attack is brief in proportion to the violence of its first symp- 
toms. When the pain ceases, swelling soon disappears, the skin undergoes a 
slight desquamation and resumes its normal appearance, the general health of 
the patient rapidly improves, and he is often found to be much better after an 
attack than he was before. 

For theoretical purposes (vide infra) it would be very advantageous to possess 
a more accurate knowledge of the condition of the urine, and in particular of the 
excretion of uric acid during the attack. As yet, however, there have been few care- 
ful investigations made. G-arrod has made a very important observation, which 
has been confirmed by Cantani : it is, that the amount of uric acid excreted dimin- 
ishes several days before the commencement of an attack, and remains diminished 
during the attack. Subsequently to the attack the excretion of uric acid is said to 
be above normal, while the amount of uric acid in the blood varies in precisely 
the opposite way — that is, during the attack it is increased, and after, it is dimin- 
ished. It has not yet been determined how far this variation in the excretion of 
uric acid may be referable to the altered diet of the patient, and how far to a 
diminished formation of uric acid or a deposition of that substance in the diseased 
joints (vide infra). 



GOUT. 



931 



If there has been one attack of gout, there are almost sure to be others. They 
come sooner or later, at regular or irregular intervals, and separated by weeks, 
months, or even years. The attacks recur at long intervals in mild cases, more 
frequently and at gradually diminishing intervals in the severe. Spring and 
autumn are regarded as the time when attacks of gout are most apt to occur. In 
these subsequent attacks the great toe still remains the part most constantly and 
severely affected ; but other joints may also suffer— for example, the wrist, the 
knee, or the shoulder. Sometimes traumatism or some previous affection of the 
joints — such as rheumatism — apparently determines the localization of the gouty 
disturbance. In each attack, the trouble is usually confined to a single joint. It 
is only in exceptional or advanced cases that several joints are simultaneously 
invaded. 

The longer the disease has lasted, the less typical are the separate attacks. 
There may now be less suffering at the time of an attack ; but the articular 
changes are more persistent. There are symptoms referable to other parts of the 
body ; and the gout gradually passes into its second chronic or " atonic " stage. 
Occasionally the disease is irregular and atypical from its incipiency ; and the 
first manifestations may not be arthritic, but referable to the kidneys {vide infra) 
or other organs. 

2. Atypical Gout. Gouty Disturbance of other Parts than the Joints. — Gout 
may affect the mucous membranes. A gouty dyspepsia is very frequent. Its 
symptoms are more or less severe. The gouty are also subject to intestinal 
catarrh of varying severity, and to bronchitis and conjunctivitis, as well as to 
catarrh of the urinary organs. Ebstein regards " gouty gonorrhoea " as essen- 
tially a catarrh of the excretory ducts of the prostate gland. It is not an easy 
matter to explain why these various forms of catarrh should occur in gout. They 
may be, some of them, complications. In other cases they are doubtless the 
result of passive congestion, due to cardiac failure (vide infra) ; but in still other 
instances it must be confessed that they are apparently due to the toxic influence 
of the accumulated uric acid. 

[My experience, though far more limited than that of Draper, nevertheless 
leads me to believe, as he does, that the irregular forms of gout are by no means 
uncommon in women as an inheritance from a previous generation. The mani- 
festations in some of these cases are so ill -defined that a diagnosis may be difficult 
without a knowledge of the family history ; in other cases, more or less deformity 
of the smaller joints, or slight recurrent swellings of those parts, throw much 
light on the condition underlying the symptoms.] 

Inflammation of serous membranes — for example, of the pleura — also occurs ; 
and there may be pneumonia. The skin not infrequently suffers from acute or 
chronic eczema, which sometimes appears to be referable directly to the gout. 
Keratitis, iritis, and other inflammatory disturbances of the eye are also said to be 
caused directly by gout. Cirrhosis of the liver has been repeatedly found, and is 
perhaps referable to the action of the uric acid upon the hepatic parenchyma. 
By far the most important of all these gouty manifestations are referable to 
the kidneys and to the circulatory system. The disorder of the latter is some- 
times symptomatic of the renal trouble, but in other instances it occurs inde- 
pendently of it. There may be severe gouty arthritis for years without any lesion 
of the kidneys ; but this is exceptional. In severe cases of gout it is the rule that, 
sooner or later, symptoms of renal disorder present themselves. The so-called 
" gouty kidney " is a form of chronic interstitial nephritis. However important 
this complication, its symptoms do not need to be discussed here, as they are pre- 
cisely similar to those seen in ordinary cases of contracted kidney {vide page 804, 
et seq.). The distinctive symptom of this disturbance is albuminuria ; and the 



932 



CONSTITUTIONAL DISEASES. 



gradually developing secondary hypertrophy of the left ventricle is the pivot on 
which turns the whole future course of the disease. So long as the heart remains 
capable of performing its functions, the condition of the patient will probably 
remain endurable if not actually comfortable. Finally, however, compensation 
is sure to become impaired ; and then appear oedema, dyspnoea, debility, and 
emaciation — in short, all the familiar symptoms of cardiac failure. A speedy 
end may be brought about by uraemia, or cerebral embolism, or haemorrhage ; 
but in other cases the patient suffers for years, both from the heart disease and 
from fresh arthritic attacks. 

The cardiac hypertrophy just mentioned is the result of the contracted kidney. 
Other disturbances of the circulatory system appear to be referable directly to the 
gout itself. Among these are chronic endocarditis or myocarditis, and perhaps 
certain " functional " symptoms, such as palpitation and angina. An important 
symptom is chronic endarteritis or arterio-sclerosis. This is often seen in gouty 
subjects, and in many instances seems to be immediately connected with the gout. 
Sometimes, also, there are gouty lesions of the veins, such as varicosities or throm- 
bosis. Of course, these changes in the blood-vessels may, in then 1 turn, give rise 
to various disorders. 

In a few very rare instances gout seems to attack the brain and spinal cord. 
Usually, however, the nervous disturbances seen in gout are, as already stated, 
symptoms of uraemia, or of circulatory disturbance, and the like. The patient 
may also have certain functional nervous troubles, like neuralgia or migraine. 
The direct cause of these is seldom evident. 

The joints, despite frequent attacks, may yet maintain an almost normal appear- 
ance, inasmuch as the acute inflammatory changes completely vanish after each 
separate attack. They may, however, undergo permanent enlargement and de- 
formity from gouty concretions {tophi arthritici). In many instances similar 
masses can be felt here and there in the muscles and tendons, the skin (for 
instance, of the eyelids), and quite often in the external ear. They consist essen- 
tially of accumulations of urates {vide infra). Occasionally these concretions 
break externally, discharging a thick pus mingled with urates, and forming indo- 
lent ulcers, slow to heal. Sometimes atmospheric germs thus find ingress into 
the system, and give rise to phlegmon. 

It should be stated, in conclusion, that gout may be complicated with other dis- 
eases. Thus, it may be associated with renal calculi, and sometimes with diabetes 
mellitus {vide supra). 

Anatomical and Chemical Changes in Gont. Theory of its Nature.— The essen- 
tial anatomical lesion in gout consists of an abundant deposit of crystalline urates 
in the tissues. This is most evident in the affected joints, the cartilaginous sur- 
faces of which are often completely covered with white, chalk-like material. In 
severe cases the same appearance may also be presented by the articular ligaments, 
tendons, and bursae, while there are at the same time numerous concretions of 
urates here and there beneath the skin. These deposits are mainly composed of 
acid sodic urate, with traces of calcic urate, calcic phosphate, and sodic chloride. 
Ebstein has lately explained how these collections are formed. He found that the 
deposition of uric acid is invariably preceded by a necrosis of the tissues. The 
uric acid while still in solution acts as a chemical irritant upon the cartilage here 
and there, and thus produces necrosis, whereupon the urates are crystallized out 
and deposited. Then a secondary inflammation develops around these foci of 
necrosis. By ligaturing the ureters in fowls, Ebstein succeeded in artificially pro- 
ducing similar changes. 

The nephritis of gout corresponds in its pathological appearances to that of the 
true contracted kidney, with one exception ; the organs usually present deposits of 



GOUT. 



933 



uric acid or urates, in stripes, both in the lumen of the urinary tubules and also 
in the epithelial cells and the interstitial tissue. In the connective tissue it is 
probable that a necrosis precedes the deposit. 

The lesions presented by the heart, blood-vessels, and remaining parts of the 
body are not especially characteristic of the disease. The blood of gouty subjects, 
as Garrod demonstrated, contains an excess of uric acid. 

There are many theoretical questions which remain unanswered : Whether in 
this disease there is an over-production, or merely a defective excretion of uric 
acid ? What the true cause of this strange anomaly in metamorphosis may be ? 
What conditions are essential to the crystallizing out of uric acid in the tissues ? 
Why certain parts, particularly the joints, and still more particularly the first joint 
of the great toe, are especially liable to suffer ? And, finally, What circumstances 
decide the course of the disease, and determine its separate attacks ? Not one of 
these questions has been satisfactorily answered. The fact that gout is prone to 
attack individuals who have led a luxurious life has led to the belief that in every 
case of gout the ingesta are not completely oxidized, and an excess of uric acid is 
consequently accumulated in the system. We have already pointed out that this 
assumption is too sweeping. And, indeed, our present knowledge with regard to 
the manufacture of uric acid out of the albuminoids, and its further transforma- 
tions, is not at all adequate for the establishment of any hypothesis of this sort. 
We must simply confess that the true cause of the accumulation of uric acid in 
the tissues is unknown. It may be conjectured, however, that the deposit of crys- 
tals of uric acid is either occasioned or promoted by an excessively acid reaction 
of the blood or lymph in which that acid is dissolved. It is not known what acids 
give rise to this reaction, nor how they are formed. It has been seen that the 
articular cartilages are especially apt to present a gouty deposit. Perhaps this is 
occasioned by the sluggishness of the circulation in these parts. It is doubtful 
whether the uric acid is produced in the cartilage itself. Ebstein believes that it 
originates mainly in the muscles and bone-marrow, and is thence conveyed to the 
cartilage. Others, and among them Cantani, believe that the uric acid is formed 
in the cartilage and the connective tissue. 

Diagnosis. — It is usually easy to recognize an acute attack of gout. The sudden 
onset of the pain at night and its localization in one of the great toes are very 
characteristic symptoms, and render it easy to distinguish between it and other 
acute affections of the joints. The diagnosis is more difficult in the advanced 
stages, where symptoms are more confused. Here the history of the case will 
often include the description of typical attacks and also setiological factors, such 
as heredity and mode of life, which may assist in diagnosis. It must be said that 
many gouty subjects are reticent as to their past experiences, and sometimes even 
deny previous attacks of gout. If there is a chronic gouty arthritis, it may be 
necessary to make a differential diagnosis between it and arthritis deformans. 
The deformities of arthritis deformans are usually seen first of all in the hands 
and fingers, and it has a persistent, chronic course. Furthermore, in gout we 
sometimes can feel the characteristic deposits in the tendons or skin (for instance, 
in the eyelids or external ear). 

If there is chronic nephritis of gouty origin, its source can be recognized only 
from its association with other indubitable symptoms of gout, unless possibly the 
knowledge of certain serological factors, such as a history of gout in the family 
or of chronic lead-poisoning, should put us upon the right track. Ebstein has 
reported cases of " primary renal gout " where there was no arthritis during the 
whole course of the disease. Such cases can seldom be correctly diagnosticated 
during life. 

Brief mention should here be made of an experiment performed by Garrod, 



934 



CONSTITUTIONAL DISEASES. 



which, may be employed to demonstrate the existence of uric acid in the blood, for 
diagnostic purposes. A drachm or two of blood-serum, or of the serum obtained 
from a fly-blister, is put into a shallow watch-glass, and six or eight drops of a 
thirty-per-cent. solution of acetic acid are added to it. A linen thread is then laid 
in the fluid, and the whole allowed to remain at a moderate temperature for about 
a day. If the proportion of uric acid in the fluid is sufficiently large, crystals of 
that acid will now be found on the thread and may be recognized by their shape 
and chemical reaction. This " thread test " of G-arrod's is not extensively used, 
because it does not succeed unless there is a comparatively large amount of uric 
acid in the blood, and, furthermore, uric acid may exist in the blood in health, or 
in other diseases than gout. 

Prognosis. — However favorable the prognosis may be with regard to the single 
gouty attack, yet a permanent release from the disease is rarely to be hoped for. 
Only such patients as, from the first appearance of gout, pursue most carefully all 
the requisite prophylactic and dietetic measures, can expect that future attacks will 
be rare and comparatively mild, and that severe lesions of the internal organs will 
not occur. So long as the kidneys and other viscera are intact, there is no imme- 
diate danger to life, and the patient may attain advanced years despite his gout. 
The gradual and chronic alterations in the joints may, however, impede locomo- 
tion as well as all other movements of the body. Except for this, the general con- 
dition of the patient in the intervals between the attacks is often one of tolerable 
comfort. Indeed, it is frequently the case that the patient will feel his very best 
directly after a severe paroxysm, while rudimentary or atypical attacks are often 
regarded as of ill omen. Really, however, there is no serious danger until a 
chronic nephritis is developed. The prognosis then becomes as unfavorable as in 
the other forms of contracted kidney (q. v.), and involves the same possibilities. 

Treatment. — All authorities agree that the first essential in treating gout is a 
proper regimen. Unless the patient has energy enough to yield the most implicit 
obedience to the injunctions regarding diet and mode of life in general, from the 
first appearance of his disease, no great benefit can be obtained from treatment.. 

Various authorities have, of late, prescribed special diets for the gouty. These 
differ considerably from one another, but the discrepancies are not actually so 
great as they seem to be at first glance ; and, after all, more importance attaches to 
the quantity of the ingesta than to their quality. As most gouty patients are cor- 
pulent, the diet to be prescribed for them is mainly that indicated by their corpu- 
lence. The first point is to limit the total amount of ingesta. No more should be 
eaten than is absolutely required to satisfy hunger. The diet may be a mixed 
one — that is, may contain albuminoids, carbohydrates, and fats ; but the quantities 
of each of these ingredients should be small (vide following chapter). The albu- 
minoids should not be too abundant, in order that the formation of uric acid may 
be limited ; the fats and carbohydrates should be cut down, in order that the albu- 
minoids may be thoroughly oxidized and thus any further deposit of adipose 
tissue avoided. Acid articles of diet should be forbidden, lest they promote the 
deposit of uric acid in the tissues. The experience of certain physicians tends to 
show that a diet mainly vegetable is better borne by gouty patients than animal 
food. In this case also, however, it will be seen that the essential point is the 
quantity. With a vegetable diet, the amount of ingested food, and still more the 
amount of nourishment absorbed from the primse viae, is almost sure to be less 
than upon an exclusive meat diet. The patient should, therefore, be told that his 
diet should consist mainly of lean meat, fish, broth, green vegetables, small 
amounts of milk, eggs, and bread. Sweet puddings, fat meat, potatoes, or sour 
and acid food of any kind should be avoided. Fruit may be allowed in small 
quantities. "Water is the best beverage; but it is not advisable, and may even be 



GOUT. 



935 



prejudicial, to drink too large an amount of any fluid {vide infra). Large quan- 
tities of alcohol are sure to injure the patient. If they can not be absolutely pro- 
scribed, yet at least their amount should be reduced to a minimum. 

[Many gouty persons, especially those suffering from the irregular form of the 
disease and acid dyspepsia, are more comfortable and seem to do better on a diet 
which is largely nitrogenous, the starches and sugars being greatly limited in 
amount. The diet, in fact, should be similar to that laid down for diabetes melli- 
tus, though not so strictly carried out. In chronic and irregular cases it is often 
desirable to prescribe a stimulant, for a time at least ; brandy, whisky, or gin, well 
diluted with water, is perhaps the best form.] 

By thus limiting the amount of food taken, we shall promote metamorphosis 
and avoid any excessive formation of uric acid. A more direct means of hasten- 
ing the conversion of the albuminoids is muscular exercise. If a corpulent 
patient is still vigorous and is not threatened by any serious internal disease, he 
should be urged to take a large amount of exercise in mountain-climbing, gym- 
nastics, gardening, or similar pursuits. The motto of such a patient should be 
" little sleep and great activity." This same indication of accelerating tissue-meta- 
morphosis is fulfilled also by bathing. In early stages cool baths and sponging 
are useful, as are also baths containing common salt, or perhaps even sea-bathing 
cautiously employed. In more advanced cases, particularly if the joints present 
permanent lesions, the warmer baths are more desirable, such as are found in 
Teplitz, Wildbad, Wiesbaden, Baden-Baden, Carlsbad, Ems, and Aix. 

The internal administration of alkalies is an efficient adjuvant to the dietetic 
and hygienic prescriptions above enumerated. For a long period the use of alka- 
line mineral- waters has been found to be most beneficial. Experience confirms 
the confidence which theoretical considerations would lead us to have in their 
value in checking the deposit of uric acid, so far as it is occasioned by excessive 
acidity of the circulatory fluids (vide supra). The sodic chloride contained in 
these waters stimulates the conversion of the albuminoids. The waters also in- 
crease the activity of the kidneys, benefit gastric catarrh, and overcome constipa- 
tion, and in all these ways combine to produce a favorable effect upon the patient's 
health. Still another factor is the judicious diet and mode of life at such health 
resorts. The waters of Carlsbad and Vichy have gained the greatest repute in 
gout, although the waters of Ems and Neuenahr have an analogous composition 
and doubtless would produce similar effects. Of the waters which contain sodic 
chloride, the most advisable are Wiesbaden, Baden-Baden, Kissingen, and Hom- 
burg. The salts of lithium especially promote the solution of uric acid, and of 
late the waters which contain lithium have been strongly recommended. The 
natural springs of this sort, such as the Crown Spring in Obersalzbrunn, and those 
of Assmannshausen and Salzschlirf, contain comparatively insignificant amounts 
of lithium ; and it might be a better way to use the artificial lithium waters, such 
as are made by Struve or Ewich. Another way is to prescribe carbonate of lith- 
ium, in powders containing two or three grains each (grm. 0 '10-0 "20), one powder 
two or three times a day, in a glass of Seltzer or Biliner water. 

Other remedies formerly in vogue were said to correct the " gouty diathesis," 
but their efficacy is extremely dubious, and they need not be especially mentioned. 

As to the treatment of the acute attack, it has ceased to be customary to employ 
any potent remedies. The patient must, of course, keep his bed. The affected 
joint should be wrapped up in cotton wool, the whole leg elevated, and a proper 
diet strictly enjoined. Free movement of the bowels should be maintained by 
means of an enema. If there is considerable gastric disturbance, bicarbonate of 
sodium, magnesia, or some bitter may be prescribed. The most certain remedy 
for severe pain is a subcutaneous injection of morphine. Less efficient are nar- 



936 



CONSTITUTIONAL DISEASES. 



cotics locally applied, and warm compresses. Whether any internal remedies are 
calculated to abbreviate the attack is doubtful. Formerly colchicum (twenty or 
thirty drops of vinum colchici seminis three or four times a day) was the favorite 
medicine, but it seems to be going out of use. Salicylic acid and salicylate of 
sodium may be administered in the same way as in acute articular rheumatism, 
and sometimes, although not always, are followed by improvement. 

[One reason why colchicum has fallen into relative disuse is that the relief 
obtained from it is often so prompt and complete that patients are tempted into 
continued indulgence in a faulty manner of life. It is also supposed by some 
that the drug interferes with the effort of nature to eliminate the poison, which 
becomes generally diffused, and sets up changes in the vessels and internal organs. 

Precisely how colchicum acts we do not know, but that it does act, and some- 
times with marvelous success, there can be no question.] 

The chronic affections of the joints in gout are treated as are other varieties of 
chronic arthritis {vide page 862). The most efficient remedies are cautious massage 
and baths, including hot sulphur baths and mud-and-sulphur baths. The internal 
administration of the alkalies, lithium, and similar drugs, to combat the general 
gouty diathesis, should be associated with these external remedies. Some phy- 
sicians report that iodide of potassium favors the absorption of the gouty deposits. 

The treatment of the nephritis and other complications need not be discussed 
at length. The gout itself should always be the main object of our therapeutic 
efforts, and beyond this we may be guided by general principles. 



CHAPTER XII. 

OBESITY. 

{Corpulence. Polysarcia adiposa.) 

Definition and iEtiology. — The amount of adipose tissue in the body is subject 
to considerable variation, and it is not possible to state absolutely what shall be 
considered as normal and what as abnormal. For practical purposes we may draw 
the line where the increased size grows burdensome to the individual. After a cer- 
tain point, any further addition to the amount of fatty tissue is almost sure to work 
serious injury, and is therefore to be regarded as an actual disease, and not merely 
an inconvenience. It should be said, however, that in such cases the symptoms of 
obesity are very frequently confounded with those springing from other disorders 
— these latter possessing, indeed, the same aetiology as obesity, but distinct from it. 

The most frequent and important cause of obesity is the habitual ingestion of 
too large an amount of food. By " too .large " is meant an amount sufficient to 
occasion a continual increase of the adipose tissue of the body, when this is already 
fairly well developed. It is a matter of indifference whether the excess is com- 
posed mainly of albuminoids, or carbohydrates, or fats ; for, in either case, if the 
quantity be sufficient, an increase of adipose tissue may take place. We shall 
soon see, however, that the excess is usually in fat and carbohydrates. Inasmuch 
as this over-feeding is almost certain to be habitual, the excess at any one time 
need not be at all large. We often hear a corpulent person express his surprise 
that he grows heavier every day, although he " does not eat any more than others 
who are lean." The explanation is easy if we consider that a daily increase of 
five grammes of fat (one and one fourth drachms) suffices to increase the weight 
in ten years, or, say between the thirty-fifth and forty-fifth years, forty pounds 
avoirdupois. In reality the daily increase is sometimes greater than this. 



OBESITY. 



937 



The basis for a detailed consideration of the causes which lead to the deposit of 
fat will be gained by a consideration of the physiological laws relating to nutrition 
discovered by Voit, Pettenkofer, and their pupils. It has been shown that both 
the albuminoids and the carbohydrates of the food may be a source of fat, formed 
within the economy, and also that the fat contained in the food may be, to a large 
extent, directly deposited in the fat-cells of the body. One product of the decom- 
position of albuminoid substances is invariably fat. This usually undergoes fur- 
ther oxidation, but it is sometimes retained unaltered in the system. It would 
even seem that the albuminoids give rise to much more of the fatty tissues of the 
body than are produced from the carbohydrates ingested, although there is no 
doubt that these latter also yield fat. Carbohydrates do promote obesity, but less 
because they are a direct source of fat than because they are easily decomposed, 
and so shield both the ingested fat and that which is formed out of the albu- 
minoids from oxidation. In this indirect way they do greatly favor a tendency 
to corpulence. 

We thus perceive that various diets may, each one of them, permit of an 
increase of adipose tissue. In actual life, of course, the most frequent conditions 
are such as result from the customs and habits of the population in general. The 
diet is almost invariably a u mixed " one — that is, it contains albumen and fat and 
carbohydrates — and in most instances the obesity is due to an excessive amount of 
all three elements, or at least of the fat and carbohydrates. A person may, how- 
ever, become corpulent who eats very little fat, provided he consumes a large 
quantity of albuminoids and carbohydrates ; or if he eats very little starchy food, 
provided he consumes a large amount of meat and fat. Perhaps these facts may 
* ? be made clearer by giving a concrete example. Voit tells us that a vigorous man 
who requires daily 118 grm. of albumen and 259 grm. of fat to maintain a physio- 
logical equilibrium as regards fat and albumen will, other things being equal, 
begin to store up fat if there is any further increase in the amount of fat in his 
diet. The same result will also take place if, instead of the rations previously 
stated, he ingests more than 118 grm. of albumen and 600 grm. of starch, or more 
than 664 grm. of albumen alone, or, finally, more than 118 grm. of albumen, 100 
grm. of fat, and 368 grm. of starch.* It is obvious that this last diet, which closely 
resembles the average diet of an adult f in good circumstances, whose weight is 
neither increasing nor diminishing, is the one most likely to be exceeded ; where- 
upon there must take place a deposition within the system of the superfluous fat. 

Among the various kinds ^of food is one group which deserves mention, as 
being an important factor in many cases of obesity ; we refer to alcoholic beverages. 
There can be no doubt that intemperance in this regard plays a prominent part in 
many instances. Sufficient illustration is furnished by brewers, hotel-keepers, 
and the inhabitants of countries like Bavaria,* where beer-drinking is prevalent. 
In this particular it is evident that beer works more harm than do wine or strong 
liquor; for beer contains, in addition to the alcohol, an appreciable amount of 
starchy material, making the sum-total from the beer drunk during the entire 
day a considerable one. Many persons who would be extremely indignant if 
called " tipplers," habitually take five or six glasses of beer a day, equivalent to 



* This statement is founded upon an important discovery of Eubner, that, as far as the storing up 
of fat is concerned, the measure of value for different foods is the amount of heat given off by them 
when they undergo oxidation into carbonic-dioxide gas and water. Measured in this way, 100 grm. 
of fat = 211 grm. of albumen = 232 grm. starch = 234 cane sugar = 256 grm. grape sugar. 

t Probably the amount of fat contained in the food is often less than the above, and the amounts 
of albumen and starch somewhat larger. Voit estimates the diet of a well-to-do person at 127 grm. 
albumen, 89 grm. fat, and 362 grm. starch; and that for a vigorous laborer at 118 grm. albumen, 56 
grm. fat, and 500 grm. starch. Of course these figures are merely approximate. 



938 



CONSTITUTIONAL DISEASES. 



150 grm. of starch, or, in other words, one half the total amount of starch required 
by the system. Even this quantity is frequently exceeded. Of course the three 
or four per cent, of alcohol which the beer contains also promotes the deposition 
of fat. Alcohol is readily oxidizable ; and it thus shields, to a considerable extent, 
the fat already present in the body ; and it also, in all probability, works such 
an injury to the tissues as to diminish their power of effecting decomposition. 

We have thus seen that in by far the larger number of cases obesity is mainly 
due to the ingestion of too much food. No weight need be attached to the usual 
statement of corpulent persons, that they eat no more than others. Few of them 
have any idea how much nourishment they do consume. Others, having already 
become corpulent, eat less, to be sure, than they used to, but nevertheless an amount 
sufficient to maintain the acquired weight. 

Other factors may, no doubt, exert an influence upon the increase of adipose 
tissue by diminishing the consumption of fat in the system. The most important 
factor of this class is physical inactivity. Muscular contractions lead to the decom- 
position of a large amount of fat. This explains why people of sedentary habits, 
and those who sleep long and exercise little, are more apt to become corpulent than 
are manual laborers. Again, there are certain diseases which seem to promote 
corpulence. In ansemia there is sometimes a striking tendency to obesity, in part 
due to the diminished supply of oxygen and in part to diminished muscular 
activity. This same inactivity is probably the main cause of corpulence in 
paralysis (hemiplegia). It may be, however, that disturbances of the nervous 
system 'may directly affect metamorphosis. Thus, idiots and other subjects of 
congenital defects of the brain are liable to obesity. Disturbances of the cir- 
culatory system seem to favor the production of corpulence by impairing oxida- 
tion. This is seen in many young persons with cardiac disease, although it is not 
easy to exclude in this case the influence of still other factors, such as a sedentary 
life. 

Finally, some cases of obesity seem to result from a constitutional and inborn 
predisposition. Young children sometimes suffer from obesity; and the condi- 
tion seems, in many cases, to be hereditary. Many races and nations exhibit an 
especial tendency to corpulence — for example, the Jews. Age and sex have some 
importance in this regard : extreme obesity is seldom seen previously to the thir- 
tieth year; and women appear to be somewhat more subject to the disease than 
men. The importance of a " tendency " to obesity should not be overrated. Upon 
careful investigation, we shall almost invariably find in the habits of the indi- 
vidual, as regards food and exercise, a satisfactory explanation of his obesity. 
Strictly speaking, the condition can not be regarded as a disease unless the habits 
as to diet and exercise fail to account for it. 

Pathology. — After corpulence has passed a certain point, the condition is evi- 
dent at the first glance. The subcutaneous cellular tissue is one of the chief places 
in which the fat is deposited. Consequently, the panniculus adiposus soon attains 
considerable thickness. The countenance grows more round and plump ; beneath 
the chin is formed a second prominence known as the " double chin " ; the chest 
appears broadened ; the waist enlarges ; and, particularly in women, the breasts 
are changed to great shapeless masses, over which the skin is so tightly stretched 
as to present linese albicantes. The abdominal walls are greatly altered. The 
belly projects more and more, until it becomes actually pendulous, and its lower 
surface touches the interior surface of the thighs. Intertrigo is apt to occur in 
the groins, below the breasts, and between the buttocks. The skin everywhere 
has a fatty feel, due to the increased secretion of the sebaceous glands. This 
hyperplasia of the fatty tissue in the panniculus adiposus is associated with a 
deposit of fat in many parts of the interior of the body, including the mesentery, 



OBESITY. 



939 



mediastinum, pericardium, and the capsules of the kidneys. Some of these will 
be mentioned again further on. 

Of course the circumference and weight of the body become greatly increased. 
As an approximate measure, it may be stated that for men of middle height a 
weight exceeding 90 kilo. (200 pounds), and for women 75 kilo. (165 pounds), may 
be regarded as abnormal.* This increase in bulk is the first cause of subjective 
symptoms. An obese person has to exert a greater effort in making any motion 
than do other people, and, as a necessary consequence, he gets easily tired, and 
seeks as far as possible to avoid exertion. The increased demand upon the muscles 
explains the familiar fact that corpulent persons perspire so readily. 

The graver symptoms of obesity, and properly the first pathological phe- 
nomena of the condition, relate to the respiration and the circulation. The patient 
begins to complain of shortness of breath, and is subject to marked dyspnoea upon 
running or climbing stairs. There may be, at the same time, cardiac disturbance, 
indicated by a rapid pulse, palpitation, intermission of the pulse, or other slight 
irregularities in cardiac action. All these symptoms grow gradually worse ; and 
to them are added symptoms of cardiac failure and consequent passive congestion. 
There is a tendency to bronchitis and other catarrhal troubles. The appetite and 
digestion are affected, and oedema appears. 

A careful analysis of all these symptoms shows that many causes combine to 
produce them, all having a common tendency to impede respiration and, still 
more, circulation. One source of disturbance is the increased deposit of fat upon 
the frame-work of the body. It is probable that the excess of adipose tissue cover- 
ing the thorax exerts a direct influence in obstructing the respiratory motion of 
the thoracic walls, and renders the respiration more superficial. In this way the 
return of venous blood to the heart and the pulmonary circulation are both 
impeded, because the negative pressure in the chest is less than normal. Likewise 
the diminished amount of bodily exercise affects the circulation unfavorably. 
Brauner has shown how numerous are the arrangements connected with the 
fasciae for promoting the venous currents, by means of the negative pressure 
resulting from the movements of the body. Whether the fat deposited around 
the heart directly obstructs the cardiac movements is somewhat doubtful, though 
this view is held by many. The fatty infiltration of the myocardium is of more 
importance: the fat is deposited in the intermuscular connective tissue. This 
lesion, however, is not of very frequent occurrence, nor does it produce so grave 
results as do certain other cardiac changes, which are either secondary to the 
obesity or complications of it. 

There is no doubt, that, in almost all cases where the corpulence actually 
induces grave disturbances, the cardiac symptoms are of prime importance. These 
are due, as has just been indicated, in part to the increased amount of adipose 
tissue, and in still greater part to complications, most of which are excited by the 
same causes as is the obesity itself. The abundant adipose tissue may obstruct 
the circulation in the smaller blood-vessels and capillaries inclosed within it. 
And, furthermore, the excessive development of fatty tissue probably leads to the 
growth of new blood-vessels, and, as a consequence, to an increase in the total vol- 
ume of the blood. This is one way in which the demands made upon the heart 
are rendered greater than normal, and explains why the corpulent frequently 
exhibit cardiac hypertrophy. Other influences are also at work to produce this 
same result: they are, in the first place, the same factor which occasions the 
obesity itself, namely, the ingestion of increased amounts of food and drink (alco- 
hol, vide page 292), and, secondly, certain other lesions which are frequently 



Even 150 kilo. (330 pounds) has been repeatedly observed. 



940 



CONSTITUTIONAL DISEASES. 



associated with obesity and are referable to the same causes as it is. Chief among 
this latter class is general arterio-sclerosis. If this involves the coronary arteries, 
it may in turn occasion still further damage — for example, degenerative myocar- 
ditis (compare page 288). Chronic interstitial nephritis is another not infrequent 
complication. This is in part referable to the same causes as is the obesity. Gout 
and diabetes are less frequent. 

We thus see that obesity is often merely one of many injurious results occa- 
sioned by an improper mode of life. It is, in a certain sense, the first danger- 
signal, warning the patient and his physician to avoid the graver disturbances 
which threaten. This is a point of great practical importance. For, when once 
we have a combination of obesity with cardiac hypertrophy, fatty infiltration of 
the heart, arterio-sclerosis, or interstitial nephritis, the various causes and effects 
act and react upon one another in a way most perilous to health and even to life. 
There is no need of describing the grave disturbances which invariably develop 
at the close of the scene. They are the result of chronic cardiac insufficiency, and 
have been fully described under cardiac disease. 

In every case of obesity the physician should examine the heart, lungs, vascu- 
lar system, and kidneys, particularly if there is already subjective disturbance. 
The examination of the heart may present considerable difficulties, because the 
results of palpation and percussion are so obscured by the thick cushion of fat 
which covers the thorax. We can, however, have recourse to auscultation, and 
can feel the pulse. The pulse may be either rapid, or slow, or irregular. We 
need not mention any minute particulars as to the examination. It may be 
stated, however, that a hepatic enlargement is often found, but it is much less 
often the result of fatty infiltration than of simple hypertrophy or passive con- 
gestion. 

We have thus seen that corpulence may sometimes be associated with grave 
and dangerous lesions ; but, on the other hand, it should be stated that this unfor- 
tunate condition by no means invariably exists. Not infrequently the corpulence 
remains moderate, in which case it is not really dangerous, however incon- 
venient. This is true of a large proportion of those cases which are due to the 
ingestion of a large amount of nourishment, associated with defective oxidation, 
and where there are no other unfavorable influences at work. The obesity of 
hard drinkers is almost always a more or less dangerous condition, while that 
seen in many elderly persons and in women is often comparatively free from 
peril. These latter individuals are, to be sure, discommoded by their great weight, 
can accomplish less than they used to, are easily put out of breath, and have a 
certain tendency to catarrhal inflammations and rheumatic difficulties ; but they 
escape the severer lesions above enumerated. Even these apparently harmless 
conditions should not be disregarded by the physician, as he can never be abso- 
lutely certain that grave complications may not be developed eventually. 

Treatment of Obesity. — To cause the disappearance of the accumulated fat, it is 
necessary to promote its oxidation in the system and to prevent the ingestion of 
new supplies of fat. To accomplish this purpose we possess only two means— first, 
a limitation of the ingestion of such kinds of food as may lead to the formation of 
fat in the system, and, secondly, stimulation of those factors which occasion the 
destruction of the fat already present. All the various methods of treating 
obesity, without exception, aim either to diminish the supply or to increase the 
destruction of fat. 

The methods vary greatly. It must be borne in mind that the diminution of 
the adipose tissue must not involve injury to the body itself. The treatment 
should not weaken the constitution, but should invigorate the patient, or at least 
be innocuous. 



OBESITY. 



941 



It is of prime importance, in every method of treatment, that the total quantity 
of ingested food should be diminished. It is a mistake to forbid the patient some 
particular kind of food — for instance, the carbohydrates or the fats — with the idea 
that they alone do harm, or to allow him unlimited quantities of other kinds of 
food, in the belief that they are harmless. Any person can eat albuminoids, fat, 
and starch at every meal, and yet not grow fat ; while, on the other hand, too 
much of any one of these may lead to an increase of adipose tissue. The amount 
of food which a person can take without increasing the amount of adipose tissue 
varies with the individual. It depends upon the amount of material already 
present in the body, and upon the various demands made upon the system, as 
well as other factors. This renders it difficult to draw up a universal dietary for 
the obese. We can best judge of the value of any course of treatment by its 
results, and these are best measured by the weight and the subjective condition of 
the patient. 

Of the various elements of food, the albuminoids should be diminished least of 
any, because it would be sure to work injury to the system if they were supplied 
in too small an amount. Of course the albuminoids must not be eaten to such 
an extent that the fat into which they decompose remains intact in the body. An 
increase in the amount of nitrogenous tissue is, however, desirable, because this 
promotes the vigor of the muscles and the heart, and so leads to the oxidation of 
larger quantities of the non-nitrogenous tissues. 

The amount of fat and starch must be much more limited. The fats and 
starches are more potent in increasing adipose tissue and in shielding from oxi- 
dation the fat already stored up in the body than is nitrogenous food. It would 
not be at all advisable to forbid the use of either one of these two constituents of a 
mixed diet, allowing the other alone to be eaten. A varied diet is extremely desir- 
able, even for one who is corpulent ; and we should exclude neither fat nor starch 
wholly from the dietary, but we should merely limit the amounts to be taken. As 
already indicated, the amount of albuminoid food remaining unchanged, a person 
can eat double the quantity of starchy food that he can of fat, without increasing 
his adipose tissue. It is therefore irrational to allow the corpulent fat in larger 
proportions than starchy foods. The diet which Ebstein has recently proposed 
for the treatment of obesity does prove successful, but the explanation of its suc- 
cess lies in the comparatively small amounts of meat and fat ingested. Precisely 
the same results would be attained if a corresponding amount of starch were sub- 
stituted for all or a portion of the fat ; and in practice it is desirable, at least in 
most cases, to allow the patient both starches and fats. Of course the likings and 
experience of the individual should be considered in each separate case. The 
Banting treatment, introduced in 1864, enjoyed for a time a great reputation. Its 
inventor applied it, first of all, to his own case, and with success. It rests upon a 
rational basis, inasmuch as the albuminoids are allowed in abundance, and the 
ingestion of fat and starch is limited. It lays too much stress, however, upon the 
exclusion of fat as compared with starch. 

The principles here expounded are direct corollaries to the laws which Voit 
has taught us in regard to the different kinds of food. The physician who bears 
them in mind can lay down his own rules for the diet of his patient. As already 
stated, it is impossible to give figures which will apply to every case. If we take 
as a basis the average diet for an adult — that is, about 125 grm. albumen, 80 grm. 
fat, and 350 grm. starch— we might say that most cases of obesity would be sure 
to undergo improvement upon a diet containing 125 grm. albumen (or possibly 
even more than this), 40 grm. fat, and 150 grm. starch. The amounts of fat and 
starch could be even more diminished, but it is usually best not to be too precipi- 
tate. A gradual diminution of, say, two or three pounds a week, extending over 



942 



CONSTITUTIONAL DISEASES. 



a long period without interruption, is to be preferred to the rapid treatment com- 
mon at many health resorts. Of course the loss of fat is greater at the commence- 
ment of treatment than later on, when the amount of adipose tissue has already 
approached more nearly to normal, and the diet must undergo a gradual and cor- 
responding change. It is of particular importance to increase the amount of non- 
nitrogenous foods in the later stages of treatment, lest the albuminoid tissues of 
the body become wasted. 

The following dietary may be taken as an illustration of what would be suit- 
able for a patient in the beginning of treatment : For breakfast, a cup of coffee 
with milk, and about 75 grm. of bread. At noon, a plate of soup, 150 to 175 grm. 
lean meat or fish, lettuce, green vegetables, and about 25 grm. bread. For dessert, 
about 75 grm. boiled rice, or some simple pudding, or 100 grm. fruit. To quench 
the thirst, water, or half a pint of light wine. In the afternoon, a cup of coffee, 
and with it not more than 20 to 30 grm. bread. For supper, two eggs, or 100 to 
120 grm. meat, with 30 grm. bread, a little fruit, lettuce, half a pint of wine, or 
one or two cups of tea, not much sweetened. Butter should be entirely proscribed 
at first ; later on it may be used in small amounts. 

Some approach to this bill of fare must be enforced, not merely for a few weeks, 
but for months. It is absolutely necessary that the patient should be weighed 
every two or three weeks. If the weight diminishes slowly and gradually, with- 
out any subjective disturbance, we have the best proof that the diet is a suitable 
one. If the weight does not diminish, then the amount of ingesta must undergo 
further reduction. If more food can be taken without the weight increasing 
again, a larger amount may be unhesitatingly permitted, and indeed may even 
be advisable if the patient is languid. The increase should at first, however, be 
mainly in the amount of albuminous food, the amount of starches and fats not 
being much increased. The "cure" can not be regarded as complete until the 
weight has been brought down to that of the average individual of the given 
age and sex. This goal having been reached, greater freedom in diet is per- 
missible. 

The object of the treatment just suggested is exclusively the limitation of the 
production of fat. "We may also promote the destruction of the fat already stored 
up in the system. A chief means to this end is muscular exercise, which undoubt- 
edly increases the oxidation of the adipose tissues. Carried out in a proper 
manner, it is therefore a most valuable adjuvant in treatment. Oertel has recently 
pointed out that muscular exertion does good in still another way — namely, by 
promoting cardiac activity and inducing deep respiratory efforts. Thus the heart 
is strengthened and circulation promoted. Mountain-climbing is one of the best 
modes in which to take the desired exercise. We needly hardly say that the 
increased muscular activity makes it possible for the patient to take an increased 
amount of food without injury. 

Baths also promote oxidation, but they are far less potent than is muscular 
exercise. Cold baths, brine baths, or baths containing carbonic-acid gas, may be 
employed. One way in which they do good is by stimulating the nervous system. 
Oertel regards it of great importance to diminish the amount of water in the sys- 
tem, a point which has until very lately received little attention. The diminution 
in the amount of fluids may ameliorate any circulatory disturbance and relieve 
venous congestion, and it undoubtedly has some value in the treatment of obesity. 
Oertel has shown that a simple diminution in the amount of fluids ingested, when 
there is no other change in the diet or mode of life, will effect a diminution of the 
adipose tissues. This result is probably due mainly to the diminished strain upon 
the heart and the consequent increase of oxidation. " Desiccation " may further 
be promoted by stimulating the perspiration by bodily exercise or by steam baths. 



SCROFULA. 



943 



This withdrawal of liquid from the system, however, is advisable only in cases 
where there is already incipient cardiac failure. 

It is evident that numerous excellent methods are at our disposal for the treat- 
ment of obesity ; but their application to any particular case should be the result 
of a careful consideration of the special circumstances presented. A very essen- 
tial point is that the injunctions of the physician should not merely be made, but 
be carried out ; and it is precisely here that the treatment of many cases suffers 
shipwreck. We may be baffled by the patient's lack of energy and persistency, 
or by the importunate demands which his profession or social position make upon 
him. Indeed, it is sometimes absolutely impossible to prosecute the treatment at 
home, in which case bathing and health resorts are to be urgently recommended. 
There alone can the patient muster up the resolution necessary for carrying out 
the desired changes in his mode of life. The incontestable success of treatment at 
Carlsbad, Marienbad, Kissingen, Tarasp, and similar resorts is doubtless only to a 
very small extent the result of their specific medicinal influence, but it is mainly 
due to a strict observance of the above-described diet and regimen. The internal 
use of mineral-waters is not entirely without a beneficial effect. Their laxative 
qualities diminish the absorption of food from the intestinal canal. It should be 
said, however, that the patient is at the same time exposed to the danger of a waste 
of his nitrogenous tissues. This is why patients frequently complain of the debili- 
tating effect of these mineral-springs ; to avoid which it would be well to increase 
the amount of albuminoids in the diet. Drinking large amounts of mineral-waters 
is inconsistent with that "desiccation" of the system which some authorities con- 
sider so desirable. 



CHAPTER XIII. 
SCROFULA. 

Definition and Symptoms of what is called Scrofula.— We desire to present, at 
the close of this section, a brief description of scrofula, but merely from a practical 
standpoint. From a scientific point of view, scrofula is not to be regarded as any 
special variety of disease. The term is applied to a group of symptoms seen most 
frequently in childhood, the essential features of which consist in the appearance 
of chronic enlargements of the lymph-glands, and in certain diseases of the skin 
and mucous membranes. The simultaneous appearance of these various phenom- 
ena does really produce a somewhat characteristic picture, which can frequently 
be recognized at the first glance. 

Most scrofulous children appear pale, with a flabby skin and soft muscles. 
The panniculus adiposus may, nevertheless, be tolerably well developed. Not 
infrequently the face is puffy, with prominent lips. This is called the " torpid 
habitus." In other cases the child has small features and a remarkably delicate 
white skin, which but partially conceals the superficial veins, and is readily suf- 
fused with blushes. To these the name u erethitic habitus " is applied. Enlarged 
lymph-glands are to be felt in the throat, at the angles of the lower jaw, and in 
the back of the neck, and occasionally in other parts of the body. These glands 
may remain indolent for a long while, or they may suppurate and break exter- 
nally. Chronic cutaneous eruptions are often seen in various places. The most 
common of these is a scaly or impetiginous eczema, affecting the face, scalp, or 
extremities. More severe affections are lupus (" lupus scrophulosorum "), prurigo, 
and lichen scrophulosorum. 



94:4 



CONSTITUTIONAL DISEASES. 



Of the mucous membranes, the conjunctiva and the lining membrane of the 
nostrils are most frequently affected. Conjunctivitis in various forms is a char- 
acteristic symptom of scrofula ; as are also blepharitis ciliaris, keratitis, and chronic 
rhinitis, which last often terminates in a pronounced ozsena (q. v.). Chronic 
diseases of the ear are also frequent, such as otitis media, with perforation of 
the tympanum, and occasionally caries of the mastoid cells and its unfortunate 
results. 

Of the deeper lying tissues, mainly the bones and joints suffer. The affections 
located here are almost exclusively " fungous " — namely, fungous ostitis and peri- 
ostitis, white swelling, and caries. Formerly there was frequent use of such terms 
as "scrofulous inflammation of the knee-joint," or " scrofulous caries of the ribs." 

If we inquire into the nature of this strange group of symptoms thus briefly 
enumerated, we shall find that by far the greater number of cases of well-marked 
scrofula are examples of tuberculosis. Tubercular bacilli have been demonstrated 
in connection with most of the fungous or " scrofulous " diseases of the bones and 
joints. Ozsena is often a tubercular disease of the nose, lupus is a tuberculosis of 
the skin, and many forms of otorrhcea are really tuberculosis of the ear. The 
aetiology of " scrofula " is, therefore, in main part, identical with that of tuber- 
culosis (q. v.), and this explains why the old physicians habitually insisted upon 
the intimate relationship between the two diseases. It was formerly thought 
that scrofula often terminated in tuberculosis — that is, a scrofulous child is apt to 
suffer eventually from tuberculosis of the lungs, intestine, or brain. To-day we 
know that most scrofulous children do not become, but that they are already, 
tuberculous. 

It must, however, be borne in mind that, in practice, many diseases are termed 
scrofulous which have nothing to do with tuberculosis. Many cases of perfectly 
innocent eczema of the face and scalp lead to swelling of the glands in the throat, 
and are therefore termed scrofulous eczema. These cases are, probably, most of 
them secondary, and the result of external irritation and the like. Again, many 
enlarged glands in the neck are the result of pharyngeal trouble, as after scarlet 
fever, and are equally devoid of a tubercular taint. Pseudo-leukaemic lymphomata 
may also occur in children; and it should be borne in mind that hereditary or 
acquired syphilis may produce in children lesions closely resembling those of 
scrofula. 

It is therefore the duty of the physician in every case of " scrofula " to analyze 
the aetiology and symptoms carefully, in order to determine with what he has to 
deal. " Scrofula" should be regarded merely as a short way of naming a certain 
group of symptoms. It is convenient to retain the term as being less likely to 
startle the friends of the child than would the true name of the disease. 

Treatment. — In the treatment of scrofula we have first to attack the various 
local diseases, and, secondly, to invigorate the general health. We can not here 
enter into all the details of local treatment, but must refer the reader to the special 
descriptions already given of the various local affections. We may, however, 
briefly mention a few facts with regard to the treatment of scrofulous swelling of 
the lymph-glands. Painting the overlying skin with tincture of iodine is a very 
common practice, but it seldom does much good. We have obtained more satis- 
factory results from iodoform collodium, or iodoform salve, or from the repeated 
inunction of sapo viridis. For particulars as to the opening of abscesses, or the 
extirpation of glands, we must refer to works on surgery. 

Secondly, in the general treatment of scrofula every possible means is to be 
employed to invigorate the system. Abundant nourishment and fresh air are 
essential. The child may be taken either to the country, or the mountains, or the 
sea-shore. Cod- liver oil is regarded by some as a specific in scrofula; but its 



SCROFULA. 



945 



undoubted value really lies in the fact that it is an easily digested fat. Some chil- 
dren can take a considerably larger dose than others without its disturbing the 
stomach. Usually we prescribe two or three tablespoonfuls per diem. Salt baths 
enjoy a great reputation as a remedy in scrofula. If circumstances permit, the 
best way is to visit some place where there are brine baths, such as Kosen, Suiza, 
Salzungen, Arnstadt, Kreuznach, Minister am Stein, Rehme, Reich enhall, Ischl, 
and Colberg. 

Treatment at these resorts is preferable to artificial baths at home, because it is 
under more favorable hygienic surroundings. 

The chief internal remedies are iron, iodine, and arsenic. A favorite prescrip- 
tion is syrup of the iodide of iron. Arsenic promotes nutrition, and perhaps 
exerts some specific influence upon certain scrofulous (tubercular) local diseases, 
particularly the " fungous " affections and lupus. 
60 



APPENDIX I. 



SUMMARY OP THE SYMPTOMS AND TREATMENT IN CASES OP 

POISONING. 

1. Sulphuric Acid.— Mucous membrane of mouth, throat, oesophagus, and 
stomach deeply corroded. In the worst cases rapid death ushered in by convul- 
sions and asphyxia, or more rarely consequent upon perforation of the stomach. 
Usually the case is more protracted. The mouth and throat are whitened, or in 
severe cases blackened. They are soon attacked by an intense ulcerative inflam- 
mation. Deglutition is extremely painful, and there are most distressing chok- 
ing and retching. The vomitus contains black lumps. Profuse salivation. Pain 
along the oesophagus. Abdomen usually distended and very tender on pressure. 
There may be intestinal discharges of a bloody character, resembling dysentery. 
Urine is generally scanty, and often contains albumen and blood. Collapse. 
Small and rapid pulse. 

In mild cases, slow recovery, the necrosed tissues gradually sloughing off. 
Cicatricial stricture of the oesophagus frequently ensues and may prove fatal. 
Neuralgia, hyperaesthesia, and various other nervous disturbances may also occur 
as sequelae. 

In fatal cases, the autopsy discloses necrosis, ulceration, and inflammation in 
the upper portion of the digestive tract. The lining of the stomach is usually 
coal-black. Well-marked parenchymatous degeneration of the liver and kidneys. 
Perhaps nephritis. In later stages, extensive cicatrices. 

Treatment. — If used at all, the stomach-pump must be introduced very cau- 
tiously, for fear of causing perforation. The best remedy to give at once is several 
teaspoonfuls of magnesia in water, or a few drops of liquor sodas in mucilage. 
Later, the symptoms are to be combated with bits of ice, disinfecting mouth- washes 
and gargles, tonics, and cautious feeding with milk, eggs, etc. If stricture of the 
oesophagus develops afterward, an endeavor should be made to dilate it with 
bougies. 

2. Hydrochloric and Nitric Acids.— Symptoms similar to those of sulphuric 
acid. The most prominent symptoms are the local ones. Nitric acid sometimes 
stains the angles of the mouth yellowish ; and the vomitus may have the same 
tinge. In poisoning from fuming nitric acid the inhaled vapors cause pulmonary 
symptoms. Prognosis and treatment as in case of sulphuric acid. 

3. Nitrous and Sulphurous Acid Fumes.— Intense local inflammation of the air- 
passages. Violent dyspnoea, cough, bloody expectoration. There may also be 
grave nervous disturbance and collapse. Treatment symptomatic : sinapisms, nar- 
cotics, expectorants, and inhalations. 

4. Oxalic Acid. — Local corrosive action similar to that of the other acids, only 
less severe. Apt to occasion certain nervous symptoms — formication, anaesthesia 
of the finger-tips, tonic and clonic convulsions. Collapse. Dyspnoea. Sometimes 
nephritis. The treatment should be symptomatic, and should also include the 



APPENDIX I. 



947 



administration of preparations of calcium — liquor calcis, calcii carbonas, or even 
egg-shells, to form insoluble calcic oxalate. Magnesia is also useful. 

5. Ammonia. — The fumes affect the air-passages chiefly ; the solution, the upper 
part of the digestive tract. The specific local effect is the production of an intense 
croupous inflammation of the mucous membrane. Accordingly, the symptoms 
are salivation, dysphagia, vomiting of strongly alkaline matter, and diarrhoea, or 
cough, dyspnoea, etc. In severe cases there is collapse, with rapid pulse, and such 
nervous symptoms as pain, paragsthesia, and vertigo. Treatment : In fresh cases 
the stomach-pump. The cautious use of acids — for instance, acetic or citric. Also, 
symptomatically, emulsions of oil, bits of ice, and narcotics. 

6. Caustic Potash or Soda.— Symptoms and treatment as in case of ammonia. 

7. Potassic Nitrate. — Vomiting and diarrhoea. Severe abdominal pain. Col- 
lapse, with cold skin and rapid, thready pulse. Occasionally the pulse is slow. 
Nervous disturbances, such as painful muscular contractions and, in severe cases, 
convulsions and coma. Treatment : symptomatic ; opium and other narcotics, 
stimulants (camphor, ether), and bits of ice. 

8. Chlorine Gas. — Violent convulsive cough. Bloody expectoration. Spasm 
of the glottis. Dyspnoea. Darting pains through the chest. Sneezing and pro- 
fuse flow of tears. In severe cases pneumonia. Treatment : Fresh air. Inhala- 
tion of warm aqueous vapor, or of ammonia to form ammonic chloride. Chloro- 
form may also be tried, and narcotics. 

9. Iodine. — 1. Acute iodism as seen, for instance, after the injection of large 
amounts of tincture of iodine into ovarian cysts : collapse, with pallor and cya- 
nosis, and small and very rapid pulse. Vomiting. Suppression of urine. Later, 
the skin becomes very red. There is albuminuria ; also sore throat, coryza, and 
cutaneous eruptions. 2. Chronic iodism, caused, for example, by long-continued 
internal administration of potassic iodide: coryza, conjunctivitis, sore throat. 
Gastric symptoms. Vertigo, headache, and similar nervous phenomena of a mild 
character. Acne or erythema. Treatment: In acute cases, white of egg and 
stimulants. Other than this, treatment must be symptomatic. Prophylaxis 
demands caution in the internal administration of iodine or its compounds. 

10. Bromine. — 1. Acute poisoning from the fumes of bromine excites the same 
symptoms as does chlorine gas. 2. Bromism, resulting from the long-continued 
use of potassic bromide, causes languor, debility, mental apathy, and impaired 
intellectual vigor. The reflexes are diminished, particularly the reflex irritability 
of the soft palate and pharynx. Anorexia. Diarrhoea. Impotence. Almost 
invariably a characteristic acne. No specific antidotes are known. 

11. Lead. — (a) Acute lead-poisoning produces severe gastro-enteritis. The 
best antidote is sulphate of sodium or magnesium ; or phosphates, white of egg, 
and milk. In fresh cases the stomach-pump, or emetics and purgatives. Other 
than this, symptomatic treatment. 

(b) Chronic lead-poisoning, seen in type-setters, type-founders, painters, potters, 
and others. General symptoms: Lead-line on the gums, lead anaemia, and lead 
cachexia. Important groups of symptoms are: 1. Lead colic: Violent colicky 
pains, radiating from the umbilicus. Usually constipation, exceptionally diar- 
rhoea. Abdomen concave and hard. Vomiting. Hard, slow pulse. Temperature 
usually normal. Urine sometimes contains a trace of albumen. Duration, one 
or two weeks. Treatment : If severe pain, opium, and hot compresses. Atropine 
may also be tried. For constipation, enemata and gentle laxatives. Warm baths. 
2. Lead paralysis (vide page 537). 3. Saturnine encephalopathy: Sudden 
development of grave cerebral symptoms; convulsions, coma, delirium, great 
mental uneasiness, and excruciating headache. Saturnine amaurosis. In severe 
cases, death. Cerebral lesions are very rarely found post mortem. Treatment is 



948 



APPENDIX I. 



symptomatic. Lukewarm baths, with, douching', narcotics, and stimulants. Later, 
potassic iodide. 4. Lead arthralgia: Most frequently attacks the knee. Also 
seen in the joints of the upper extremities. Sometimes associated with painful 
muscular contractions. Objective lesions are rarely seen. The treatment consists 
in warm baths and the administration of potassic iodide. It should be remem- 
bered that chronic lead-poisoning may occasion gout and chronic interstitial 
nephritis. The reader is referred to the chapters describing these diseases. 

12. Copper. — (a) Acute copper poisoning: Vomiting of greenish matter, 
colic, tenesmus, and bloody stools. Collapse. Dyspnoea. Treatment : White of 
egg, milk, wood charcoal. Magnesia is also valuable, (b) Chronic copper poison- 
ing is rare. It occasions gastro-intestinal disturbance, colic, and a reddish or 
greenish discoloration of the hair. 

13. Mercury. — (a) Acute poisoning from corrosive sublimate : The mucous 
membrane of the mouth, throat, oesophagus, stomach, and intestines is deeply 
corroded. Vomiting. Diarrhoea with painful tenesmus. Ischuria or complete 
anuria. Collapse. Generally quickly fatal. Treatment : White of egg, reduced 
iron, narcotics, (b) Chronic mercurial poisoning : Seen in the makers of ther- 
mometers, scientific instruments, and mirrors. Rarely occasioned by the pro- 
longed use of anti-syphilitic remedies. The symptoms are anaemia, emaciation, 
and gastro-intestinal disturbance. Mercurial tremor. Stomatitis, salivation. 
Sometimes there are psychical symptoms. In severe cases there is marked tremor 
and paralysis (exclusively motor). Treatment : Warm baths. Potassic iodide. 
Abundant nourishment. Electricity. 

14. Phosphorus. — (1) Acute phosphorus poisoning, as from matches : Violent 
epigastric pain, vomiting — the vomitus smells of phosphorus and may be phos- 
phorescent. After these initial symptoms usually comes a period of comparative 
comfort, lasting two or three days. Then appear grave symptoms: jaundice, 
severe pain in the hepatic region and whole abdomen, hepatic enlargement, fever, 
feeble and rapid pulse, sometimes gastric or intestinal haemorrhage, cutaneous 
ecchymoses, haematuria, epistaxis, or metrorrhagia. The intellect usually remains 
clear, except that just before death there may be drowsiness or convulsions. The 
urine contains albumen, blood, casts, and sometimes leucin and tyrosin. No urea 
is excreted. Death occurs usually at the end of one or two weeks, but may be 
more speedy. In mild cases the above symptoms are not strongly marked, and 
recovery may ensue. The prognosis should be very grave in every case at the 
start. Post-mortem appearances in acute phosphorus poisoning: Jaundice. 
Numerous internal ecchymoses — for example, in the serous and mucous mem- 
branes and kidneys. Fatty degeneration of most of the internal organs, including 
the liver, heart, muscles, and kidneys. Treatment : In fresh cases, washing out 
of the stomach. Laxatives. As an emetic, sulphate of copper. The best anti- 
dote is old oil of turpentine (30-40 drops in mucilage). Oily substances should be 
avoided, as phosphorus is soluble in oil. Narcotics and other symptomatic reme- 
dies may also be indicated. (2) Chronic phosphorus poisoning : Necrosis of the 
lower jaw, less often of the upper jaw, extending from caries of the teeth. Necro- 
sis of the bone, with exuberant growth of osteophytes. 

15. Arsenic (Arsenious Acid, Schweinfurth Green, Scheele's Green, Arsenical 
Wall-paper. — (1) Acute arsenic poisoning: Symptoms of intense gastroen- 
teritis, suggesting cholera. Violent vomiting. Rice-water stools. Severe abdomi- 
nal pain. Collapse. Not infrequently a cutaneous eruption resembling urticaria 
or eczema. Sometimes albumen and blood are present in the urine. Severe cases 
are fatal in one or two days. With regard to arsenical paralysis, vide page 538. 
Treatment: At first the stomach-pump or emetics — for example, sulphate of 
zinc. The best antidotes are freshly prepared ferric hydrate in water, two to four 



APPENDIX I. 



949 



tablespoonfuls every fifteen to thirty minutes; ferrum oxydatum saccharatum 
solubile (P. G.), in teaspoonfnl doses; magnesia; and, best of all, the compound of 
magnesia and ferric hydrate known as k ' antidotum arsenici " (P. G.), of which a 
tablespoonful may be given every fifteen to thirty minutes. (2) Chronic arsenic 
poisoning: Acquired in arsenic-works and glass-factories, or from arsenical 
fabrics, papers, and flowers. Conjunctivitis, chronic gastro-intestinal catarrh, 
eczema, and cutaneous ulcerations. Anseinia and cachexia, falling out of the 
hair, loss of sleep. Treatment is purely symptomatic, except as regards prophy- 
laxis. 

16. Alcohol. — 1. Acute alcoholic poisoning : Unconsciousness ; anaesthesia ; 
pupils either dilated or contracted, usually not reacting to light; pulse small, 
sometimes slow : skin cold and clammy ; vomiting ; stertorous respiration. There 
may be delirium and clonic convulsions instead of coma. Such cases last three or 
four days. Death has been repeatedly observed. Treatment: Bathing and 
douching. Stimulants [ammonia]. 

2. Chronic alcoholism, (a) Physical and mental debility : Chronic catarrh 
of the throat, larynx, stomach, and intestines. Alcoholic tremor. Numerous 
organic diseases, including cirrhosis of the liver, contracted kidney, cerebral dis- 
ease, and neuritis. 

(b) Delirium tremens : Usually a sudden onset, as in connection with some 
acute disease or after a surgical injury. Disordered intellect. Great restlessness, 
hallucinations (vermin, etc.), excitement, and loss of sleep. Treatment : Bathing 
and douching. Injections of strychnine, The use of chloral and other narcotics 
should be cautious. Physical restraint should be avoided if possible. The patient 
may often be allowed to go about the room as he likes, if only he is watched. 
Alcohol should be given if collapse is threatened. 

17. Chloroform. — Unconsciousness. Paralysis of the heart and of respiration. 
Pupils dilated. Treatment: Artificial respiration. Injections of strychnine. 
Stimulants. Counter-irritation. 

18. Carbonic Oxide Gas (Illuminating Gas).— At first, vertigo, headache, throb- 
bing in the temples, ringing in the ears, and spots before the eyes. The patient 
gradually becomes unconscious. Skin pale and cyanotic. Eespiration intermit- 
tent. Subnormal temperature. The urine may contain albumen and sugar. The 
carbonic oxide may be demonstrated in the blood by means of the spectroscope. 
Subsequently paralysis, disturbances of sensation and of speech. Treatment: 
Fresh air, artificial respiration, stimulants, transfusion. 

19. Sulphuretted Hydrogen. — Headache, vomiting, diarrhoea. In severe cases, 
unconsciousness, dyspnoea, cyanosis, convulsions, and death. Treatment : Artifi- 
cial respiration, fresh air, and the cautious inhalation of chlorine gas. 

20. Hydrocyanic Acid (Potassic Cyanide ; Bitter Almonds).— Characteristic 
odor of bitter almonds. In severe cases death may occur in a few minutes. If 
the course is more protracted, convulsive and extremely slow respiration, the 
expiratory act being much prolonged ; the eyeballs protrude, and the pupils are 
somewhat enlarged and do not react to light. Cardiac weakness, cyanosis, uncon- 
sciousness. Twitching of the muscles. Trismus. Treatment : Merely symptom- 
atic. Emetics, artificial respiration, cool douches, stimulants. Atropine may be 
tried ; also, hydrated ferric oxide and chlorine- water. 

21. Nitrobenzine (Nitrobenzole, Oil of Mirbane). — Strong odor of bitter almonds. 
At first, dizziness. The skin soon assumes a bluish hue, rapidly increasing to the 
deepest cyanosis. Increasing anxiety, sense of suffocation, and gradual loss of 
consciousness. In severe cases, death, ushered in by convulsions. In milder 
cases, gradual recovery. Treatment: Stomach-pump. Artificial respiration. 
Stimulants. In the Leipsic clinique, transfusion has worked admirably in two 



950 



APPENDIX I. 



cases. The symptoms caused by aniline and the aniline-dyes closely resemble 
poisoning from nitrobenzole. 

22. Carbolic Acid. — Corrosion of mouth, throat, and stomach. In mild cases, 
vertigo and headache ; in severe cases, coma, preceded in rare instances by symp- 
toms of cerebral irritation. Contracted pupils. Vomiting. Pulse slow at first, 
then rapid. The urine has a dark, olive-green color. Treatment : Stomach-pump. 
Slaked lime and water. Large doses of sulphate of sodium are especially to be 
recommended. 

23. Atropine {Belladonna). — Dryness of the mouth and throat. Excessive 
thirst. Dizziness and headache. Peculiar mental disturbances: hallucinations 
are particularly frequent. Pupils very widely dilated. Cutaneous erythema 
resembling that of scarlet fever. In severe cases, pulse enormously accelerated, 
with violent pulsation in the arteries. Convulsions may occur. Nervous symp- 
toms persist for some time. Treatment : The following physiological antidotes 
should be tried: physostigmine (eserine), pilocarpine, and morphine. 

24. Digitalis. — Vomiting. Diarrhoea. Pulse very slow (forty beats per min- 
ute, or less). Dyspnoea. Symptoms of collapse. Somnolence. In the worst cases, 
sopor and death. Even the milder cases are protracted. Treatment : Emetics, 
stomach-pump. Tannin. Camphor, strong cafe noh\ ether, ammonia. Counter- 
irritation. 

25. Mcotine. — 1. Acute : Pulse small and slow, syncope, sense of oppression, 
vomiting. In severe cases, loss of consciousness, tetanic spasms, both pulse and 
respiration intermittent. 2. Chronic (from excessive use of tobacco) : Palpitation, 
irregular action of the heart, paroxysms of asthma and angina pectoris. Tremor, 
muscular weakness. Loss of sleep. Sometimes there are symptoms of ataxia 
(" nicotine tabes " seen in cigar-makers). Amblyopia. Gastric disturbance, chronic 
catarrh of the pharynx and larynx. Treatment : In acute cases, stimulants. 
Chronic poisoning necessitates the giving up of tobacco. Further treatment is 
symptomatic. 

26. Strychnine. — Violent tetanic reflex convulsions. Exaggeration of the 
cutaneous and tendon reflexes. Trismus. Opisthotonos. Pulse small and very 
rapid. The convulsions come in paroxysms, with intervals between them. The 
intellect is usually perfectly clear. Recovery occurs only in mild cases. Treat- 
ment : Emetics, stomach-pump. Tannin. Tincture of iodine. Castor-oil. The 
convulsions are to be combated by morphine, chloroform, chloral, or potassic 
bromide. Curare has also been tried. 

27. Morphine (Opium). — 1. Acute : In mild cases, headache, languor, dizziness, 
and somnolence. In all cases of any severity, coma. Muscles completely relaxed. 
Respiration slow, and often irregular. Contracted pupils. Treatment : Sulphate 
of zinc, or some other emetic; stomach-pump. Tannin. Cafe noir. Atropine 
may be tried as a physiological antidote. Artificial respiration. Stimulants. 
2. Chronic (morphine habit): Emaciation, anaemia, headache, vertigo, wakeful- 
ness. Tremor. Mental disturbance. Unconquerable longing for morphine ; and, 
if this be denied, the appearance of grave symptoms. To break up the morphine 
habit is almost impossible except in hospitals and special asylums. The with- 
drawal of the drug is abrupt according to the practice of some, and gradual 
according to others. For particulars consult monographs. 

28. Ergot (Ergotine). — 1. Acute : At first nausea, vomiting, colic, and diarrhoea. 
Then vertigo, headache, and muscular weakness. Pulse slow. In severe cases, 
sopor, disturbance of respiration, and sometimes death. Treatment : Emetics and 
purgatives. Tannin. Ether, camphor, and cafe noir, as stimulants. 2. Chronic 
ergotism : Gastric symptoms, vertigo, languor, cardiac weakness. The nervous 
disturbances are, however, of especial importance. Of these, paraasthesia has long 



APPENDIX I. 



951 



been recognized. Recently attention has been attracted to the great resemblance 
of the nervous symptoms to those of locomotor ataxia; and there is, moreover, an 
anatomical change in the posterior columns of the cord. Psychical phenomena 
are also observed. A second form of chronic ergotism is called gangrenous 
ergotism. It results in dry gangrene of the hands and feet. A line of demarka- 
tion forms and the gangrenous parts slough off. The process may be attended 
by fever and pyaemia. The probable explanation is that the minute blood-vessels 
become spasmodically contracted under the influence of the poison. The treat- 
ment of chronic ergotism is purely symptomatic. 

29. Poison Mushrooms. — 1. Poisoning from morels : Fresh morels (" morcheln " 
or " lorcheln ") contain a poison which is readily soluble in hot water, and which 
evaporates completely if the morels are dried. Morels that have been dried or 
parboiled are therefore perfectly harmless ; but the fresh ones are poisonous. 
The symptoms are nausea, vomiting, diarrhoea, headache, coma, and. above 
all, haemoglobinaemia and haemoglobinuria (q. v.), associated with which is a 
haematogenous icterus. In severe cases death occurs, ushered in by convulsions. 
Treatment is symptomatic, and includes the administration of emetics, purgatives, 
and stimulants. 2. Poisoning from the red agaric (amanita muscaria) : This 
contains the poisonous alkaloid muscarine. Gastric symptoms and diarrhoea. 
Mental excitement, delirium, tetanic and epileptiform convulsions. A slow pulse, 
dilated pupils, disturbed vision, salivation, and in most of the severe cases sopor 
and death. Treatment : Emetics, etc. Atropine, which acts as a physiological 
antidote to muscarine. Also tannin and stimulants. 

30. Poisoning from Sausages (Botulismus).— This sometimes occurs as the result 
of eating partially decayed sausages. The peculiar poisonous principle has not yet 
been isolated. The symptoms are pain in the stomach, nausea, vomiting, colic, and 
diarrhoea. There are also marked feebleness, praecordial anxiety, and dyspnoea ; 
vertigo, headache, somnolence ; and very often disturbance of vision (amblyopia, 
spots before the eyes), and, what is surprising, ptosis. In severe cases, dysphagia, 
as a result of more or less complete paralysis of the tongue and the constrictors of 
the pharynx. The mouth is dry. The heart is feeble ; this and the general pros- 
tration and malnutrition may prove fatal. The cases are usually protracted, rarely 
being very acute. Treatment : Emetics, purgatives (calomel), stimulants, and, if 
indicated, artificial feeding. 

31. Poisoning from Meat. — In repeated instances severe symptoms have been 
occasioned by eating tainted meat, or possibly that obtained from animals which 
had been diseased. The special poison is not yet fully known. Probably there 
are several poisons, either chemical or organic and infectious. The usual symp- 
toms are vomiting and diarrhoea. The case may closely simulate cholera. In 
most instances certain nervous phenomena are also observed — wakefulness, deliri- 
um, headache, and changes in the pupils. There may be roseola or wheals or 
erythema. Frequently there is a high fever, but sometimes the temperature is 
subnormal. The pulse is small and slightly accelerated, although it may occa- 
sionally be slower than normal. There is a sense of thoracic oppression. The 
cases are often protracted. Tendency to relapses. Death may occur. Post-mortem, 
there is usually found an intense and often haemorrhagic enteritis, with secondary 
changes in the spleen, kidneys, lungs, and other organs. Treatment : Symptom- 
atic : calomel, emulsions, stimulants, and baths. Food should be given cau- 
tiously. 

32. Poisoning from Fish. — The eating of tainted fish has likewise caused grave 
disturbance. The symptoms vary. Usually there are pain in the stomach, prae- 
cordial anxiety, vertigo, dryness of the throat, aphonia, and labored respiration. 
There may also be disturbance of vision, amblyopia, and colored vision, or paraly- 



952 



APPENDIX I. 



sis of the motores oculi and of accommodation. In severe cases there may he 
dysphagia and general paresis. Sometimes dyspnoea and cardiac weakness are 
observed. The cases are frequently very tedious. There is an undeniable resem- 
blance in these symptoms to those caused by the ingestion of tainted sausages. 
Treatment similar to that recommended in the two preceding paragraphs. 

33. Poisoning from Cheese. — Vomiting, colicky pains, diarrhoea, vertigo, sense 
of thoracic oppression, headache, languor, and disturbance of vision. Treatment 
as in paragraphs 31 and 32. 



APPENDIX II. 



TABLE OF WEIGHTS AND MEASURES. 

Table of Relation of U. S. Fluid to Metric Measure. 



Cubic 

Minims. Centimetres. 

1 = -06 

2 = -12 
5 = -31 

10 = -62 

15 = -92 

16* = 1-00 

20 = 1-23 



Cubic 

Minims. Centimetres. 

30 = 1-85 

40 = 246 

Fluid Cubic 

Drachms. Centimetres. 

1 = 3-70 

2 = 7-39 

3 = 11-09 



Fluid Cubic 
Drachms. Centimetres. 

4 = 14-79 

6 = 22-18 

Fluid Cubic 

Ounces. Centimetres. 

1 = 29-57 

2 = 59-10 

3 = 88-67 



Fluid 


Cubic 


Ounces. 


Centimetres. 


4 


= 118-24 


6 


= 177-39 


8 


= 236-53 


12 


= 354-82 


16 


= 473-11 



Table of Relation of Troy Weight to Grammes. 



Grains. 




Grammes. 


Grains. 




Grammes. 


Drachms. 


Grammes. 


Ounces. 




Grammes. 


* 




•008 


8 




•52 


1 = 


3-89 


1 




31-1 






•011 


10 




•65 


H = 


5-83 


11 




46-6 


i 




•016 


15 




•97 


2 = 


7-77 


2 




62-2 


\ 




•032 


15-43 




1-00 


3 = 


11-66 


3 




93-3 


1 




•065 


20 




1-29 


4 = 


15-55 


4 




124-4 


2 




•13 


30 




1-94 


6 = 


23-3 


6 




186-6 


4 




•26 


40 




2-59 






8 




248-8 


5 




•32 


61-73 




4-00 












6 




•39 



















The Metric System in Medicine. 



Old Style. 
TU j or gr. j 
f 3 j or 3 j 



Metric. 

06 grm. 

4 

32 



The decimal line, instead of points, makes errors impossible. As "06 (drug) is 
less than a grain, while 4* and 32' (vehicle) are more than the drachm and ounce, 
there is no danger of giving too large doses of strong drugs. 

C.c. (cubic centimetres), used for grms. (grammes), causes an error of five per 
cent (excess). 

A teaspoonful is usually 5 grms. ; a tablespoonful, 20 grms. 



> 



INDEX. 



Abducens nerve, paralysis of, 524. 

Abortion in acute yellow atrophy of the liver, 45S ; 
in pernicious anaemia, 889 ; in typhoid fever, 16. 

Abscesses, embolic, 230 ; in glanders, 105 ; in paroti- 
tis, 326 ; in perinephritis, 818 ; in perityphlitis, 393 ; 
in small-pox, 52 ; in septico-pyaemia, 98 ; in typhoid 
fever, 8 ; sub-diaphragmatic, in peritonitis, 423. 

Absorption, impaired, in chronic gastric catarrh, 352. 

Accessorius nerve, spasm of, 541 ; position of head 
in spasm of, 541 ; paralysis of, 530. 

Acetonaemia in diabetes, 912. 

Acetone, odor of, in diabetes, 918. 

Achilles 1 tendon reflex, 513. 

Acholia, 459. 

Achromatopsia, 760. 

Aconitia in neuralgia, 489 ; in trigeminal neuralgia, 
492. 

Acoustic nerve, atrophy of, in locomotor ataxia, 607. 

Actinomycosis, 249. 

Acupuncture for aneurism, 315. 

Addison's disease, 826. 

Adenia, 896. 

Adeno-carcinoma, 398. 

JSgophony, 243. 

After-sensations, 479 ; in locomotor ataxia, 479. 
Agaricine in pulmonary tuberculosis, 218. 
Ageusia, 502. 
Agraphia, 680. 

Air, inspired, as carrier of infection, 193. 
Alalia, 646. 

Albuminuria, 772, 789, 790 ; in acute ascending spinal 
paralysis, 637 ; in anaemia, 880, 888 ; in bulbar apo- 
plexy, 653 ; in diabetes, 916 ; in gout, 931 ; in osteo- 
malacia, 872 ; in scarlet fever, 39 ; in scurvy, 904 ; in 
small-pox, 53 ; in typhoid fever, 16 ; in yellow fever, 
91 ; genuine renal, 773 ; spurious, accidental, 773 ; 
transitory, 774. 

Alcoholic beverages in anaemia, 882 ; in diabetes, 923, 
924 ; in gout, 935 ; in neurasthenia, 769 ; in obesity, 
937 ; in pneumonia, 191 ; in pulmonary tuberculosis, 
215 ; paralysis, 538 : poisoning, acute, 949. 

Alcoholismus, chronic, 949. 

Alexia, 680. 

Alkalies in diabetes, 925 ; in gout, 935. 
Allantiasis, 951. 

Alum in intestinal catarrh of children, 390. 
Amaurosis in gastric ulcer, 361 ; uraemic, 781. 
Amblyopia in hysteria, 760. 
Aminia, 680. 
Ammoniaemia, 831, 842. 

Ammonia in asthma, 158 ; in diabetes, 925 ; poisoning 
from, 947. 



Amyl nitrite in asthma, 158 ; in epilepsy, 737 ; in hemi- 
crania, 558 ; in trigeminal neuralgia, 493 ; in valvu- 
lar disease, 286. 

Amyloid disease of liver, 468 ; of kidney, 812 ; com- 
bined with chronic nephritis, 814. 

Anaemia, 874 ; as a complication of intestinal tuber- 
culosis, 396 ; combined with general malnutrition, 
8?6 ; fever in, 880 ; hepatic, 466 ; in Addison's dis- 
ease, 828 ; in articular rheumatism, 853 ; in gastric 
cancer, 366 ; in gastric ulcer, 361 ; primary, 874 ; 
secondary, 876. 

Anaemia, pernicious, 884 ; associated with atrophy of 
gastro-intestinal walls, 884 ; chemical examination 
of blood in, 889 ; diagnosis of, 889 ; fever in, 889 ; 
post-mortem lesions in, 885 ; symptoms of, 886 ; 
treatment of, 890. 

Anaemia, simple, constitutional, 875 ; diagnosis of, 
881 ; symptoms of, 877 ; treatment of, 882. 

Anaemia, spastic, 481 ; splenic, 886, 888, 896. 

Anaesthesia, 475 ; dolorosa, 482 ; in hysteria, 759 ; in 
myelitis, 586 ; in neuralgia, 487 ; in neuromata, 552 ; 
in railway-spine, 573 ; in unilateral lesions of the 
spinal cord, 644 ; of the skin, 480 ; of the trigemi- 
nus, 482, 483. 

Analgesia, 478 ; in locomotor ataxia, 604. 

Anarthria, 646 ; in bulbar apoplexy, 653. 

Anchylostomum duodenale, 419. 

Aneurism, cylindrical, 311 ; diffuse, 311 ; dissecting, 
316 ; fusiform, 311 ; sacciform, 311 ; of abdominal 
aorta, 316 ; of carotid artery, 316 ; of cerebral ar- 
teries, 316 ; of pulmonary artery, 316 ; of subcla- 
vian artery, 316. 

Angina, 328. See Sore Throat. 

Aniline, poisoning from, 950. 

Ankle clonus, 513 ; in cerebral haemorrhage, 692 ; in 

tetanus, 750. 
Anosmia, 501. 
Anthracosis of lungs, 228. 
Anthrax, 106. 

Antidotes in poisoning from atropine, 950 ; lead, 947 ; 

mushrooms, 951 ; phosphorus, 948. 
Antidotum arsenici, 949. 

Antimony, arsenite of, in cardiac valvular disease, 
283. 

Antipyrine in typhoid fever, 22. 
Antiseptics in pyelitis, 831. 

Anuria in hydronephrosis, 839 ; in nephritis, 789. 

Aorta, narrowing of, 317 ; rupture of, 316. 

Apex of lung, catarrh affecting, 206. 

Aphasia, 677 ; amnesic, 678 ; anatomical localization 
of, 677 ; ataxic, 678 ; diagnosis of, 680 ; in cerebral 
haemorrhage, 696 ; prognosis, 680 ; treatment, 680. 



956 



INDEX. 



Aphthae, 320. 

Aplasia of the lungs, 167. 

Apoplectic cyst, 688 ; habit, 686 ; scar, 688. ' 

Apoplexy, 688 ; delayed, 689 ; from cerebral syphilis, 
717 ; from haematoma of the dura mater, 658 ; from 
haemorrhage into medulla and pons,t552 ; from tu- 
mors of the brain, 710 ; in multiple sclerosis, 594 ; 
meningeal, 568 ; premonitory symptoms of, 689 ; 
symptoms of, 688. 

Apraxia, 680. 

Apyrexia in relapsing fever, 32. 
Arbutine in cystitis, 843. 

Arsenic in anaemia and chlorosis, 883 ; in angina pec- 
toris, 296 ; in cerebral tumor, 714 ; in chorea, 742 ; 
in diabetes, 924, 925 ; in exophthalmic goitre, 563 ; 
in habitual headache, 501. 

Arsenic in hysteria, 765 ; in leukaemia, 895 ; in loco- 
motor ataxia, 612 ; in lymphatic pseudo-leukaemia, 
898 ; in malaria, 87 ; in neuralgia, 491 ; in paralysis 
agitans, 745 ; in scrofula, 945 ; in spasm of the mus- 
cles of the neck, 542 ; paralysis from, 528 ; poison- 
ing from, 948. 

Arteriosclerosis, 308 ; in diabetes, 916 ; in obesity, 
940. 

Arthralgia from lead, 948. 

Arthritis deformans, 858 ; monarticular form of, 859 ; 
in locomotor ataxia, 608 ; of the poor, 858 ; of the 
rich, 929 ; polyarticular form of, 859 ; senile, 859 ; 
sicca, 859. 

Arthrogryposis, 543. 

Asafoetida in hysteria, 765. 

Ascaris lumbricoides, 417. 

Ascites, 432 ; in cancer of the liver, 462 ; in cancer 
of the pancreas, 474 ; in cirrhosis of the liver, 
450 ; in chronic endocarditis, 279 ; in suppurative 
hepatitis, 447 ; in scarlet fever, 39 ; in syphilis 
of the liver, 461 ; in thrombosis of the portal vein, 
472. 

Associated movements, 510 ; in cerebral haemorrhage, 
695 ; in facial paralysis, 528 ; in infantile cerebral 
paralysis, 705 ; of the facial muscles in progressive 
paralysis, 721. 

Asthenopia, neurasthenic, 768. 

Asthma, bronchial, 154 ; cardiac, 156, 276 ; crystals, 
155 ; humid, 140 ; Millar's, 129 ; nervous, 154 ; origin 
of, 156 ; symptomatic, 156 ; thymic, 129 ; uraemic, 
808. 

Ataxia, 510 ; cerebellar, 684'; drunkard's, 551 ; heredi- 
tary, 612 ; in diphtheria, 66 ; in locomotor ataxia, 
600 ; in myelitis, 586 ; in progressive general pa- 
ralysis, 723 ; in typhoid fever, 15 ; locomotor, 596. 
See also Locomotor Ataxia. 

Atelectasis, pulmonary, 167. 

Atheroma of the arteries, 268, 308. 

Atheroma of the veins, 308. 

Athetosis, 745 ; congenital, 747 ; idiopathic, 747 ; in 
cerebral paralysis of children, 705, 746 ; movements 
of, 509 ; nature of, 747 ; symptomatic, 746. 

Athrepsia, 388. 

Atresia ani, 404. 

Atrophy, 388 ; juvenile muscular, 621 ; of the cardiac 
muscle in pericarditis, 304 ; unilateral, of the face, 
559. 

Atropine in asthma, 158 ; in epilepsy, 737 ; in exoph- 
thalmic goitre, 563 ; in progressive bulbar paraly- 
sis, 651 ; in pulmonary tuberculosis, 218 ; in neu- 
ralgia, 490 ; poisoning from, 950. 



Bacilli of Asiatic cholera, 73 ; of malaria, 81, 82 ; of 
malignant pustule, 106 ; of tuberculosis, 192 ; of 
typhoid fever, 1. 

Bacteria in diphtheria, 62 ; in septicopyeemia, 99 ; in 
urinary casts, 776. 

Balsams in chronic bronchitis, 141 ; in pulmonary 
emphysema, 166. 

Bandage for compression in chronic hydrocephalus, 
727 ; for extension in pressure paralysis of the 
spinal cord, 581 ; for the legs in locomotor ataxia, 
612 ; in anaesthesia of the trigeminus, 484 ; in neu- 
ralgia of the joints, 499. 

Banting treatment of obesity, 941. 

Baraesthesiometer, 477. 

Basedow's disease. See Exophthalmic GoItre, 560. 
Basilar meningitis, 663. 

Baths in acute ascending spinal paralysis, 638 ; in 
acute poliomyelitis, 633 ; in anaesthesia of the 
trigeminus, 484 ; in bronchitis, 137 ; in cerebral 
haemorrhage, 697 ; in cerebral hyperaemia, 671 ; in 
cholera morbus, 386 ; in chorea, 742 ; in chronic 
spinal leptomeningitis, 566 ; in cutaneous anaesthe- 
sia, 484 ; in cystitis, 843 ; in diabetes, 924, 925 ; in 
diphtheria, 69 ; in erysipelas, 61 ; in gout, 935 ; in 
habitual headache, 500 ; in hysteria, 765 ; in multi- 
ple sclerosis, 596 ; in myelitis, 591 ; in nephritis, 795, 
796 ; in nephrolithiasis, 835 ; in neuralgia, 490 ; in 
neurasthenia, 770 ; in neuritis, 550 ; in obesity, 942 ; 
in osteomalacia, 873 ; in paralysis agitans, 745 ; in 
paralysis of the upper limbs, 535 ; in pachymenin- 
gitis cervicalis hypertrophica, 568 ; in pneumonia, 
190 ; in progressive bulbar paralysis, 651 ; in pro- 
gressive paralysis of the insane, 725 ; in pyelitis, 832 ; 
in purulent meningitis, 662 ; in rachitis, 870 ; in rail- 
way spine, 574 ; in rheumatism (acute articular), 
858 ; in rheumatism (muscular), 865 ; in small-pox, 
56 ; in spasm of the respiratory muscles, 544 ; in 
tetanus, 752 ; in tetany, 749 ; in typhoid fever, 20, 21. 

Baths, electric, in neurasthenia, 770. 

Belladonna in bronchial asthma, 158 ; in diabetes, 
924 ; in epilepsy, 737 ; in whooping-cough, 150 ; 
poisoning from, 950. 

Bell's palsy, 525. 

Benzine in trichinosis, 112 ; in whooping-cough, 150. 
Biermer's change of note in pneumothorax, 252. 
Bile in intestinal catarrh, 380, 381 ; in typhoid fever, 
11. 

Bile-ducts, cancer of the, 463. 

Biliary abscess, 444, 446 ; acids in the blood, 437 ; 

acids in the urine, 438. 
Bismuth, subnitrate of, in gastric catarrh, 357 ; in 

intestinal catarrh of children, 390. 
Bitters in gastric catarrh, 356, 357 ; in scurvy, 905 ; in 

valvular cardiac disease, 286. 
Black vomit, 92. 

Bladder, cancer of, 844 ; catarrh of, 840 ; diphtheria 
of, 841 ; "haemorrhoids" of, 401 ; paralysis of, in 
injuries to spinal cord, 572 ; paralysis of, in loco- 
motor ataxia, 607 ; paralysis of, in myelitis, 587 ; 
paralysis of, in pressure paralysis of the spinal 
cord, 579 ; paralysis of, in progressive paralysis, 
723 ; paralysis of, in spinal apoplexy, 570. 

Bleeding. See Hemorrhage. 

Bleeding for cerebral haemorrhage, 696. 

Bleeding (local) for cystitis, 843 ; for cerebral abscess, 
704 ; for cerebral haemorrhage, 697 ; for cerebral 
hyperaemia., 671 ; for haematoma of the dura mater, 



INDEX. 



957 



659 ; for haemorrhage into the spinal meninges, 
568 ; for infantile spinal paralysis, 632 ; for menin- 
geal haemorrhage, 568 ; for meningitis, 662 ; for 
pericarditis, 305 ; for peritonitis, 427 : for pneu- 
monia, 190 ; for sciatica, 496 ; for typhlitis, 394. 

Blepharitis ciliaris, 944. 

Blepharospasm, 540. 

Blindness from anaemia, 877 (amaurosis, anaemic) ; 

from tumors of the brain, 711. 
Blisters for neuralgia, 488, 489 ; for sciatica, 496. 
Blood-casts, 776. 
Blood, changes in the, 874. 

Blood, character of, in anaemia, 874 ; in cancer of the 
stomach, 366 ; in chlorosis, 881 ; in cholera, 78 ; in 
diabetes, 919 ; in gout, 933 ; in haemoglobinuria, 899; 
in haemophilia, 908 ; in leukaemia, 893 ; in perni- 
cious anaemia, 888 ; in pseudo-leukaemia, 897. 

Blood, poverty of the, 874. 

Blood-test, Heller's, 777. 

Blood, transfusion of, in leukaemia, 896 ; in pernicious 
anaemia, 890 ; in poisoning from carbonic-oxide 
gas, 949 ; in poisoning from nitrobenzine, 949. 

Bones, growth of, in infantile spinal paralysis, 631 ; 
in rachitis, 868. 

Bones, lesions of, in scrofula, 944 ; marrow of, in 
leukaemia, 891, 892, 892 ; in osteomalacia, 871 ; in 
pernicious anaemia, 886 ; in pseudo-leukaemia, 896, 
897 ; pain in, in leukaemia, 893 ; in pernicious anae- 
mia, 887, 888 ; softening of, in osteomalacia, 871 ; 
in rachitis, 867. 

Borborygmi in intestinal catarrh, 379. 

Borosalicylic solution in diphtheria, 67. 

Bothriocephalus latus, 413. 

Botulismus, 951. 

Brachial spasm, 542. 

Brachial paralysis, 532 ; in acute ascending spinal 
paralysis, 636 ; combined, 534 ; peripheral, progno- 
sis and treatment of, 535. 

Brain, abscess of, 701 ; diagnosis of, 703 ; distin- 
guished from tumor of, 713 ; encapsulated, 702 ; 
focal symptoms, 703 ; idiopathic, 701 ; metastatic, 
701 ; traumatic, 701 ; treatment of, 703. 

Brain, anaemia of, 670 ; aetiology of, 670 ; symptoms 
of, 670 • treatment of. 670. 

Brain and cord, multiple sclerosis of, 592, 704. See 
also Multiple Sclerosis. 

Brain, atrophy of, in progressive general paralysis, 
724. 

Brain, cancer of, 709. 

Brain, diffuse sclerosis of, 704. 

Brain, diseases of, 657, 669 ; remarks in regard to 
topical diagnosis of, 671. 

Brain, glioma of, 708 ; haemorrhages into, 709 ; situa- 
tion of, 709. 

Brain, hyperaemia of, 669, 670 ; symptoms of, 671 ; 
treatment of, 671. 

Brain, in cerebro-spinal meningitis, 94, 95. 

Brain, localization of diseases in, 671. 

Brain, oedema of, in uraemia, 780. 

Brain psammoma of, 709 ; sarcoma of, 709. 

Brain, softening of, 698 ; aetiology of,. 698 ; diagnosis 
of, 700 ; idiopathic, 704 ; in tumor of, 711. 

Brain, syphiloma of, 709, 716 ; situation of, 716. 

Brain, syphilis of, 715 ; apoplectic symptoms in, 717 ; 
diagnosis of, 717 ; disease of arteries in, 717 ; heredi- 
tary, 715 ; new growths in, 716 ; symptoms of, 716 ; 
varieties in course of, 716, 717. 



Brain, tumors of, 708 ; at base, 712 ; cerebral com- 
pression caused by, 710 ; diagnosis of, 713 ; in the 
cerebellum, 713 ; in the cerebral hemispheres, 711 ; 
in the cortex, 712 ; involving nerves at base, 712 ; 
originating in the meninges, 712 ; symptoms of, 
709 ; treatment of, 714 ; varieties of, 708. 

Breakbone fever, 89. 

Breathing. See Respiration. 

Bright's disease, 771 ; acute, 784 ; second stage of, 
797 ; third stage of, 804. 

Bromide of ammonium in epilepsy, 736. 

Bromide of potash in abscess of the brain, 703 ; in 
athetosis, 747 ; in bronchial asthma, 158 ; in chorea, 
742 ; in diabetes, 924 ; in epilepsy, 736 ; in epilepti- 
form attacks following cerebral paralysis of chil- 
dren, 705 ; in habitual headache, 500 ; in hysteria, 
765 ; in locomotor ataxia, 612 ; in neuralgia, 489 ; 
in neurasthenia, 770 ; in paralysis agitans, 745 ; in 
spasm of the face, 540 ; in spasm of the glottis, 
130 ; in spasm of the muscles of the neck, 542 ; in 
spasm of the muscles of mastication, 539 ; in teta- 
nus, 752 ; in tetany, 749 ; in whooping-cough, 150. 

Bromide of sodium in epilepsy, 736. 

Bromine, poisoning from, 947. 

Bronchi, casts of the, 176, 179 ; dilatation of, 150 ; 

stenosis, 152, 153. 
Bronchial blenorrhcea, 139. 
Bronchial catarrh. See Bronchitis. 
Bronchiectasis, 150. 
Bronchiolitis, exudative, 157. 

Bronchitis, acute, 133 ; after whooping-cough, 149 ; 
asthmatic, 157 ; capillary, 136 ; chronic, 138 ; croup- 
ous, 145 ; fibrinous, 145 ; foetid, 142 ; haemorrhagic, 
135 ; in children, 136 ; in erysipelas, 60 ; in gout, 
931 ; in malaria, 84 : in measles, 46 ; in rachitis, 
869 ; in small-pox, 52 ; in typhoid fever, 11 ; in val- 
vular cardiac disease, 276 ; pseudo-membranous, 
145 ; putrid, 142 ; secondary, 134 ; symptomatic 
croupous, 145 ; tubercular, 197. 

Bronchophony, 180. 

Broncho-pneumonia, 170. 

Bronchorrhoea, serous, 139. 

Bronzed skin, 826. 

Brown-Sequard's spinal paralysis, 643. 
Bruit. See Murmur. 

Bruit de diable in anaemia, 879 ; in chlorosis, 880 ; in 

pernicious anaemia, 888. 
Bulbar. See also Medulla. 
Bulbar myelitis, acute, 655. 

Bulbar paralysis, acute, 655 ; inflammatory, 655 ; 
treatment of, 656 ; progressive, 646 ; progressive, 
aetiology of, 646 ; progressive, complications of, 
620, 649, 650; progressive extension of, to the nerves, 
651 ; progressive treatment of, 650. 

Bulbar symptoms in acute ascending spinal paralysis, 
636; in amyotrophic lateral sclerosis, 615. 650; in 
compression of the medulla, 656 ; in embolism and 
thrombosis of the basilar artery, 654 ; in progres- 
sive general paralysis, 723 ; in tubercular meningi- 
tis, 665. 

" Bulbar pulse, 1 1 272. 

Butyl chloral in neuralgia of the trigeminus, 492. 

Cachexie pachydermique, 555. 

Caecum, cancer of, 399 ; inflammation of, 391. 

Caffeine in hemicrania, 558. 

Caisson disease, 574. 



958 



INDEX. 



Calabar-bean in tetanus, 752. 

Calcaneus in paralysis of the tibial nerve, 537. 

Calculus, renal, 832. 

Calm stage in yellow fever, 91. 

Calomel in cholera morbus, 386 ; in intestinal catarrh 
of children, 390 ; in purulent meningitis, 663 ; in 
relapsing fever, 34 ; in tubercular meningitis, 667 ; 
in typhoid fever, 19. 

Camphor in articular rheumatism, 857 ; in scarlet 
fever, 42 ; in typhoid fever, 24. 

Cancer of the bile-ducts, 462 ; brain, 709 ; intestines, 
398; larynx, 131; liver, 462; lungs, 233; oesophagus, 
346 ; pancreas, 473 ; peritoneum, 434 ; pleura, 254 ; 
stomach, 364. 

Cancer, colloid, 365 ; fibroid, 365 ; medullary, 365. 

Cancer, metastatic, in cancer of the oesophagus, 347 ; 
in the bones, 366, 367 ; in the pleura, 254. 

Cancrum oris, 323. 

Cannabinum tannicum in neurasthenia, 770. 

Cannabis indica in diabetes, 924 ; in hemicrania, 558 ; 
in neurasthenia, 770. 

Cantata's dietary for diabetes, 922. 

Cantharides as a cause of cystitis, 840. 

Capsule, internal, lesions of, 681 ; involving facial 
nerve, 682 ; as a cause of cerebral hemianaesthesia, 
682, 685 ; as a cause of hemiplegia, 682, 685 ; as a 
cause of post-hemiplegic chorea, 682, 685. 

Caput Medusae, 451, 472. 

Caput obstipum, 541. 

" Carbolic mask,'" 144. 

Carbolic acid in articular rheumatism, 857 ; in dia- 
betes, 925 ; in erysipelas, 61 ; in scarlet fever, 42 ; 
in whooping-cough, 150 ; poisoning from, 950. 

Carbunculus contagiosus, 106. 

Carcinoma. See Cancer. 

Carcinosis, miliary, of the lungs, 233 ; of the perito- 
neum, 434. 
Cardiac. See also Heart. 
Cardiac failure, 264. 

Cardiac murmurs, anaemic, 879 ; in leukaemia, 894. 

Cardiac muscle, atrophy of, from pericarditis, 300 ; 
cloudy swelling of, 15, 278 ; fatty degeneration of, 
294 ; lesions of, 278. 

Cardiac neuroses, 296 ; overstrain, 291. 

Cardialgia in gastric ulcer, 360 ; in malaria, 86. 

Carlsbad salts in gastric ulcer, 363. 

Carotids, aneurism of, 316 ; compression of, in epi- 
leptic paroxysms, 737. 

Castoreum in hysteria, 765. 

Castration for hysteria, 766. 

Catalepsy, 754 ; hypnotic, 754 ; hysterical, 754, 763 ; 
in cerebral disease, 754 ; in connection with psy- 
choses, 754. 

Cataract in diabetes, 917. 

Catarrh, chronic bronchial, 138 : chronic laryngeal, 
119. 

Catarrh, dry bronchial, 135, 139 ; gastro-duodenal, 

435 ; of the bladder, 840. 
Catarrhe pituiteux, 139 ; sec, 139. 
Cats 1 purr, 265. 

Cathartics in anaemia and chlorosis, 883 ; in cerebral 
haemorrhage, 697 ; in cerebral hyperaemia, 671 ; 
in cirrhosis of the liver, 453 ; in dysentery, 72 ; in 
haematoma of the dura mater, 659 ; in haemophilia, 
910 ; in infantile convulsions, 738 ; in intestinal 
catarrh, 383 ; in locomotor ataxia, 612 ; in trichino- 
sis, 112. 



Catheterization in myelitis, 591. 

Caustic potash, poisoning from, 947 ; soda, poisoning 
from, 947. 

Cautery, actual, in acute ascending spinal paralysis, 
638 ; in neuralgia, 489 ; in pachymeningitis cervica- 
lis hypertrophica, 568 ; in pressure paralysis of the 
spinal cord, 581 ; in spasm of the muscles of the 
face, 540 ; in spasm of the muscles of the neck, 
542. 

Cavities and fissures in the spinal cord, 639. 

Centrum ovale, lesions of, as a cause of ataxic apha- 
sia, 681 ; as a cause of word deafness, 681 ; as a 
cause of hemiopia, 681 ; as a cause of hemiplegia, 
681 ; as a cause of monoplegia, 681. 

Cephalaea (see Headache, Habitual), 499. 

Cephalalgia (see Headache, Habitual), 499. 

Cerebral arteries, aneurism of, 686 ; syphilis of, 716 ; 
syphilis of, histology of, 716 ; syphilis of, as a cause 
of cerebral softening, 716 ; syphilis of, as a cause of 
apoplectiform attacks, 717. 

Cerebral embolism, 698 ; in gout, 932 ; repeated at- 
tacks caused by, 700. 

Cerebral haemorrhage, 686 ; aetiology of, 686 ; as a 
cause of cerebral hemiplegia, 691 ; diagnosis of, 
696 ; focal symptoms of, 690, 691 ; hereditary tend- 
ency to, 686 ; in arterio-sclerosis, 686 ; in gout, 686 ; 
in tumors of the brain, 713 ; in valvular cardiac 
disease, 281 ; symptoms of, 688 ; treatment of, 696 ; 
usual situation of, 687. 

Cerebral meninges, diseases of, 657. 

" Cerebral rheumatism,''' 852. 

Cerebral sinuses, thrombosis of the, 668. 

Cerebral symptoms in contracted kidney, 809, 810 ; 
in gout, 932 ; in nephritis, 802 ; in pneumonia, 183 ; 
in purpura haemorrhagica, 907 ; in pseudo-leukae- 
mia lymphatica, 897 ; in relapsing fever, 31 ; in 
scarlet fever, 35 ; in septico- pyaemia, 100. 

Cerebral tuberculosis, 709, 714 ; symptoms of, 714. 

Cerebro-spinal meningitis, epidemic, 93 (see also Men- 
ingitis) ; distinguished from tubercular meningi- 
tis, 97 ; encephalitic foci in, 94 ; sequelae of, 93 ; 
treatment of, 97 ; varieties of, 94. 

Cervical muscles, paralysis of, 530 ; in acute ascend- 
ing spinal paralysis. 636 ; resulting from stasis, 639. 

Cervical muscles, spasm of, 541 ; in hysteria, 759 ; 
prognosis of, 541 ; treatment of, 541, 542. 

Cervico-brachial neuralgia, 493. 

Cestodes, 411. 

Chalicosis pidmonum, 228. 

Champagne in yellow fever, 93. 

Charbon, 106. 

Charcot's crystals, 155. 

Cheek, gangrene of, 323. 

Cheese, poisoning from, 952. 

Chicken-pox, 57. 

Chloral in chorea, 742 ; in diabetes, 924 ; in intestinal 
catarrh of children, 390 ; in neuralgia, 490 ; in teta- 
nus, 752 ; in trigeminal neuralgia, 492. 

Chlorine gas, poisoning from, 947. 

Chloroform in epilepsy, 737 ; in hepatic colic, 445 ; in 
hysteria, 759 ; in infantile convulsions, 738 ; in renal 
colic, 835 ; in spasm of the diaphragm, 544. 

Chloroform, poisoning from, 949. 

Chloroform-test for bile, 438. 

Chlorosis, 874, 880 ; distinguished from gastric dis- 
eases, 882 ; from renal diseases, 882 ; from syphilis, 
882 ; front tuberculosis, 882. 



INDEX. 



959 



Chlorosis, Egyptian, 420. 

Chlorosis, relapses of, 881 ; treatment of, 882 ; with 

regard to sexual disturbances, 881. 
Choked disc. See Neuritis, Optic. 
Cholaemia, 439, 459. 
Cholelithiasis, 440. 

Cholera (Asiatic), 73 ; asphyxia in, 75 ; complications 
of, 77 ; contagiousness of, 74 ; dejections in, 75 ; 
diagnosis of, 79 ; distinguished from acute arsenical 
poisoning, 79 ; eruption in, 77 ; exciting causes of, 
74, 75 ; period of incubation in, 75 ; post-mortem 
appearances in, 77 ; predisposition to, 75 ; progno- 
sis of, 79 ; specific poison of, 73 ; treatment of, 79. 

Cholera morbus, 384 ; diagnosis of, 385 ; mortality in, 
385 ; treatment of, 386. 

Cholera sicca, 76. 

Choleraic diarrhoea, simple, 75 ; premonitory, 75. 

Choleraic nephritis, 77. 

Choleraic typhoid, 77 ; uraemic, 77. 

Cholerine, 75. 

Cholesterine, calculi formed of, 442. 

Cholesterine and pigment, calculi formed of, 442. 

Chorditis tuberosa, 120. 

Chorditis vocalis inferior hypertrophica, 120. 

Chorea, 739 ; aetiology of, 739 ; as related to chorea 
major, 739 ; as related to embolic processes, 741 ; 
complications of, 739, 740 ; diagnosis of, 741 ; gravi- 
darum, 739 ; in articular rheumatism, 739 ; nature 
and situation of the disease, 741 ; predisposition to, 
739 ; premonitory symptoms of, 739 ; prognosis and 
treatment of, 741 ; relapses in, 741 ; unilateral, 740. 

Choroid, tuberculosis of the, in meningitis, 667. 

Chyluria, 822, 823. 

Cicatricial induration caused by syphilis of the brain, 
716. 

Cicatrices of the larynx after syphilis, 132 ; of the 
oesophagus, 343 ; of the oesophagus from sulphuric 
acid, 946. 

Cinchona, decoction of, in purpura haemorrhagica, 

907 ; in scurvy, 905. 
Circumcision, dangerous in haemophilia, 908. 
Cirrhosis of the liver, 448. 
Cirrhosis, hypertrophic, of the liver, 453. 
11 Clap-threads " in cystitis, 842. 
Clavicles, deformed, in rachitis, 869. 
Clavus hystericus, 761. 
Claw-shaped hand, 534. 

Climate, change of, in asthma, 158 ; in pulmonary 

tuberculosis, 215. 
Clitoris, cauterization of, in hysteria, 766. 
Clownismus in hysteria, 762. 

Club-foot, resulting from infantile spinal paralysis, 
631. 

Coagulation-necrosis, 197. 

Coccyodynia, 497 ; in locomotor ataxia, 497, 607 ; 

operative removal of coccyx for, 497. 
Cod-liver oil in diabetes, 923 ; in osteomalacia, 873 ; 

in pulmonary tuberculosis, 215 ; in rachitis, 870 ; in 

scrofula, 944. 

Colchicum in articular rheumatism, 856 ; in gout, 936. 
Colic, hepatic, 440. 

Collapse in cholera morbus, 385 ; in hepatic colic, 442 ; 
in peritonitis, 425 ; in pneumonia, 182 ; in pneumo- 
thorax, 251 ; in typhoid fever, 7. 

Colloid cancer of the stomach, 365. 

Colon, cancer of the, 399. 

Colo-typhoid, 9. 



Columns, posterior, gray degeneration of, 596. 

Coma in acute yellow atrophy, 457 ; in cerebral 
haemorrhage, 689 ; in cerebral syphilis, 717 ; in 
thermic fever, 707 ; in thrombosis of the cerebral 
sinuses, 668 ; in typhus fever, 29 ; in uraemia, 782. 

Coma, diabetic, 917 ; causes of, 918 ; treatment of, 
925. 

Coma, post-epileptic, 732. 
Commotio spinalis, 572. 

Complexion in anaemia, 877, 880, 887 ; in diabetic 
coma, 918 ; in leukaemia, 894 ; in pseudo-leukaemia, 
897. 

Compression of the medulla oblongata, 656 ; diagnosis 

and prognosis of, 656. 
Compression of the oesophagus, 343. 
Compression as a cause of thrombosis, 471. 
Conchinine in malaria, 87. 
Concretio pericardii, 303. 

Conjugate deviation of the eyeballs in cerebral 
haemorrhage, 689. 

Conjunctivitis in difficult dentition, 327 ; in diphtheria, 
65 ; in gout, 931 ; in measles, 45 ; in scarlet fever, 
38 ; in scrofula, 944 ; in whooping-cough, 147. 

Conscience musculaire, 760. 

Constipation, habitual, 402 ; in diseases of the nervous 
system, 402 ; treatment of, 403. 

Constipation in anaemia and chlorosis, 878 ; in case of 
cerebral tumors, 711 ; in cirrhosis of the liver, 450 ; 
in gastric catarrh, 354 ; in intestinal stenosis, 407 ; 
in jaundice, 438 ; in locomotor ataxia, 607 ; in mye- 
litis, 588 ; in typhlitis, 392 ; in typhoid fever, 9. 

Consumption. See Tuberculosis. 

Consumption, galloping, 201. 

Contracted kidney, 804 ; embolic, 820 ; genuine, 804 ; 
in arterio-sclerosis, 805 ; in gout, 804 ; in obesity, 
940 ; secondary, 799, 804. 

Contractions, rhythmical, 509. 

Contracture des nourrices, 747. 

Convexity, meningitis of the, 659. 

Convulsions, cataleptic, 510. 

Convulsions, epileptiform, 509, 729, 735. 

Convulsions in acute yellow atrophy, 457 ; in cerebral 
embolism, 699 ; in cerebral haemorrhage, 690 ; in 
cerebral hydatids, 715 ; in cerebral syphilis, 717 ; in 
cerebral tumors, 710 ; in compression of the medul- 
la, 656 ; in diffuse sclerosis of the brain, 704 ; in 
focal lesions of the cortex, 675, 685 ; in haematoma 
of the dura mater, 658, 659 ; in hepatic colic, 442 ; 
in hydrophobia, 103 ; in hysteria, 758, 763, 765 ; in 
infantile cerebral paralysis, 705 ; in infantile spinal 
paralysis, 630 ; in meningitis, 95, 661, 665, 667 ; in 
multiple sclerosis, 594 ; in tape -worm, 415 ; in 
thermic fever, 707 ; in uraemia, 780, 792. 

Convulsions, infantile, 737. 

Co-ordination, impaired, in locomotor ataxia, 600, 601. 
Copaiba, balsam of, in cirrhosis of the liver, 453 ; in 

cystitis, 843. 
Copaiba, resin of, in cirrhosis of the liver, 453. 
Copper, paralysis due to, 538 ; poisoning from, 948 ; 

sulphate of, in chorea, 742. 
Coprostasis, 404. 
Cor adiposum, 294. 
Cor villosum, 300. 

Corpora quadrigemina, lesions of, 683 ; as a cause af 

ocular disturbances, 685. 
Corpulence, 936. \ 
Corset-liver, 469. 



960 



INDEX. 



Coryza, 113 ; fever caused by, 114. 

Cortical epilepsy, 675. 

Cough, spasmodic, 544 ; in hysteria, 758. 

Cows 1 milk as food for infants, 389. 

Cramps in the legs, 542 ; after severe physical exer- 
tion, 542 ; in hysteria, 543 ; liability to, 542. 

Craniometric anomalies in the epileptic, 734 ; in the 
rachitic, 868. 

Craniotabes in rachitis, 868. 

Cranium in osteomalacia, 872 ; in rachitis, 868. 

Creasote in gastric catarrh, 356 ; in intestinal ca- 
tarrh of children, 390 ; in tuberculosis of the lungs, 
214. 

Cremaster reflex, 512 ; in cerebral haemorrhage, 693. 
Crepitant rales in croupous pneumonia, 180. 
Crepitatio redux, 180. 
Croup, 61 ; ascending, 64. 
Crural, anterior, paralysis of, 536. 
Cry, cephalic, 666. 

Cundurango bark in cancer of the stomach, 368. 

Cups, dry, in acute ascending spinal paralysis, 638 ; 
in pressure paralysis of the spinal cord, 581. 

Curare in paralysis agitans, 745 ; in spasm of the 
facial muscles, 540 ; in tetanus, 752 ; in tetanie, 749. 

Cutaneous. See also Skin. 

Cutaneous abscesses in erysipelas, 60. 

Cutaneous anaesthesia, 480 ; bilateral, 481 ; cerebral, 
481 ; in diseases of the internal capsule, 682, 685 ; in 
hysteria, 481, 759 ; in laundresses, 481 ; in locomotor 
ataxia, 481 ; painful, 482 ; peripheral, 481 ; spinal, 
481 ; symptoms of, 482 ; treatment of, 483. 

Cutaneous ecchymoses in articular rheumatism, 851, 
852 ; in typhoid fever, 16. 

Cutaneous reflexes, 511 ; diminution or absence of, 
512 ; exaggeration of, 512 ; in cerebral haemorrhage, 
693 ; in epilepsy, 732 ; in infantile spinal paralysis, 
631, 632 ; in locomotor ataxia, 605 ; in myelitis, 586 ; 
in poliomyelitis of adults, 633, 634 ; in pressure pa- 
ralysis of the spinal cord, 579 ; in tetanus, 750 ; in 
the extremities, 511 ; sluggishness of, 512. 

Cutaneous sensibility, electro-, 478 ; in locomotor 
ataxia, 604 ; in tubercular meningitis, 665 ; varie- 
ties, and modes of testing, 475. 

Cyanosis in epileptic paroxysms, 731 ; in stenosis of 
the pulmonary orifice, 274. 

Cynanche contagiosa, 61 ; gangraenosa, 326. 

Cysts of the larynx, 131. 

Cysticercus cellulosae, 412 ; in the brain, 715. 

Cysticercus racemosus, 413. 

Cystine, calculi composed of, 832. 

Cystitis, 840 ; aetiology of, 840 ; chronic, 842 ; compli- 
cations of, 841, 842 ; in locomotor ataxia, 607 ; in 
myelitis, 591 ; in pressure paralysis of the spinal 
cord, 579 ; in spinal apoplexy, 570 ; symptoms of, 
841 ; treatment of, 843 ; varieties of, 841. 

Deafness in embolism and thrombosis of the basilar 
artery, 655 ; in epidemic cerebro-spinal meningitis, 
95 ; in epilepsy, 731 ; in hysteria, 760 ; in lesions of 
the centrum ovale, 681 ; in locomotor ataxia, 607 ; 
in Meniere's disease, 728 ; in scarlet fever, 38 ; in 
uraemia, 781. 

Debility, nervous, 767. 

Degeneration, fatty, in acute phosphorus poisoning, 
948 ; in acute yellow atrophy, 456 ; in anaemia, 879, 
885 ; in typhoid fever, 15 ; of the heart, 294 ; of the 
liver, 456. 



Degeneration, parenchymatous, in typhoid fever, 11, 
15 ; of the kidney, 785. 

Degeneration, sclerotic, of the heart, 287. 

Degeneration, reaction of, 518 ; anatomical changes 
in nerves and muscles in, 521 ; complete, 519, 520 ; 
in amyotrophic lateral sclerosis, 615 ; in infantile 
spinal paralysis, 631 ; in lead paralysis, 537 ; in 
myelitis, 588 ; in paralysis of the deltoid, 532 ; in 
paralysis of the facial, 528, 529 ; in poliomyelitis 
of adults, 634 ; in progressive bulbar paralysis, 
648 ; in progressive muscular atrophy, 620 ; in 
secondary neuritis, 548 ; partial, 521. 

Degeneration, physical signs of, in epileptics, 734. 

Deglutition, impairment of, in acute bulbar myeli- 
tis, 655 ; in acute bulbar paralysis, 655 ; in amy- 
otrophic lateral sclerosis. 615 ; in angina, 328 ; in 
chronic poliomyelitis, 635 ; in compression of the 
medulla, 656, 685 ; in dilatation of the oesophagus, 
341 ; in diphtheria, 63, 66 ; in laryngeal catarrh, 
118 ; in pericarditis, 302 ; in progressive bulbar 
paralysis, 647 ; in progressive muscular atrophy, 
620 ; in pseudo-leukaemia lymphatica, 897 ; in tho- 
racic aneurism, 313, 314 ; in trichinosis, 111. 

Deglutition, paralysis of, in bulbar haemorrhage, 653 ; 
in embolism and thrombosis of the basilar artery, 
655 ; in hysteria, 759 ; in progressive general pa- 
ralysis, 723. 

Delirium in acute yellow atrophy, 456 ; in cerebral 
haemorrhage, 689 ; in dengue, 90 ; in diabetes, 917 ; 
in hysteria, 762 ; in meningitis, 95, 661, 664 ; in pneu- 
monia, 183 ; in pylephlebitis suppurativa, 471 ; in 
typhoid fever, 5, 13 ; in typhus fever, 28. 

Delirium tremens, 949 ; in croupous pneumonia, 186. 

Delivery paralyses, 534. 

Deltoid, paralysis of, 532. 

Dementia from epilepsy, 734. 

Dementia paralytica, 719. 

Dengue, 89. 

Dentitio difficilis, 326. 

" Desiccation " in the treatment of obesity, 942. 
Diabetes inositus, 927. 

Diabetes insipidus, 926 ; related to diabetes mellitus, 
926, 927 ; related to polyuria, 926. 

Diabetes mellitus, 910 ; "accidental," 911 ; complica- 
tions of, 911, 912, 920 ; decipiens, 912, 920 ; diagnosis 
of, 921 ; intermittent, 920 ; related to glycosuria, 
910. 

Diaphoresis for bronchitis, 137 ; for nephritis, 795. 

Diaphragm, paralysis of the, 535 ; in acute bulbar 
paralysis, 655 ; modifying the movements of res- 
piration, 535 ; treatment of, 536. 

Diaphragm, spasm of the, clonic, 543 ; in hysteria, 
758 ; tonic, 543. 

Diarrhoea in cholera Asiatica, 75 ; in cholera morbus, 
385 ; in cirrhosis of the liver, 450 ; in dysentery, 70 ; 
in exophthalmic goitre. 562 ; in gastric catarrh, 350 : 
in intestinal catarrh, 378 ; in locomotor ataxia, 607 ; 
in noma, 324 ; in pneumonia, 182 ; in pulmonary 
gangrene, 226 ; in pulmonary tuberculosis, 210 ; in 
pylephlebitis, 471, 472 ; in rachitis, 869 ; in septico- 
pyaemia, 100 ; in typhoid fever, 9 ; in uraemia, 781 ; 
in whooping-cough, 149. 

Diathesis, gouty, 936. 

Diathesis, haemorrhagic, in acute articular rheuma- 
tism, 851 ; in anaemia, 879 ; in jaundice, 437 ; in 
scurvy, 903. 

"Digitalis eaters," 284. 



INDEX. 



961 



Digitalis in pericarditis, 305 ; in pleurisy, 246 ; in pul- 
monary emphysema, 166 ; in nephritis, 796 ; in 
typhoid fever, 24 ; in valvular cardiac disease, 283 ; 
poisoning from, 950. 

Dicrotism of the pulse in typhoid fever, 15. 

Dilatation, bronchial, 150. 

Dilatation of the stomach, 369. 

Diphtheria, 61 ; diagnosis of, 66 ; gangrenous, 65 ; in 
measles, 46 ; prognosis of, 67 ; septic, 65 ; treat- 
ment of, 67. 

Diplopia, 523 ; in multiple sclerosis, 594. 

Disease, trichinatous, 109. 

Disinfection in infectious diseases, 25. 

Dislocation, paralysis of the upper arm following, 
534. 

Displacement, symptoms resulting from, of other or- 
gans, in pleurisy, 242 ; in pneumonia, 181 ; in pneu- 
mothorax, 251. 

Distoma haematobium, 822. 

Disuse, atrophy from, 583. 

Dittrich's plugs, 143. 

Diuretics in cirrhosis of the liver, 453 ; in pleurisy, 
246 ; in pulmonary emphysema, 166 ; in nephritis, 
796 ; in valvular cardiac disease, 284, 286. 

Diverticula of the oesophagus, 340. 

Dochmius duodenalis, 419. 

Double vision in paralysis of the ocular muscles, 523. 

Dorso-intercostal neuralgia, 494. 

Douche, cold, in cutaneous anaesthesia, 484 ; in dia- 
betes, 924 ; in hysteria, 765 ; in neuralgia of the 
joints, 499 ; in neurasthenia, 770 ; in scarlet fever, 
42 ; in spasm of the diaphragm, 543, 544. 

Drainage in relation to the occurrence of tonsillitis, 
328. 

Drinkers 1 , gin-, liver, 448. 

Drinking water as a cause of cholera, 74 ; of typhoid 

fever, 2. 
Dropsy. See also (Edema. 

Dropsy in amyloid disease of the kidney, 815 ; in re- 
nal diseases, 777, 790, 801 ; in scarlet fever, 39, 40 ; 
in typhoid fever, 15 ; in valvular cardiac disease, 
282. 

Dropsy, intermittent, of the joints, 555. 

Dropsy of the gall-bladder, 443 ; of the vermiform 

appendix, 393. 
Duodenum, cancer of the, 399 ; catarrh of the, 380, 

436 ; fistula of the, 444, 445 ; ulcer, perforating, of 

the, 395. 

Durande's remedy for biliary calculi, 445. 
Duroziez's double murmur, 270. 
Dust, diseases due to the inhalation of, 227 ; prophy- 
laxis of, 229. 
Dysarthria, 646, 680. 

Dysentery, 69 : catarrhal, 70 ; chronic, 71 ; diagnosis 
of, 71 ; diphtheritic, 70 ; gangrenous, 70 ; prognosis 
of, 71 ; secondary, 70 ; treatment of, 71. 

Dyspepsia, acute, 348 ; chronic, 350 ; nervous, 375 ; of 
children, 387. 

Dysphagia, convulsive, in tetanus, 750 ; lusoria, 343. 

Dyspnoea in anaemia, 878, 887 ; in anthrax, 108 ; in 
bronchitis, 139 ; in contracted kidney, 808 ; in dia- 
betes, 918 ; in oedema of the glottis, 123 ; in miliary 
tuberculosis, 220 ; in new growths of the lungs, 233 ; 
in new growths of the mediastinum, 255, 256 ; in 
paralysis of the muscles of the larynx, 127 ; in 
pleurisy, 239 ; in pneumonia, 177, 178 ; in pulmo- 
nary emphysema, 162 ; in pulmonary tuberculosis, 



204 ; in septico-pyaemia, 101 : in stenosis of the 
bronchi, 154 ; in stenosis of the trachea, 153*; in 
trichinosis. 111 ; in valvular cardiac disease, 276. 
Dyspnoea, uraemic, 782. 

Ear, symptoms in the, in anaemia, 878. 887 ; in cais- 
son disease, 574 ; in cerebral anaemia, 670 ; in com- 
pression of the medulla oblongata, 656 ; in facial 
paralysis, 527, 528 ; in haemorrhage into the medul- 
la oblongata, 652 : in hysteria, 760 ; in leukaemia, 
894 ; in Meniere's disease. 728 ; in meningitis, cere- 
brospinal, 95 ; in scarlet fever. 38 ; in scrofula, 944. 

Echinococcus, 464 ; diagnosis, 465 ; treatment, 466 ; 
granulosus, 464 ; hydatidosus, 464 ; multilocularis, 
464 ; of the kidney, 822. 

Eclampsia. See also Convulsions. 

Eclampsia gravidarum in acute nephritis, 793. 

Eclampsia infantum, 737 ; aetiology of, 738 ; asso- 
ciated with spasm of the glottis, 129 ; liability of 
rachitic children to, 738. 

Eclampsia, uraemic, 780, 792. 

Ectasis, alveolar, 159. 

Electricity in acute ascending spinal paralysis, 638 ; 
in acute bulbar paralysis, 654 ; in amyotrophic 
lateral sclerosis, 616 ; in anaesthesia of the trigemi- 
nus, 483 ; in anomalies of the sense of smell, 502 ; 
in anomalies of the sense of taste, 502 ; in articular 
neuroses, 499 ; in articular rheumatism, 856 ; in 
asthma, 158 ; in athetosis, 747 ; in cerebral abscess, 
703 ; in cerebral haemorrhage, 697 ; in cerebral 
syphilis, 718 ; in cervico-brachial neuralgia, 494 ; in 
chorea, 742 ; in chronic poliomyelitis, 635 ; in cu- 
taneous anaesthesia, 483, 484 ; in diabetes, 925 ; in 
dilatation of the stomach, 374 ; in epilepsy, 737 ; in 
exophthalmic goitre, 563 ; in facial paralysis, 529 ; 
in facial spasm, 540 ; in habitual constipation, 403 ; 
in habitual headache, 501 ; in hemicrania, 558 ; in 
hysteria, 765 ; in incontinence of urine, 845 ; in in- 
fantile cerebral paralysis, 705 ; in infantile spiral 
paralysis, 632 ; in intercostal neuralgia, 495 ; in 
lead paralysis, 538 ; in locomotor ataxia,. 611 ; in 
mastodynia, 495 ; in multiple sclerosis, 596 ; in 
muscular rheumatism, 865 ; in myelitis, 590 ; in 
nervous dyspepsia, 377 ; in neuralgia, 489 ; in neu- 
rasthenia, 769 ; in neuritis, 550 ; in occipital neu- 
ralgia, 493 ; in pachymeningitis cervicalis hyper- 
trophica, 568 ; in paralysis, 507 ; in paralysis agitans, 
745 ; in paralysis of the diaphragm, 536 ; in pa- 
ralysis of the motor branch of the trigeminus, 525 ; 
in paralysis of the ocular muscles. 525 ; in periphe- 
ral paralysis of the arm, 535 ; in pressure paralysis 
of the spinal cord, 581 ; in progressive muscular 
atrophy, 621 ; in progressive bulbar paralysis, 650 ; 
in progressive general paralysis, 725 ; in pseudo- 
muscular hypertrophy, 625 ; in railway spine, 574 : 
in sciatica, 496 ; in spasm of the diaphragm, 543. 
544 ; in spasm of the muscles of the neck, 541 ; in 
spasm of the muscles of the shoulder, 542 ; in spasm 
of the trigeminus, 539 ; in spastic spinal paralysis, 
628 ; in splenic leukaemia, 896 ; in tetany, 749 ; in 
unilateral progressive facial atrophy, 560 ; in writ- 
er's cramp, 545. 

Electricity used to test sensibility, 478. 

Electro-cutaneous sensibility, 478. 

Embolic processes in the lungs, 229. 

Embolism and thrombosis of the basilar artery, 654 ; 
a cause of softening of the medulla and pons, 654 ; 



61 



962 



INDEX. 



aetiology of, 654 ; symptoms of, 654 ; treatment of, 
655. 

Emetics in bronchitis, 138 ; in dysentery, 72 ; in in- 
fantile convulsions, 738 ; in pulmonary oedema, 170. 

Emphysema, 159 ; acute, 155 ; complementary, 161 ; 
connected with whooping-cough, 161 ; diagnosis of, 
165 ; essential, 161 ; followed by pulmonary tubercu- 
losis, 163 ; interlobular, 161 ; interstitial, 161 ; prog- 
nosis of, 165 ; treatment of, 166 ; vesicular, 161 ; 
vicarious, 154, 161, 243. 

Emotion, convulsive expressions of, in hysteria, 758. 

Empyema, 245 ; necessitatis, 238. 

Encephalitis, curable form of. 704 ; in children, 704 ; 
non-purulent, 704 ; purulent, 701. 

Encephalomalacia, 698. 

Encephalopathy, saturnine, 947. 

Enchondroma of the lungs, 233. 

Endarteritis chronica deformans, 308. 

Endocarditis, acute, 257 ; acute recurrent, 260 ; 
chronic, 261 ; diagnosis of, 260 ; diphtheritic, 258 ; 
foetal, 258 ; in articular rheumatism, 850 ; in chorea, 
257, 739, 740 ; in pneumonia, 182 ; in septic diseases, 
98, 100, 260 ; prognosis of, 261 ; rheumatoid, 259 ; 
ulcerative, 258 ; verrucosa, 257, 258. 

Endothelial carcinoma of the pleura, 255. 

Enema ta of cold water in jaundice, 440. 

"English disease," 865. 

Engouement, 175. 

Enteritis catarrhalis, 377 ; membranous, 382. 
Enuresis nocturna, 845. 
Eosinophilous blood-globules, 893. 
Epidemic of typhoid fever in Plymouth, Pennsyl- 
vania, 3. 

Epidermis, desquamation of, in scarlet fever, 38 ; in 
typhoid fever, 16. 

Epilepsy, 729 ; aetiology of, 729 ; diurnal, 733 ; in re- 
gard to cerebral ansemia, 735 ; in regard to sudden 
somnolence, 732 ; in regard to teething convulsions, 
733 ; nocturnal, 733 ; occurrence of various forms 
of, 730 ; reflex, 730 ; seat of the disease, 735 ; trau- 
matic, 730 ; treatment of, 736. 

Epileptic paroxysm, 730 ; aura preceding the, 730 ; 
convulsive stage of, 731 ; frequency of, 733 ; in 
progressive general paralysis, 723 ; rudimentary 
forms of, 732. 

Epileptoid confusion of intellect, 733 ; sweating, 733. 

Epistaxis, 116. 

Erethitic habitus, 943. 

Ergot (ergotine) in acute ascending spinal paralysis, 
638 ; in aneurism of the thoracic aorta, 315 ; in dia- 
betes insipidus, 928 ; in exophthalmic goitre, 563 ; 
in habitual headache, 501 ; in haemophilia, 910 ; in 
hemicrania, 558 ; in locomotor ataxia, 612 ; in mye- 
litis, 591 ; in neuralgia, 489 ; in paralysis agitans, 
745 ; in poliomyelitis of adults, 634 ; in progressive 
general paralysis, 725 ; in pulmonary tuberculosis, 
217 ; in purpura haemorrhagica, 907 ; in railway 
spine, 574 ; in spastic spinal paralysis, 629 ; in 
spinal apoplexy, 570 ; poisoning from, 950 ; psy- 
choses due to, 951. 

Ergotism, 951 ; gangrenous, 951. 

Erosion, ulcers due to, in laryngeal catarrh, 117, 120. 

Eructations in anaemia, 878, 888 ; in diabetes, 912 ; 
in intestinal obstruction, 407 ; in peritonitis, 425. 

Eruption, acute, in scarlet fever, 35 ; haemorrhagic, 
in small-pox, 53. 

Erysipelas, 57 ; bulbous, 59 ; contagiousness of, 58 ; 



diagnosis of, 60 ; gangrenous, 59 ; idiopathic, 58 ; 

inoculation of, 58 ; in small-pox, 52 ; migratory, 59 ; 

of the new-born, 58 ; prognosis of, 61 ; puerperal, 

58 ; pustulous, 59 ; traumatic, 58 ; treatment of, 61 ; 

vesicular, 59. 
Erythema exsudativum, 906. 
Erythromelalgia, 554. 
Etat de mal, 733. 

Eucalyptus, oil of, in splenic leukaemia, 895. 
Eustrongylus gigas, 823. 

Exophthalmic goitre, 560 ; aetiology of, 560 ; diagno- 
sis of, 563 ; examination of heart in, 561 ; " Graefe 
symptom 11 in, 561 ; nervous symptoms in, 561, 562 ; 
treatment of, 563. 

Exophthalmus in exophthalmic goitre, 561 ; in pa- 
ralysis of the motores oculi, 524. 

Expectorants in bronchitis, 138, 141 ; in pneumonia, 
174, 190 ; in pulmonary emphysema, 166 ; in pul- 
monary tuberculosis, 217. 

" Expectoration albumineuse " in pleurisy, 248. 

Expectoration in asthma, 155 ; in bronchiectasis, 152 ; 
in bronchitis, 135, 139, 143, 146 ; in laryngeal catarrh, 
120 ; in pleurisy, 239 ; in pneumonia, 172, 178, 179 ; 
in pulmonary cancer, 233 ; in pulmonary emphy- 
sema, 152 ; in pulmonary gangrene, 225 ; in pul- 
monary tuberculosis, 202. 

Eyes. See also Ocular and Ophthalmia. 

Eyes, conjugate deviation of, in cerebral haemor- 
rhage, 689. 

Eyes, disorders of, in acute bulbar paralysis, 655 ; in 
acute hydrocephalus, 665 ; in anaemia, 877, 887 ; in 
cerebral haemorrhage, 693 ; in cerebral tumor, 712 ; 
in chorea, 739 ; in chronic hydrocephalus, 727 ; in 
diabetes, 917 ; in hasmatoma of the dura mater, 
658 ; in hemicrania, 557 ; in hysteria, 760 ; in lesions 
of the central ganglia, 683 ; in lesions of the corpora 
quadrigemina and crura cerebri, 683 ; in lesions of 
the occipital cortex, 676 ; in leukaemia, 894 ; in loco- 
motor ataxia, 606 ; in measles, 44 ; in meningitis, 
661, 665 ; in miliary tuberculosis, 219, 222 ; in multi- 
ple sclerosis, 594 ; in progressive bulbar paralysis, 
648 ; in relapsing fever, 33 ; in septico-pyaemia, 100 ; 
in thrombosis of the cerebral sinuses, 668, 669 ; in 
trichinosis, 111. 

Face-ache, FothergilPs, 491. 

Facial atrophy, unilateral progressive, 559 ; paraly- 
sis, 525 ; aetiology of, 525 ; diagnosis of, 529 ; in 
acute bulbar paralysis, 655 ; in cerebral haemor- 
rhage, 691 ; in cerebral tumor, 712 ; in compression 
of the medulla oblongata, 656 ; in haemorrhage into 
the medulla oblongata, 653 ; in progressive bulbar 
paralysis, 647 ; mimetic, 525 ; treatment of, 529 ; 
varieties of, 527. 

Facial spasm, clonic, 539 ; in epilepsy, 731 ; in menin- 
gitis, 95 ; treatment of, 540 ; spasm, mimetic, 539 ; 
spasm, tonic, in tetanus, 750. 

Faecal vomiting, 407 ; concretions, 391, 392. 

Faeces in jaundice, 437. 

Fainting, 670 ; aetiology of, 670 ; in anaemia, 877 ; in 
cerebral haemorrhage, 689, 690 ; in cerebral tumor, 
710 ; in epilepsy, 732 ; in insolation, 706 ; in leukae- 
mia, 894 ; in pernicious anaemia, 887 ; liability to, 
670 ; symptoms of, 670 ; treatment of, 670. 

Falling sickness, 729. 

Famine fever, 27. 

Farcy, 104. 



INDEX. 



963 



Fascia, reflex, 513 ; in cerebral haemorrhage, 693. 
Fat, ingestion of, in diabetes, 923. 
Fat-drops in urinary casts, 776. 

Fatty acids, crystals of, in the sputum of foetid 

bronchitis, 143. 
Fatty granular globules in urinary casts, 776 ; heart, 

294 ; kidney, inflammatory, 799 ; liver, 468 ; liver in 

pulmonary tuberculosis, 211 ; liver in trichinosis, 

111. 
Febricula, 29. 

Febris continua, 6 ; erratica, 84 ; gastrica, 17 ; inter- 
mittens, 82 ; nervosa stupida, 13 ; nervosa versa- 
tilis, 13 ; quotidiana, 83 ; recurrens, 30. 

Feeding, artificial, in progressive bulbar paralysis, 
651 ; in stenosis of the oesophagus, 354 ; in trismus, 
539. 

Fever, anaemic, 361, 880 ; cerebro-spinal, 93 ; " cold,''' 
76 ; enteric, 1 ; gastric, 17 ; hectic, 208, 396 ; in 
acute ascending spinal paralysis, 636, 637 ; in an- 
gina, 329 ; in arthrogryposis, 543 ; in articular rheu- 
matism, 848 ; in bronchitis, 135, 136 ; in cardiac 
valvular disease, 281 ; in cerebral abscess, 702, 703 ; 
in cholera, 76 ; in cirrhosis of the liver, 451 ; in cys- 
titis, 842 ; in dengue, 89 ; in diabetes, 915 ; in diph- 
theria, 64 ; in dysentery, 71 ; in endocarditis, 259 ; 
in erysipelas, 59 ; in gastric catarrh, 349, 350 ; in 
glanders, 105 ; in gout, 930 ; in haeinoglobinaemia, 
899 ; in hepatitis, suppurative, 447 ; in infantile 
cerebral paralysis, 704 ; in infantile spinal paraly- 
sis, 630 ; in intestinal catarrh, 379 ; in measles, 44 ; 
in meningitis, 94, 96, 661, 665 ; in noma, 324 ; in os- 
teomalacia, 872 ; in parotitis, 325 ; in pericarditis, 
300, 301 ; in perinephritis, 818 ; in pleurisy, 239 ; in 
pneumonia, 172, 177, 183 ; in poliomyelitis of adults, 
633 ; in primary multiple neuritis, 549 ; in pulmon- 
ary emphysema, 165 ; in pulmonary gangrene, 226 ; 
in pulmonary tuberculosis, 208 ; in purpura hem- 
orrhagica, 907 ; in purpura rheumatica, 906 ; in 
pyelitis, 831 ; in pylephlebitis, suppurative, 471 ; in 
rachitis, 868 ; in relapsing fever, 31 ; in scarlet 
fever, 36 ; in septico-pyeemia, 100 ; in small-pox, 
51 ; in thermic fever, 707 ; in trichinosis, 111 ; in 
tuberculosis of the genito-urinary organs, 837 ; in 
typhlitis, 392 ; in typhoid fever, 5 ; in typhus fever, 
28 ; in yellow fever, 91. 

Fever, lung, 174 ; ship, 27 ; splenic, 106 ; spotted, 27, 
93 ; swamp, 81 ; typho-malarial, 88 ; yellow, 90. 

Fibroma of the larynx, 131. 

Filaria Bancrofti, 823 ; sanguinis, 823. 

Fish, poisoning from the ingestion of, 951. 

Flapping joints in infantile spinal paralysis, 831. 

Flatulence in jaundice, 438. 

Flexibility, waxy, 754. 

Follicular catarrh of the intestines, 378. 

Forced movements, 510 ; in disease of the crura cere- 
belli ad pontem, 684, 685 ; in paralysis agitans, 744. 

Forced positions, 510. 

Forearm, paralysis of, 532 ; paralysis of, in amyo- 
trophic lateral sclerosis, 614. 

Foreign bodies in the intestinal canal, 404. 

FothergilTs face-ache, 491. 

Fowler's solution. See Arsenic. 

Fowler's solution in chorea, 742 ; in endocarditis, 
261 ; in valvular cardiac disease, 283. 

Fractures in rachitis, 869. 

Friction-sounds in pericarditis, 301, 302 ; in pleurisy, 
240. - 



Frontal convolutions, lesions of the, 676 ; connected 
with the cortical motor centers, 676 ; connected 
with the centers of speech, 676. 680. 

Frontal sinuses, catarrh of the, 114. 

Fuchsine in nephritis, 794. 

Furunculosis in diabetes, 917, 921, 927 ; in scarlet 
fever, 38 ; in typhoid fever, 16 ; in typhus fever, 29. 
Foot-baths in asthma, 158. 

Gait in amyotrophic lateral sclerosis. 615 ; in locomo- 
tor ataxia, 601 ; in multiple sclerosis, 594 ; in osteo- 
malacia, 872 ; in rachitis, 869. 

Gall-stones, 440 ; diagnosis of, 444 ; prognosis of, 444 ; 
treatment of, 445. 

Gall-stones, impaction of, 443. 

Galvano-cautery in hypertrophic pharyngitis, 337. 

Galvano-puncture in aneurism of the thoracic aorta. 
315. 

Ganglia, central, of the brain, lesions of, 682 ; lesions 
of, causing hemiplegia, 682 ; lesions of, causing 
hemiopia, 683, 685 ; lesions of, causing post-hemi- 
plegic chorea, 683, 685. 

Gangrene, embolic, 224, 230, 280. 

Gangrene in diabetes, 917 ; in exophthalmic goitre, 
562 ; in small-pox, 52 ; in typhoid fever, 16 ; of the 
lungs, 223 ; senile, 310. 

Garrod's thread-test for uric acid, 934. 

Gastrectasis, 369. 

Gastric. See also Stomach. 

Gastric abscess, 357 ; cancer, 364. 

Gastric catarrh, acute, 348 ; absorption impeded by, 
352 ; chronic, 350 ; diagnosis of, 355 ; exciting 
causes of, 348, 350 ; gastric juice in, 351 ; liability 
to, 349 ; mucus secreted in, 351 ; peristalsis in, 351 ; 
treatment of, 350, 355. 

Gastric crises in locomotor ataxia, 607 ; haemorrhage. 
362, 374 ; haemorrhage in cancer, 365 ; haemorrhage 
in ulcer, 359, 360, 362 ; pain in case of ulcer, 359, 
360 ; ulcer, 358 ; ulcer, peptic, 358 ; ulcer, round, 
358 ; vertigo, 376. 

Gastritis, acute, 348 ; chronic, 350 ; phlegmonous, 
357. 

Gastro-intestinal symptoms in emphysema, 165. 
Gastromalacia, 358. 

Gelsemium, tincture of, in neuralgia, 489 ; in trigemi- 
nal neuralgia, 492. 

General paralysis, progressive, 719 ; aetiology of, 719 ; 
depressive form, 722 ; development of, 720 ; diag- 
nosis of, 725 ; hereditary predisposition to, 720 ; 
maniacal exaltation in, 722 ; symptoms of, 720 ; 
treatment of, 725. 

Genito-urinary organs, tuberculosis of, 836 ; diagno- 
sis of, 837 ; treatment of, 837. 

German measles, 48. 

Gin-drinker's liver, 448. 

Girdle-sensation in locomotor ataxia, 604. 

Glanders, 104 ; diagnosis of, 105 ; period of incuba- 
tion in, 105 ; treatment of, 106. 

Globus hystericus, 758. 

Glomeruli, abnormal permeability of the walls ofj 
773. 

Glomerulo-nephritis, 789 ; in scarlet fever, 40. 
Glossitis, acute parenchymatous, 322 ; treatment of., 
322. 

Glossitis dissecans, 323. 

Glossy fingers in cervico-brachial neuralgia, 494 ; in 
trophic disorders of the nerves, 555. 



964 



INDEX. 



Glossy skin in trophic disorders of the nerves, 555. 

Glottis, oedema of, 122 ; in nephritis, 802 ; in small- 
pox, 52 ; in scarlet fever, 37. 

Glottis, openers of, paralysis of, 127. 

Glottis, spasm of, 129 ; in hysteria, 758 ; in rachitis, 
129, 869 ; in tetanus, 750 ; treatment of, 129. 

Glotzaugenkrankheit, 560. 

Gluteal paralysis, 536 ; reflex, 512. ■ 

Glycerine in diabetes, 923 ; in trichinosis, 112. 

Glycosuria, 910 ; aetiology of, 910 ; in bulbar haemor- 
rhage, 633 ; in cerebral haemorrhage, 690 ; in teta- 
nus, 751. 

Goll, columns of, 480. 

Gout, 928 ; atypical, 931 ; chronic, 931 ; complications 
of, 932 ; diagnosis of, 933 ; geographical distribu- 
tion, 929 ; nature of, 932 ; symptoms of, 930 ; treat- 
ment of, 934 ; with regard to lead-poisoning, 929. 

Graphospasm, 544. 

Grande hysterie, 762 ; contortions in, 762 ; epilepti- 
form paroxysms in, 762 ; statuesque postures and 
" attitudes of passion " in, 762. 

Grandeur, delusions of, in progressive general paraly- 
sis, 722. 

Gravel, renal, 832. 

Graves's disease, 560. 

Green-sickness, 880. See also Chlorosis. 

Guarana in habitual headache, 501 ; in hemicrania, 
558 ; in intestinal catarrh of children, 390. 

Gummata in cerebral syphilis, 716 ; in hepatic sj~phi- 
lis, 460 ; in laryngeal syphilis, 132. 

Gums, affections of, in diabetes, 915, 916 ; in scurvy, 
904 ; in typhoid fever, 11. 

Gymnastics in articular rheumatism (chronic), 862 ; 
in diabetes, 924 ; in gout, 935 ; in infantile spinal 
paralysis, 632 ; in neurasthenia, 769 ; in progressive 
muscular atrophy, 621 ; in writer's cramp, 545. 

Habitus apoplectic, 686; emphysematous, 163; erethi- 
tic, 943 ; phthisical, 204. 

Haematemesis, hysterical, 761 ; in acute yellow atro- 
phy, 457 ; in gastric ulcer, 360. 

Haematidrosis, 556. 

Haematoidine, granules of, in urinary casts, 776. 

Hasmatoma of the dura mater, 657 ; apoplectic symp- 
toms in, 658 ; diagnosis of, 659 ; in chronic alcohol- 
ism, 658 ; in connection with the haemorrhagic 
diathesis, 658 ; in progressive general paralysis, 
658 ; origin of, 657 ; seat of, 657 ; treatment of, 659. 

Haematomyelia, 569. 

Haematorrhachis, 568. 

Haematothorax, 254. 

Haematuria, 777 ; in chyluria, 823 ; in tumor of the 

kidney, 821 ; tropical, 823. 
Haemine test, 365. 
Haemoglobinaemia, 898. 

Haemoglobineemia, aetiology of, 898 ; in connection 

with malaria, 900 ; in connection with syphilis, 900 ; 

in poisoning from mushrooms, 898 ; paroxysmal, 

899, 900 ; symptoms of, 899. 
Haemoglobine, granules of, in the urine, 899. 
Haemoglobinuria, 898; in poisoning from mushrooms, 

898. 

Haemopericardium, 307. 

Haemophilia, 907 ; aetiology of, 907 ; complications 
of, 909 ; connected with anaemia, 909 ; rudimentary 
forms of, 908 ; prognosis of, 909 ; treatment of, (a) 
prophylactic, 909 ; (b) surgical, 910. 



Haemoptysis in bronchial catarrh, 135 ; in pulmo- 
nary gangrene, 226 ; in pulmonary tuberculosis, 
202. 

Haemorrhage in acute yellow atrophy, 457 ; in anae- 
mia, 879, 885, 887 ; in cirrhosis of the liver, 450 ; in 
contracted kidney, 809, 810 ; in endocarditis, 260 ; 
in epileptic paroxysms, 732 ; in haemophilia, 908 ; 
in hysteria, 761 ; in leukaemia, 895 ; in malignant 
pustule, 108 ; in meningitis, epidemic cerebro- 
spinal, 94 ; in nephrolithiasis, 834 ; in pseudo-leu- 
kaemia, 897 ; in pyelitis, 830 ; in purpura haemor- 
rhagica, 907 ; in scarlet fever, 38 ; in scurvy, 903 ; 
in syphilis of the rectum, 397 ; in typhoid, 9 ; in 
yellow fever, 92. 

Haemorrhoids, 400 ; " attacks of," 400 ; bleeding from, 
400 ; treatment of, 401. 

Hair, loss of, in typhoid fever, 16 ; in unilateral facial 
atrophy, 559. 

Hallucinations in hysteria, 762, 763. 

Halo surrounding the pocks of small-pox, 50. 

Hay fever, 113. 

Headache, habitual, 499 ; in acute ascending spinal 
paralysis, 636 ; in anaemia, 878 ; in bronchitis, 135 ; 
in bulbar paralysis, acute, 655 ; in cerebral abscess, 
702 ; in cerebral anaemia, 670 ; in cerebral haemor- 
rhage, 689 ; in cerebral syphilis, 717 ; in cerebral 
tumors, 710 ; in chlorosis, 880 ; in compression of 
the medulla oblongata, 656 ; in diabetes, 912, 917 ; 
in diseases of the cerebellum, 684 ; in epilepsy, 732 ; 
in exophthalmic goitre, 562 ; in haematoma of the 
dura mater, 658; in hysteria, 761 ; in infantile spinal 
paralysis, 630 ; in leukaemia, 894 ; in meningitis, 
epidemic, 95 ; in meningitis, purulent, 661 ; in 
meningitis, tubercular, 664, 666 ; in nervous dys- 
pepsia, 376 ; in neurasthenia, 767 ; in paroxysmal 
haemoglobinuria, 899 ; in pernicious anaemia, 887 ; 
in pleurisy, 240 ; in pneumonia, 177 ; in poliomye- 
litis of adults, 633 ; in primary multiple neuritis, 
549 ; in railway spine, 573 ; in small-pox, 49 ; in 
tetanus, 749 ; in thrombosis of the cerebral sinuses, 
668 ; in typhoid fever, 4, 5 ; in writer's cramp, 545. 

Headache, nervous, 499. 

Head, deviation of, in cerebral haemorrhage, 689 ; 
rheumatism in, 864 ; sense of pressure in, in neu- 
rasthenia, 767 ; in progressive general paralysis, 
720. 

Head, tetanus of the, 750. 

Heart, aneurism of, 288 ; arhythmia of, in valvular 
disease, 277. 

Heart, dilatation of, 291 ; in chlorosis, 880 ; in ma- 
laria, 84. 

Heart, disorders of, in diabetes, 916 ; in obesity, 939 ; 
in pneumonia, 182 ; in scurvy, 904. 

Heart, fatty degeneration of, 294. 

Heart, hypertrophy of, 291 ; diagnosis of, 293 ; idio- 
pathic, 291 ; in arteriosclerosis, 309 ; in obesity, 
939 ; in renal disease, 783, 791, 801, 807 ; in scarlet 
fever, 40 ; treatment of, 294. 

Heart, indurated degeneration of, 287. 

Heart, infarctions in, 287. 

Heart, lesions of, compensated, 263 ; congenital, 274 ; 

lungs altered by disease of, 232. < 
Heart, over-exertion of, 291. 

Heart, palpitation of, diagnosis of the nervous form 
of, 297 ; in cardiac valvular disease, 276 ; in case of 
tape-worm, 415 ; in hysteria, 761 ; in neurasthenia, 
j 768 ; in obesitj r , 939 ; in pernicious anaemia, 887 ; in 



INDEX. 



965 



scurvy, 903 ; nervous, 297 ; treatment of the ner- 
vous form of, 298. 

Heart, rupture of, in cardiac aneurism, 288. 

Heart, valvular disease of, 261 ; complications of, 
276 ; multiple, 275 ; prognosis of, 281 ; treatment 
of, 282. 

Heart, weakened, 291. 

Heartburn in chronic gastric catarrh, 352. 

Hegar's funnel for rectal irrigation, 383. 

Heller's test for blood in the urine, 777. 

Helminthiasis, 411. 

Hemianaesthesia, 481 ; in cerebral haemorrhage, 693 ; 
in hysteria, 760, 766 ; in lesions of the internal cap- 
sule, 682, 685 ; in tumors of the cerebral hemi- 
spheres, 712. 

Hemianopia in cerebral haemorrhage, 693 ; in hemi- 
crania, 557 ; in lesions of the central ganglia, 683, 
685 ; in lesions of the corpora quadrigemina, 683, 
685 ; in lesions of the occipito-cortical region, 677, 
685 ; in tumors of the base of the brain, 712 ; in 
tumors of the cerebral hemispheres, 712. 

Hemiathetosis, post-hemiplegic, 746. 

Hemiatrophy, progressive facial, 559 ; loss of hair in, 
559 ; seat of, 559, 560 ; treatment of, 560. 

Hemichorea, post-hemiplegic, 695, 746 ; in infantile 
cerebral paralysis, 705 ; in lesions of the internal 
capsule, 682, 685 ; in lesions of the optic thalamus, 
683, 685. 

Hemicrania, 556 (see also Migraine) ; course of, 558 ; 
in diabetes, 917 ; ophthalmic, 557 ; paralytic, 557 ; 
spastic, 557 ; symptoms of, 557 ; treatment of, 
558. 

Hemiplegia, 505. 

Hemiplegia, crossed, 653 ; in cerebral haemorrhage, 
691, 693, 695 ; in cerebral syphilis, 717 ; in diffuse 
cerebral sclerosis, 704 ; in haematoma of the dura 
mater, 658 ; in hysteria, 759 ; in infantile cerebral 
paralysis, 705 ; in lesions of the central ganglia, 
682 ; in lesions of the crura cerebri, 683, 685 ; in 
lesions of the internal capsule and centrum ovale, 
681, 682 ; in lesions of the motor cortical region, 
673 ; in locomotor ataxia, 609 ; in multiple sclero- 
sis, 595 ; in progressive general paralysis, 723 ; in 
purulent meningitis, 661 ; in tumors of the cerebral 
hemispheres, 711. 

Hepatic. See also Liver. 

Hepatic abscess, 446 ; in dysentery, 71 ; in pylephle- 
bitis, suppurative, 471. 

Hepatic colic, 440 ; pulse, 270, 273. 

Hepatitis, chronic diffuse interstitial, 448 ; diffuse 
syphilitic, 460 ; suppurative, 446. 

Hepatization of the lungs, 176. 

Hernia, diaphragmatic, 405 ; duodeno-jejunal, 405 ; 
hitersigmoid, 405 ; of the omental bursa, 405 ; retro- 
peritoneal, 405 ; subcoccal, 405. 

Herpes in acute gastric catarrh, 350 ; in facial paraly- 
sis, 528 ; in intercostal neuralgia, 494 ; in locomo- 
tor ataxia, 608 ; in neuralgia, 487 ; in neuritis, 548 ; 
in pressure paralysis of the spinal cord, 579 ; in 
sciatica, 496 ; in trigeminal neuralgia, 491. 

Herpes labialis in angina, 329 ; in intestinal catarrh, 
379 ; in malaria, 84 ; in meningitis, epidemic cere- 
brospinal, 96 ; in pneumonia, 177 ; in relapsing 
fever, 31 ; in scarlet fever, 38 ; in typhoid fever, 16 ; 
in typhus fever, 28. 

Hiccough, 543 ; hysterical, 543, 758 ; in anaemia, 878 ; 
in cholera, 76 ; in dysentery, 71 ; in hepatitis, sup- 



purative, 447 ; in uraemia, 781 ; reflex, 543 ; treat- 
ment of , 544. 

Hoarseness in diphtheria, 64 ; in laryngeal catarrh, 

119 ; in laryngeal syphilis, 132 ; in trichinosis, 111. 
Hodgkin's disease, 896. 
Hydatid thrill, 465. 
Hydraemia, 774. 

Hydrocephaloid symptoms, 385. 

Hydrocephalus, acute, 663, 664 ; aetiology of, 663 ; 
chronic, 726 ; congenital, ?26 ; congenital, diagno- 
sis of, 727 ; course of, 726 ; effect of, upon shape of 
brain, 726 ; enlargement of head caused by, 726 ; 
following epidemic cerebro-spinal meningitis, 97 ; 
of adults, 727 ; skull in, different from the rachitic, 
727 ; symptoms of, 726 ; the fluid of, 726 ; treat- 
ment of, 727. 

Hydrochloric acid in anaemia and chlorosis, 883 ; in 

gastric catarrh, 350, 356 ; poisoning from, 946. 
Hydrocyanic acid, poisoning from, 949. 
Hydromyelus, 639. 
Hydronephrosis, 838. 
Hydropericardium, 306. 
Hydroperitoneum, 432. 

Hydrophobia, 102 ; diagnosis of, 104 ; hydrophobic 
stage, 103 ; maniacal stape of, 103 ; paralytic stage 
of, 103, 104 ; period of incubation in, 103 ; quiet 
form of, 102 ; raving form of, 102 ; treatment of, 
104. 

Hydrorrhachis, 640. 

Hydrothorax, 253 ; in scarlet fever, 40 ; in valvular 

cardiac disease, 279 ; treatment of, 254. 
Hyoscyamine in paralysis agitans, 745. 
Hyperacusis in facial paralysis, 527. 
Hyperaemia, 669. 

Hyperaesthesia, 475 ; in hysteria, 760 ; in myelitis, 
586 ; in neuralgia, 487 ; in neurasthenia, 767 ; in 
pulmonary tuberculosis, 209 ; in relapsing fever, 
31 ; in spinal meningitis, 565 : in typhoid fever, 15 ; 
in unilateral lesions of the spinal cord, 644 ; of smell* 
501 ; of taste, 502. 

Hyperidrosis, unilateral, 556. 

Hypertrophy, unilateral, 560. 

Hypnotic phenomena in hysteria, 763. 

Hypochondriasis in gastric catarrh, 354 ; in habitual 
constipation, 402 ; in nervous dyspepsia, 376. 

Hypoglossus, paralysis of, in cerebral tumor, 712. 

Hysteria, 755 ; aetiology of, 755 ; artificial production 
of spasms in, 758 ; complications of, 758, 760 ; course 
of, 763 ; development of, 756, 757 ; diagnosis of, 764 ; 
grand paroxysms of, 762 ; in connection with float- 
ing kidney, 825 ; liability to, 756 ; metallotherapeu- 
tics in, 766 ; produced by sexual influences, 75? ; 
symptoms of, 757 ; treatment of, 764 ; with regard 
to exophthalmic goitre, 562. 

Hysterical insanity in typhoid fever, 14. 

Hystero-epilepsy, 758. 

Ice in cerebral hemorrhage, 696 ; in spinal apoplexy, 
570 ; in spinal meningeal haemorrhage, 568 ; in in- 
fantile spinal paralysis, 632 ; in injuries of the spinal 
cord, 572 ; in meningitis, 97, 662, 667. 

Ichthyosis linguae et oris, 323. 

Icteric casts in the urine, 438. 

Icterus, catarrhal, 435. 

Ileocaecal region, gurgling in, in typhoid fever, 9; 

tumor, 392. 
Ileotyphus, 1. 



966 



INDEX. 



Ileus from intestinal obstruction, 407 ; in typhoid 
fever, 10 ; paralytic, 404. 

Illuminating-gas, poisoning from, 949. 

Imbecility in multiple sclerosis, 594. 

Inanition in nervous dyspepsia, 376. 

Incarceration, internal, of the intestines, 405 ; symp- 
toms of, in case of floating kidney, 825. 

Incontinence, nocturnal, of urine, 845. 

Indican, test for, 408. 

Induction of labor, artificial, in chorea gravidarum, 
742. 

Induration, brown, of the lungs, 232 ; rheumatic, of 
the muscles, 863. 

Infantile paralysis, cerebral, 704 ; acute, 704 ; course 
of, 705 ; pathology of, 705 ; treatment of, 705. 

Infantile paralysis, spinal, 629. See Spinal Paraly- 
sis op Children. 

Infarction, embolic, of the kidneys, 819 ; hemorrha- 
gic, of the lungs, 229. 

Influenza, 134. 

Inhalation-pneumonia, 171, 406. 

Inhalations in bronchitis, 141 ; in diphtheria, 67 ; in 
laryngitis, 119 ; in pharyngitis, 336 ; in pulmonary 
gangrene, 227 ; in pulmonary tuberculosis, 214 ; in 
whooping-cough, 149. « 

Injury, mechanical, due to chorea, 741 ; due to epi- 
lepsy, 732. 

Insects, the sting of, a cause of malignant pustule, 
107. 

Inspection of meat, governmental, to prevent trichi- 
nosis, 112. 
Insufficiency, valvular, 262. 

Insufflation of powders in chronic pharyngitis, 336. 
Intention tremor in multiple sclerosis, 593 ; in myeli- 
tis, 586. 
Intercostal neuralgia, 494. 
Intermeningeal apoplexy, 657. 

Intermittent fever, 82 ; masked, 86 ; pernicious, 84 ; 

tertian, 83. 
Intestinal calculi, 404. 

Intestinal catarrh, 377 ; acute, 381 ; chronic, 381 ; f ol- 
licular, 378 ; from the ingestion of poisons, 377 ; in 
rachitis, 869 ; of children, 387 ; treatment of, 382, 
388. 

Intestinal glands enlarged in leukaemia, 893]; in pseu- 
do-leukaemia, 897. 

Intestinal haemorrhage in pylethrombosis, 472 ; in ty- 
phoid fever, 9. 

Intestinal parasites, 411 ; polypi, 406. 

Intestinal symptoms in cholera, 75 ; in dysentery, 70 ; 
in erysipelas, 60 ; in gastric catarrh, 350, 354 ; in 
glanders, 105 ; in malignant pustule, 108 ; in mea- 
sles, 46 ; in pulmonary gangrene, 226 ; in pulmo- 
nary tuberculosis, 210 ; in purpura haemorrhagica, 
907 ; in typhoid fever, 8, 9. 

Intestine, cancer of, 398 ; diagnosis of, 398 ; treat- 
ment of, 399. 

Intestine, compression of, from without, 406 ; con- 
struction of, 405 ; incarceration of, 405 ; intussuscep- 
tion of, 405 ; invagination of, 405 ; obstruction of, 
404. 

Intestine, obstruction of, diagnosis of the cause, 409 ; 
perforation of, in typhoid fever, 10 ; twists of, 405. 

Intestine, large, catarrh of, 381 ; desquamative, 382. 

Inunction, mercurial, in acute ascending spinal pa- 
ralysis, 638 ; in acute bulbar paralysis, 656 ; in 
cerebral syphilis, 718 ; in haemoglobinuria, 901 ; in 



locomotor ataxia, 611 ; in myelitis, 590 ; in progres- 
sive general paralysis, 725 ; in spastic spinal pa- 
ralysis, 629 ; in tumors of the brain, 714 ; in tumors 
of the spinal cord, 639. 

Iodide of potassium in acute ascending spinal pa- 
ralysis, 638 ; in aneurism of the thoracic aorta, 
315 ; in asthma, 158 ; in bronchitis, 142, 146 ; in 
cerebral syphilis, 718 ; in cerebral tumors, 714 ; in 
chronic hydrocephalus, 727 ; in gout, 936 ; in ha- 
bitual headache, 500 ; in lead paralysis, 538 ; in lep- 
tomeningitis, spinal, 566 ; in locomotor ataxia, 611, 
612 ; in meningitis, cerebro-spinal, 98 ; in multiple 
sclerosis, 596 ; in myelitis, 590, 591 ; in neuralgia, 
490 ; in pachymeningitis cervicalis hypertrophica, 
568 ; in peritonitis, chronic, 431 ; in railway spine, 
574 ; in sciatica, 497 ; in spasm of the trigeminus, 
539 ; in spastic spinal paralysis, 629 ; in syphilitic 
paralysis of the motores oculi, 525 ; in tumor of the 
spinal cord, 639. 

Iodide of iron in peritonitis, chronic, 431 ; in pressure 
paralysis of the spinal cord, 581 ; in scrofula, 945. 

Iodine coryza, 113. 

Iodine, poisoning from, 947. 

Iodine, tincture of, externally, in articular rheuma- 
tism, chronic, 862 ; in chronic nasal catarrh, 116 ; 
in pharyngitis, chronic, 336 ; in pleurisy, 246 ; in 
pressure paralysis of the spinal cord, 581 ; in spinal 
leptomeningitis, 566. 

Iodine, tincture of, internally, in diabetes, 925 ; in 
scrofula, 945. 

Iodoform in diabetes, 925 ; in pleurisy, 246 ; in pseudo- 
leukaemia lymphatica, 898. 
Ipecacuanha in dysentery, 72. 

Iron baths in anaemia and chlorosis, 883 ; in infantile 
spinal paralysis, 633 ; in locomotor ataxia, 611 ; in 
railway spine, 574. 

Iron, chloride of, in purpura haemorrhagica, 907 ; re- 
action caused by, in diabetic urine, 914. 

Iron in anaemia and chlorosis, 882 ; in cardiac valvu- 
lar disease, 283 ; in exophthalmic goitre, 563 ; in 
habitual headache, 500 ; in hemicrania, 558 ; in 
nephritis, 803 ; in neurasthenia, 770 ; in osteoma- 
lacia, 873 ; in paralysis of the muscles of the larynx, 
129 ; in pernicious anaemia, 890 ; in pulmonary tu- 
berculosis, 217, 218 ; in rachitis, 870 ; in scurvy, 905 ; 
in scrofula, 945. 

Irradiation, 487. 

Irrigation in intestinal catarrh, 383 ; in the intestinal 

catarrh of children, 390. 
Ischuria in hysteria, 762. 

Jaundice, catarrhal, 435 ; chronic, 436 ; diagnosis of, 
439 ; haematogenous, 460 ; hepatogenous, 435 ; in 
acute phosphorus poisoning, 948 ; in acute yellow 
atrophy, 456, 457 ; in cancer of the liver, 463 ; in 
cancer of the pancreas, 474 ; in cirrhosis of the 
liver, 450, 454 ; in diabetes, 916 ; in gastric catarrh, 
&50 ; in gastro-duodenitis, 435 ; in haemoglobinuria, 
899 ; in hepatic colic, 443 ; in hepatitis, suppurative, 
447 ; in pneumonia, 187 ; in pylephlebitis, suppura- 
tive, 471 ; in syphilis of the liver, 461 ; in yellow 
fever, 91 ; of the new-born, 460 pernicious, 459 ; 
treatment of, 439. 

Jaw. See Maxilla. 

Joints, disorders of, in acute neuritis, 549 ; in cerebral 
haemorrhage, 695 ; in dengue, 89 ; in endocarditis, 
260 ; in erysipelas, 60 ; in gout, 930, 936 ; in haemo- 



INDEX. 



967 



philia, 909 ; in locomotor ataxia, 608 ; in meningitis, 
cerebro-spinal, 96 ; in pernicious anaemia, 888 ; in 
purpura haemorrhagica, 907 ; in scrofula, 944 ; in 
scurvy, 904 ; in septico-pyaemia, 101 ; in small-pox, 
53 ; in typhoid fever, 16 ; in valvular cardiac dis- 
ease, 281. 

Joints, neuroses of, 498. 

Joints, sensibility of, 479. 

Kidney, abscess of, 816 ; calculus of, 832 ; diseases of, 
771 ; disturbances of circulation in, 819 ; genuine 
contracted, 804 ; granular, 804 ; hydatids of, 822 ; 
in diabetes, 916 ; in diphtheria, 66 ; in gout, 931 ; in 
haemoglobinuria, 899 ; in leukaemia, 892 ; in obesity, 
940 ; in pneumonia, 182 ; in pseudo-leukaemia, 897 ; 
in pulmonary emphysema, 165 ; in pulmonary tu- 
berculosis, 211 ; in scarlet fever, 39 ; in septico-py- 
eemia, 101 ; large red, 798 ; large white, 799 ; mov- 
able, 824 ; new growths of, 820 ; parasites of, 822 ; 
pelvis of, dilatation of, 838 ; pelvis of, inflammation 
of, 829 ; sclerosis of, 804 ; secondary contracted, 
797. 

Knee-phenomenon, 513. See also Patella Reflex. 
Koumyss as a food in pulmonary tuberculosis, 215. 
Kousso for tape-worm, 416. 
Kyphosis in osteomalacia, 872 ; in rachitis, 869. 

Lactic acid in diabetes, 925 ; in nephrolithiasis, 836 ; 

in the bones in osteomalacia, 871 ; in the urine in 

osteomalacia, 872. 
Laennec's cirrhosis, 448. 
Lagophthalmus in facial paralysis, 526. 
Lancinating pains in locomotor ataxia, 604. 
Landry's paralysis, 635. 

Lardaceous liver, 468 ; in pulmonary tuberculosis, 
211. 

Lard, inunction of, in scarlet fever, 42. 

Laryngeal crises in locomotor ataxia, 607. 

Laryngitis, acute, 117 ; chronic, 119 ; hypoglottica 
acuta gravis, 118 ; hypoglottica chronica hyper- 
trophica, 120 ; in measles, 46. 

Laryngitis, phlegmonous, 121 ; treatment of, 122. 

Larynx, abscess of, 121 ; affected by typhoid fever, 
13 ; cancer of, 131 ; disturbances of sensibility in, 
130 ; examination of, 117 ; muscles of, paralysis of, 
125 ; in acute bulbar paralysis, 655 ; in progressive 
bulbar paralysis, 647 ; treatment of, 128 ; muscles 
of, spasm of, in hysteria, 758 ; new growths in, 130 ; 
treatment of, 132 ; polypi of, 131 ; stenosis of, 
chronic, 120 ; in diphtheria, 64 ; in laryngitis, acute, 
118 ; syphilis of, 132 ; tuberculosis of, 123 ; diag- 
nosis of, 124 ; treatment of, 125. 

Lateral sclerosis, amyotrophic, 613 ; diagnosis of, 
616 ; involving the medulla oblongata, 615 ; symp- 
toms and course of, 614 ; treatment of, 616. 

Laughter, spasmodic, 544 ; in hysteria, 758. . 

Lead colic, 947. 

Lead paralysis, 537 ; bilateral, 537 ; localization of, 
537 ; treatment of, 538. 

Lead poisoning, chronic, 947 ; chronic, related to con- 
tracted kidney, 804, 948 ; chronic, related to gout, 
929, 948. 

Leptomeningitis, cerebral purulent, 659 ; tubercular, 
663. 

Leptomeningitis, chronic spinal, 566 ; primary, 566 ; 
secondary, 566 ; symptoms of, 566 ; treatment of, 
566. 



Lesions, cerebral, topical diagnosis of, 671. 
Lethargy in hysteria, 763. 

Leukaemia, 890 ; aetiology of, 890 ; complications, 894 ; 
diagnosis of, 895 ; lymphatic, 892, 895 ; myelogenous, 
891 ; splenic, 891, 895 ; symptoms of, 892 ; treatment 
of, 895 ; with regard to anaemia, 894. 

Leukocythaemia, 890. 

Leukocytosis, 890. 

Lids, spasm of, 540. 

Lime in osteomalacia, 873 ; in poisoning from oxalic 

acid, 947 ; in rachitis, 870. 
Lingua geographica in glossitis, 323. 
Lips, atrophy of, in amyotrophic lateral sclerosis, 615; 

in progressive bulbar paralysis, 647. 
Lithium, carbonate of, in nephrolithiasis, 835. 
Lithium- water in gout, 935. 
Liver. See also Hepatic. 

Liver, anomalies in the shape and position of, 469 ; 
atrophy of, 467 ; atrophy of, acute yellow, 455 ; 
atrophy of, acute yellow, diagnosis of, 458 ; atrophy 
of, acute yellow, treatment of, 458. 

Liver, cancer of, 462 ; diagnosis of, 463 ; prognosis of, 
464 ; secondary to cancer of stomach, 463 ; treat- 
ment of, 464. 

Liver, cirrhosis of, 448 ; biliary, 453 ; diagnosis of, 
452, 455 ; hypertrophic, 453 ; prognosis of, 452 ; 
treatment of, 452, 455. 

Liver, disturbances of circulation in, 466 ; gin-drink- 
ers', 448 ; granulated, 449 ; hydatids of, 464 ; hyper- 
aemia of, 466, 467 ; hypertrophy of, 468 ; in gout, 
931 ; in haemoglobinuria, 899, 900 ; in jaundice, 439 ; 
in leukaemia, 892 ; in pseudo-leukaemia, 897 ; in pul- 
monary emphysema, 165 ; in pulmonary tuberculo- 
sis, 211 ; in rachitis, 869 ; in yellow fever, 91 ; tabu- 
lated, 449 ; syphilis of, 460. 

Lobelia, tincture of, in asthma, 159. 

Locality, testing the sense of, 476. 

Lock-jaw, 749. 

Locomotor ataxia, 596 ; ataxic stage of, 600 ; devel- 
opment of, 596 ; diagnosis and prognosis of, 609 ; 
Friedreich's form of, 612 ; hereditary predisposition 
to, 596 ; histology of, 597 ; in chronic ergotism, 597 ; 
initial stage of, 599 ; involving cranial nerves, 606 ; 
symptoms of, 599 ; terminal stage of, 600 ; treat- 
ment of, 610 ; with regard to progressive general 
paralysis, 609. 

Loins, pains in, in relapsing fever, 31 ; in small-pox, 
49 ; in typhus fever, 28. 

Lordosis in pseudo-muscular hypertrophy, 623. 

Lower extremities, in rachitis, 869 ; spasm of, 542 ; 
spasm of, in amyotrophic lateral sclerosis, 615 ; 
spasm of, in tetanus, 750. 

Lower jaw. See Maxilla. 

Lumbago, 864. 

Lungs, abscesses of, in septico-pyaamia, 101 ; aplasia 
of, 167 ; aplasia of, in kyphoscoliosis, 168 ; atelec- 
tasis of, 167 ; capillaries of, atrophy of. in emphy- 
sema, 161 ; cancer of, 233 ; compression of, 167, 241 ; 
consumption of, 191 ; contraction of, 151, 198, 201, 
206 ; disorders of, in diabetes, 920 ; disorders of, in 
leukaemia, 892 ; disorders of, in progressive bulbar 
paralysis, 648 ; disorders of, in tj^phoid fever, 12 ; 
echinococcus of, 234 ; embolic changes in, 229. 

Lungs, emphysema of, 159 ; caused by pertussis, 161 ; 
diagnosis of, 165 ; followed by pulmonary tubercu- 
losis, 165 ; prognosis of, 165 ; treatment of, 166. 

Lungs, gangrene of, 223 ; circumscribed, 224 ; devel- 



968 



INDEX. 



opment of, 223 ; diagnosis of, 226 ; diffuse, 224 ; in 
cancer of oesophagus, 347 ; liability to, in diabetes, 
224 ; prognosis of, 226 ; treatment of, 227. 

Lungs, haemorrhage from, 202 ; increased volume of, 
159 ; induration of, brown, 232 ; infarctions in, 
hemorrhagic, 229 ; infarctions in, hsemorrhagic, 
diagnosis and prognosis of, 231 ; infarctions in, 
hasmorrhagic, symptoms of, 231 ; infarctions in, 
hgemorrhagic, treatment of, 231 ; inflammation of, 
174 (see also Pneumonia) ; oedema of, 169 ; oedema 
of, inflammatory, 169 ; oedema of, influencing res- 
piration, 169 ; oedema of, treatment of, 170 ; pig- 
mentation of, 228 ; syphilis of, 235 ; tuberculosis of, 
J91 ; tumors of, 233 ; tumors of, causing symptoms 
of compression, 234 ; tumors of, prognosis of, 234 ; 
tumors of, treatment of, 234. 

Lymph, animal, for vaccination, 56. 

Lymph-glands, extirpation of, in pseudo-leukaemia, 
898 ; progressive multiple hypertrophy of, 896. 

Lymph-glands, swollen, in dengue. 90 ; in diphtheria, 
64 ; in erysipelas, 60; in leukaemia, 892, 893, 894, 895 ; 
in malignant pustule, 108 ; in pseudo-leukaemia, 896; 
in pulmonary cancer, 234 ; in pulmonary tubercu- 
losis, 211 ; in scarlet fever, 37 ; in scrofula, 943, 944; 
in typhoid fever, 10. 

Lympho-sarcoma, malignant, 896. 

Magnesia in gastric catarrh, 350 ; in sulphuric-acid 

poisoning, 946. 
Magnet, application of, in hysteria, 766. 
Main en griffe, 534. 

Malaria, 81 ; diagnosis of, 86 ; distribution of, 81 ; 
germs of, 82 ; liability to, 82 ; period of incubation 
of, 82 ; pigment-formation in, 85 ; treatment of, 86. 

Malarial cachexia, 85. 

Malarial fever, remittent and continuous, 85. 
Malarial neuralgia, 486, 488. 
Malarial poison, 81. 

Malignant pustule, 106, 108 ; in animals, 106 ; bacilli 
of, 106 ; diagnosis of, 109 ; prophylactic inoculation 
of, 109 ; spores of, 106 ; transmission to man, 107 ; 
treatment of, 109. 

Male fern, ethereal extract of, for tape-worm, 416. 

Mai perf orant du pied in locomotor ataxia, 608. 

Malum Cotunnii, 495. See Sciatica. 

Mamillary reflex, 512. 

Marasmus in diabetes, 915. 

Massage in articular neuralgia, 499 ; in articular 
rheumatism, 856, 862 ; in brachial paralysis, 535 ; 
after cerebral haemorrhage, 697 ; in facial paraly- 
sis, 529 ; in gout* 936 ; in hysteria, 765 ; in infantile 
paralysis (cerebral), 705 ; in infantile paralysis (spi- 
nal), 632 ; in muscular rheumatism, 865 ; in neural- 
gia, 490 ; in neurasthenia, 769, 770 ; in paralysis agi- 
tans, 745 ; in progressive muscular atrophy, 621 ; in 
pseudo-hypertrophic muscular paralysis, 625 ; in 
sciatica, 497 ; in scorbutic ecchymoses, 905 ; in 
writer's cramp, 545. 

Mastication, disturbances of, in progressive bulbar 
paralysis, 647, 648. 

Mastication, muscles of, paralysis of, 525 ; in general 
paralysis of the insane, 723 ; in tumors at the base 
of the brain, 712 ; spasm of, clonic, 539 ; conic, 538. 

Mastodynia, 495 ; treatment of, 495. 

Measles, 43 ; black, 45 ; catarrh in, 44 ; complications 
of, 45 ; contagiousness of, 43 ; diagnosis of, 47 ; 
diphtheria in, 46 ; inoculation of, 44 ; period of in- 



cubation in, 44 ; prognosis of, 47 ; prophylaxis of, 
47 ; relation of, to pulmonary tuberculosis, 46 ; re- 
lation of, to whooping-cough, 46 ; treatment of, 
47 ; typhoid, 46. 

Measles in pork, 412. See Taenia. 

Measles, German, 48. See Rotheln. 

Meat, compulsory inspection of, in trichinosis, 112 ; 
poisoning from, 951. 

Meckel's diverticulum in obstruction of the intestine, 
405. 

Median paralysis, 534 ; disturbances of the functions 
of the forearm and hand in, 534 ; traumatic, 534. 

Mediastinal tumors, 255 ; diagnosis of, 256 ; prognosis 
of, 256 ; treatment of, 256. 

Mediastino-pericarditis, 302. 

Medulla oblongata, acute apoplectiform paralysis of, 
652 ; compression of, 656 ; diseases of, 646 ; progres- 
sive paralysis of, 646. 

Medulla oblongata and pons, haemorrhages into, 652 ; 
apoplexy from, 652 ; cysts and scars from, 652 ; 
seat and extent of, 652 ; treatment of, 654, 

Melaena neonatorum, 374. 

Melanaemia in malaria, 85. 

Mellituria, 910. See Glycosuria. 

Memory, weakness of, in exophthalmic goitre, 562. 

Meniere's disease, 723 ; implication of the semi- 
circular canals in, 723 ; in locomotor ataxia, 607 ; 
treatment of, 728. 

Meningeal apoplexy, 568. 

Meningeal haemorrhage, 568. 

Meningeal tumors, 638 ; different forms of, 638 ; prog- 
nosis and treatment of, 639 ; symptoms of, 639. 
Meningitis, basilar, 663. 
Meningitis of the convexity, 659. 

Meningitis, epidemic cerebro-spinal, 93, 659, 662 (see 
also Cerebro-spinal Meningitis) ; diagnosis of. 
97 ; in pneumonia, 97 ; prognosis of, 97 ; secondary, 
97, 659 ; sequelae of, 96 ; siderans, 94 ; treatment of, 
97. 

Meningitis, purulent, 659 ; aetiological factors in, 659 ; 
complications of, 660 ; diagnosis of, 662 ; localiza- 
tion of the morbid process in, 660 ; metastatic, 660 : 
primary, 659 ; symptoms of, 661 ; treatment of, 662. 

Meningitis, tubercular, 663 ; causes of, 663 ; duration 
of, 666 ; haemorrhages into the pia mater in, 664 ; 
hydrocephalic effusion into the ventricles in, 664 ; 
implication of the spinal cord in, 664 ; inflammatory 
changes in, 664 ; seat of miliary tubercles in, 664 ; 
symptoms of, 664. 

Meningitis, tubercular, in children, 666 ; diagnosis of, 
667 ; loud outcry of child in, 666 ; treatment of, 667. 

Meningocele, 640. 

Menstruation in chlorosis, 881 ; influence of, on epi- 
lepsy, 733 ; vicarious, 116. 

Mental disturbances in acute general miliary tuber- 
culosis, 222 ; in anaemia, 877 ; in articular rheuma- 
tism, 853 ; in athetosis, 747 ; in bulbar haemorrhage, 
632 ; in cerebral abscess, 702 ; in cerebral anaemia, 
670 ; in cerebral embolism, 700 ; in cerebral haemor- 
rhage, 689, 690, 693 ; in cerebral hyperaemia, 671 ; 
in cerebral syphilis, 717 ; in cerebral tumor, 710 ; 
in cerebro-spinal meningitis, 95 ; in cholera, Asiatic. 
76 ; in cholera morbus, 385 ; in chorea, 739, 740 ; in 
convulsions, 510 ; in cutaneous anaesthesia, 482. 

Mental disturbances in diabetic coma, 917 ; in epi- 
lepsy, 729, 731, 732, 734, 736 ; in fainting attacks, 
670 ; in general paralysis of the insane, 720 ; in 



INDEX. 



969 



habitual constipation, 402 ; in haematoma of the 
dura mater, 658 ; in hydrocephalus, 727 ; in hys- 
teria, 757, 758 ; in infantile paralysis (cerebral), 705 ; 
(spinal), 030 ; in jaundice, 437 ; in meningitis, 661, 
664 ; in multiple sclerosis, 594, 595 ; in neuralgia 
487 ; in neurasthenia, 768 ; in peritonitis, 426 ; in 
poliomyelitis of adults, 633 ; in pseudo-hypertrophic 
muscular paralysis, 624 ; in pulmonary tuberculosis, 
209 ; in pylephlebitis, 471 ; in sinus thrombosis, 668 ; 
in spinal concussion, 573 ; in typhoid fever, 13, 14 ; 
in typhus fever, 29 ; in uraemia, 780 ; in valvular 
heart disease, 281 ; in writers' cramp, 545. 

Mercuriahsm, chronic, 948. 

Mercurial poisoning, 948. 

Metallic tinkling, 252, 253. 

Metalloscopy in hysteria, 760, 766. 

Meteorism in hysteria, 761 ; in intestinal obstruction, 
407 ; in intestinal tuberculosis, 396 ; in peritonitis, 
424 ; in pulmonary tuberculosis, 210 ; in typhlitis, 
392 ; in typhoid fever, 9. 

Micrococci in cystitis, 841 ; in endocarditis, 258 ; in 
erysipelas. 5?, 58 ; in pneumonia, 174 ; in septico- 
pyaemia, 93, 99. 

Migraine, 556 (see Hemicrania) ; duration of the at- 
tacks of, 558 ; in general paralysis of the insane, 
722 ; treatment of, 558. 

Milk-cure in anaemia, 882 ; in nephritis, 795 ; in pul- 
monary tuberculosis, 215 ; in pyelitis, 832. 

Miliary tuberculosis, acute general, 218 ; cerebral 
symptoms in, 220 ; causes of, 218 ; diagnosis of, 
222 ; intermittent form of, 220 ; prognosis of, 223 ; 
relation of, to tubercular meningitis, 220 ; symp- 
toms of, 219 ; treatment of, 223 ; typhoid form of, 
219. 

Milkers' cramp, 546. 

Millar's asthma, 129. See Glottis, Spasm of. 
Mineral acids in scurvy, 905. 

Mineral springs in anaemia and chlorosis, 883 ; in 
bronchitis, 141 ; in cholelithiasis, 445 ; in diabetes, 
924 ; in exophthalmic goitre, 563 ; in gastric catarrh, 
356 ; in gout, 935 ; in habitual headache, 500 ; in in- 
testinal catarrh, 384 ; in laryngeal catarrh, 121 ; in 
nephrolithiasis, 835 ; in neuritis, 550 ; in obesity, 943 ; 
in pulmonary emphysema, 166 ; in pyelitis, 832. 

Miserere in intestinal obstruction, 407. 

Mitral insufficiency, 264. 

Mitral stenosis, 266. 

Mogigraphia, 544. See Writers' Cramp. 
Monophasia, 679. 

Monoplegia, 505 ; in focal diseases of the centrum 
ovale, 681 ; in focal diseases of the motor cortex, 
673, 685 ; in general paralysis of the insane, 723 ; in 
meningitis, 661, 665. 

Morbilli, 43. See Measles. 

Morbus Addisonii, 826. _ See Addison's Disease. 

Morbus Basedowii, 560. See Exophthalmic Goitre. 

Morbus Brightii, 784. See Nephritis. 

Morbus Gravesii, 560. See Exophthalmic Goitre. 

Morbus maculosus Werlhofli, 906. See Purpura. 

Morbus sacer, 729. See Epilepsy. 

Morphine in angina pectoris, 297 ; in cholelithi - sis, 
445 ; in endocarditis, 261 ; in gastric ulcer, 363 ; in 
intercostal neuralgia, 495 ; in intestinal obstruction, 
411 ; in locomotor ataxia, 612 ; in myelitis, 592 ; in 
myocarditis, 291 ; in nephritis, 797 ; in neuralgia, 
490 ; in occipital neuralgia, 493 ; in peritonitis, 428 ; 
in pleurisy, 246 ; in pneumothorax, 253 ; in sciatica, 



496 ; in spasm of the diaphragm, 543. See also 
Opium. 

Morphine, poisoning from, 950. 
Morphinism, chronic, 950. 
Mosquitoes, relation of, to chyluria, 824. 
Mothers' milk, substitutes for, in feeding children, 
389. 

Motility, disturbances of, 503 ; in caisson disease, 574 ; 
in chronic hydrocephalus, 727 ; in locomotor ataxia, 
600 ; in pressure paralysis of the spinal cord, 
578. 

Motion, sensations of, 477. 

Motor nerves, diseases of, 503 ; changes of electrical 
excitability in, 514. 

Motor region of the cortex and its focal diseases, 672, 
703 ; centers of different muscular territories in, 
672 ; diagnosis of focal lesions of, 673 ; relation of 
hemiplegia to, 673, 685 ; relation of monoplegia to, 
673, 685 ; relation of symptoms of irritation in differ- 
ent muscular territories to, 674, 675, 685 ; relation of 
tonic-clonic spasms to, 674, 675. 

Mouth, cavity of inflammation of, 318 ; in pulmonary 
tuberculosis, 210 ; in typhoid fever, 11. 

Mucous haemorrhoids, 400. 

Mucous patches in syphilis of the larynx, 132. 

Mucous polypi in the larynx, 131. 

Mud-baths in locomotor ataxia, 611 ; in muscular 
rheumatism, 865 ; in myelitis, 591. 

Muguet, 321. See Thrush. 

Mulberry calculi in nephrolithiasis, 832. 

Mumps, 324. See Parotitis. 

Muscles, abscess of, in septico-pyaemia, 98 ; regenera- 
tion of. 521 ; sensory nerves to, 480 ; stretching of, 
in facial paralysis, 529 ; trichinae in, 110. 

Muscular atrophy in amyotrophic lateral sclerosis, 
614, 615, 616 ; in articular rheumatism, 852 ; in cere- 
bral haemorrhage, 695 ; degenerative, 521, 618 ; in 
deltoid paralysis, 532 ; in infantile paralysis (cere- 
bral), 705 ; (spinal), 630, 631 ; in lead paralysis, 537 ; 
in locomotor ataxia, 608. 612 ; in myelitis, 588 ; in 
neuritis, 549, 550 ; in pachymeningitis cervicalis 
hypertrophica, 567 ; in paralysis, 507 ; in poliomye- 
litis in adults, 634, 635 ; in pressure paralysis of the 
spinal cord, 579 ; in progressive bulbar paralysis, 
646-649 ; in radial paralysis, 532 ; in ulnar paralysis, 
533 ; in unilateral lesion of the spinal cord, 645. 

Muscular atrophy , progressive, 618; beginning of, 618 ; 
causes of, 618 ; complication of, with progressive 
bulbar paralysis, 620 ; diagnosis of, 620 ; hereditary, 
618, 621, 624 ; juvenile form of, 624 ; pathological 
lesion in, 618 ; symptoms of, 618 ; treatment of, 
621. 

Muscular contractures in amyotrophic lateral sclero- 
sis, 615 ; in cerebral haemorrhage, 694 ; in cholera, 
76 ; in Friedreich's ataxia, 612 ; in hysteria, 759, 
765, 766 ; in infantile paralysis (cerebral), 705 ; 
(spinal), 631 ; in paralysis agitans, 743 ; in second- 
ary degeneration of the spinal cord, 643. 

Muscular degeneration, 521. 

Muscular excitability in acute ascending spinal pa- 
ralysis, 636 ; in amyotrophic lateral sclerosis, 615 ; 
in cerebral haemorrhage, 693, 695 ; electrical, 514 ; 
in facial paralysis, 528 ; in hysteria, 763 ; in loco- 
motor ataxia, 606 ; mechanical, 514 ; in myelitis, 
588 ; in neuritis, 551 ; in progressive muscular 
atrophy, 619 ; in pseudo-hypertrophic muscular 
paralysis, 623 ; in radial paralysis, 533 ; in spinal 



970 



INDEX. 



infantile paralysis, 631 ; in unilateral lesion of the 

spinal cord, 645. 
Muscular hypertrophy in congenital myotonia, 753. 
Muscular pains in cholera morbus, 385 ; in intestinal 

catarrh, 379 ; in muscular rheumatism, 864 ; in 

scarlet fever, 16 ; in typhoid fever, 40. 
Muscular rheumatism, 863 ; acute, 863 ; chronic, 863 ; 

diagnosis of, 865 ; in haemophilia, 909 ; treatment 

of, 865. 

Muscular rigidity in congenital myotonia, 753 ; in 

paralysis agitans, 743, 744 ; in tetanus, 749. 
Muscular sense, 479. 

Muscular sensibility, abnormal, 480 ; electro-muscu- 
lar, 430 ; in locomotor ataxia, 600, 603, 605 ; test of, 
479. 

Muscular stiffness after cerebral haemorrhage, 690 ; 

in cholera, 78. 
Muscular tonus in locomotor ataxia, 603 ; in spastic 

spinal paralysis, 626. 
Mushroom poisoning, 951. 
Musk in spasm of the glottis, 129. 
Mustard in asthma, 158 ; in pleurisy, 246. 
Myalgia, cervical, 864 ; lumbar, 864 ; rheumatic, 863. 
Mycoderma vini in relation to thi'ush-formation, 

321. 

Mycosis, intestinal, 108. See Malignant Pustule. 

Mydriasis in oculo-motor paralysis, 524. 

Myelitis, 581 ; acute bulbar, 655 ; cervical, 589 ; diag- 
nosis of diffuse transverse, 590 ; diffuse, 581, 5S2 ; 
dorsal, 539 ; lumbar, 589 ; pathological changes in 
the spinal cord in, 533 ; symptoms of, 585 ; trans- 
verse, 531 ; treatment of, antisyphilitic, 590 ; by 
baths, 591 ; electrical, 590 ; hygienic and symp- 
tomatic, 591. 

Myelocele, 640. 

Myocarditis, 287 ; diagnosis of, 290 ; prognosis of, 291 ; 

treatment of, 291. 
Myodegenerati on of the heart, 287. 
Myositis, rheumatic, 863. 

Myotonia, congenital, 752 ; congenital muscular anom- 
alies in, 753. 

Myxcedema in diseases of the trophic nerves, 555. 
Nails in typhoid fever, 16. 

Narcotics in acute bulbar paralysis, 656 ; in asthma, 
158 ; in bronchitis, 142 ; in cerebral abscess, 703 ; in 
cerebral syphilis, 718 ; in cystitis, 843 ; in diabetes, 
924 ; in epilepsy, 737 ; in habitual headache, 501 ; in 
hemicrania, 55S ; in hiccough, 544 ; in hysteria, 
766 ; in mastodynia, 495 ; in meningitis, 97, 663, 667 : 
in nephrolithiasis, 835 ; in neuralgia, 490 ; in neu- 
rasthenia, 770 ; in neuritis, 550 ; in osteomalacia, 
873 ; in palpitation of the heart, 298 ; in pneumonia, 
190, 191 ; in progressive bulbar paralysis, 651 ; in 
pulmonary emphysema, 166 ; in pulmonary tuber- 
culosis, 217 ; in pyelitis, 832 ; in spasm of the cervi- 
cal muscles, 542 ; in spasm of the glottis, 130 ; in 
spasm of the trigeminus, 539 ; in spermatic neu- 
ralgia, 497 ; in tetanus, 752 ; in trigeminal neuralgia, 
492 ; in valvular disease of the heart, 286 ; in whoop- 
ing-cough, 150. 

Nasal catarrh, chronic, 114 ; diagnosis of, 115 ; treat- 
ment of, 115. 

Nasal catarrh in typhus fever, 28. 

Nasal douche in diphtheria, 68 ; in nasal catarrh, 115 ; 
in pharyngeal catarrh, 336. 

Naso-pharyngeal catarrh, 335. 



Nationality in relation to hysteria, ?57 ; to neurasthe- 
nia, 767. 

Nephritis, acute, 784, 787 ; acute hemorrhagic, 788 ; 
acute infectious, 785 ; in articular rheumatism, 786, 
853 ; in cholera, 77, 785 ; chronic, 797 ; chronic 
hemorrhagic, 797 ; chronic interstitial, 804 ; chronic 
parenchymatous, 797 ; in diabetes, 916 ; diagnosis 
of, 793, 803, 818 ; in diphtheria, 66, 786 ; in endocar- 
ditis, 260, 786 ; in epidemic meningitis, 96, 786 ; 
gravidarum, 786 ; in intestinal affections, 786 ; in 
measles, 46, 785 ; in pneumonia, 182, 786 ; primary 
idiopathic acute, 786, 792 ; prognosis of, 793, 803 ; in 
pulmonary tuberculosis, 211, 786 ; in purpura haem- 
orrhagica, 907 ; purulent, 816 ; in relapsing fever, 
34, 785 ; in rotheln, 785 ; in scarlet fever, 39, 785 ; in 
scurvy, 904 ; in septico-pyaemia, 101 ; septic, 786 ; in 
small-pox, 785 ; in sore throat, 786 ; in syphilis, 786 ; 
in tetanus, 750, 786 ; toxic, 786 ; treatment of, 794, 
803, 819 ; in typhoid fever, 16, 785. 

Nephritis, chronic and subchronic, 797 ; diagnosis of, 
803 ; prognosis of, 803 ; treatment of, 803. 

Nephrolithiasis, 832 ; diagnosis of, 834 ; heredity of, 
833 ; origin of, 832 ; treatment of, 835. 

Nephrophthisis, 836. See Tuberculosis, Genito-urin- 

ARY. 

Nerves, atrophy of, in amyotrophic lateral sclerosis, 
614 ; degenerative, 521,554 ; in lead paralysis, 537; 
in locomotor ataxia, 597, 599 ; in paralysis, 507, 508. 

Nerves, degeneration of, 521 ; in amyotrophic lateral 
sclerosis, 614 ; in the lumbar cord in locomotor 
ataxia, 603 ; in spinal paralysis of children, 630. 

Nerves, excitability of, changes of electrical, 514 ; in 
facial paralysis, 528 ; in hysteria, 763 ; in locomotor 
ataxia, 603 ; in neuritis, 549 ; in spinal paralysis of 
children, 631 ; in tetany, 748. 

Nerves, regeneration of, 521. 

Nerve-stretching in cervico-brachial neuralgia, 494 ; 
in facial spasm, 540 ; in locomotor ataxia, 612 ; in 
neuralgia, 490 ; in paralysis agitans, 745 ; in sci- 
atica, 497 ; in spasm of the cervical muscles, 542 ; 
in trigeminal neuralgia, 493. 

Nervous fever, 13. 

Nervines in palpitation of the heart, 298. 

Neuralgia, 485 ; in the anaemic, 486 ; in aneurism of 
the thoracic aorta, 313 ; brachial, 493 ; causes of, 
486 ; cervico-brachial, 493 ; in diabetes mellitus, 
486, 917 ; dorso-intercostal, 494 ; epileptiform, 492 ; 
in general paralysis of the insane, 722 ; of the geni- 
tals and rectal region, 497 ; in gout, 486 ; in haemo- 
philia, 909 ; hereditary predisposition to, 486 ; idio- 
pathic, 486 ; intercostal, 494 ; ischiatic, 495 ; lum- 
bar, 495 ; in malaria, 85, 438 ; in neuromata, 552 ; 
occipital, 493 ; phrenic, 493 ; reflex, 486 : rheumatic, 
486 ; sciatic, 495 ; spermatic, 497 ; symptomatic, 
486 ; syphilitic, 486, 493 ; treatment of, 488 ; trigem- 
inal, 491 ; in typhoid fever, 15. 

Neurasthenia, 767 ; causes of, 767 ; course of, 768 ; 
diagnosis and prognosis of, 768 ; disposition to, 767 ; 
symptoms of, 767 ; treatment of, 769. 

Neurectomy in neuralgia, 490. 

Neuritis, 546 ; of alcoholic subjects, 550 ; ascending, 
547, 583 ; causes of, 547 ; chronic 547, 550 ; diag- 
nosis and prognosis of multiple, 550 ; hypertrophic, 
after cerebral haemorrhage, 696 ; multiple, 548 ; new 
formation of connective tissus in, 543 ; nodosa, 546 ; 
purulent, 546 ; in relation to primary degenerative 
atrophy of the nerves, 547 ; secondary, 548 ; spon- 



INDEX. 



971 



taneous, 547 ; symptoms and cause of, 549 ; trau- 
matic, 547 ; treatment of, 550, 551. 

Neuritis, optic, in acute general miliary tuberculo- 
sis, 222 ; in cerebral tumor, 710 ; in chronic hydro- 
cephalus, 727 ; in hgematoma of the dura mater, 
658 ; in meningitis, 661, 665 ; in myelitis, 589. 

Neuroma, 551 ; amputation, 552 ; diagnosis of, 552 : 
extirpation of, 552 ; false, 551 ; hereditary predis- 
position to, 552 ; after injuries of the nerves, 552 ; 
multiple occurrence of, 552 ; symptoms of, 552 ; 
treatment of, 552 ; true, 551. 

Neuroses, articular, 498 ; of the heart, 296 ; of the 
vagus, 296. 

Neurotomy in neuralgia, 490. 

Nicotine poisoning, 950. 

Night-sweats in phthisis, 199. 

Nitric acid in diabetes insipidus, 928 ; in nephritis, 

794 ; poisoning from, 946. 
Nitrous-acid fumes, poisoning from, 946. 
Nitro-benzine poisoning, 949. 
Nitro-glycerine in hemicrania, 558. 
Nocturnal incontinence of urine, 845. See Enuresis. 
Nodding spasm, 541. 

Nodules, myocarditic, in valvular disease of the heart, 
278. 

Noma, 323 ; in measles, 46 ; treatment of, 324. 

Nose, affections of, in diphtheria, 64 ; in glanders, 105 ; 

in measles, 45 ; in scarlet fever, 37, 38 ; in typhoid 

fever, 13. 

Nose-bleed, 116 ; in contracted kidney, 808, 810 ; ha- 
bitual, 116 ; in nephritis, 791 ; in relapsing fever, 33 ; 
in typhoid fever, 13 ; as vicarious menstruation, 
116. 

Nutmeg liver, 466. 

Nux vomica in dilatation of the stomach, 374. 

Nystagmus in hereditary ataxia, 612 ; in lesions of 
the corpora quadrigemina, 683 ; in multiple sclero- 
sis, 593 ; in purulent meningitis, 661 ; in sinus throm- 
bosis, 668. 

Obesity, 936 ; causes of, 936 ; complications of, 939 ; 

treatment of, 940. 
Obstruction, intestinal, 404, 444 ; tables for diagnosis 

of, 409. 

Obturator paralysis, 536 ; symptoms of, 536. 
Occipital lobes, focal diseases of their cortex, 676, 

703 ; relation of, to hemiopia, 677, 685 ; relation of, 

to soul-blindness, 677 ; seat of the visual sense in 

the cortex of, 676. 
Occipital neuralgia, 493 ; bilateral, 493 ; painful points 

in, 493. 

Ocular nerves in meningitis, 661. 

Oculo-motor paralysis, 522 ; in diphtheria, 66 ; diplo- 
pia in, 523 ; in lesions of the corpora quadrigemina, 
683 ; in lesions of the crura cerebri, 683, 685 : in lo- 
comotor ataxia, 608 ; partial, 524 ; periodical, 525 ; 
in purulent meningitis, 661 ; in tumor of the brain, 
712. 

(Edema, 777. 

03dema, acute angioneurotic, 554 ; in acute ascend- 
ing spinal paralysis, 636 ; in aneemia, 880 ; in can- 
cer of the stomach, 367 ; in contracted kidney, 808 ; 
in diabetes, 917. 

(Edema in leukaemia, 894 ; in myelitis. 589 ; in ne- 
phritis, 790, 801 : in neuritis, 549 ; in scarlet fever, 
39 ; in tetany, 748 ; in trichinosis, 111 ; in typhoid 
fever, 15 ; in valvular disease of the heart, 279. 



Oesophagitis, 338 ; catarrhal, 338 ; corrosive, 339 ; 
croupous-diphtheritic, 338 ; purulent, 339 ; treat- 
ment of, 339. 

(Esophagomalacia, 348. 

(Esophagus, cancer of, 346 ; complications of, 347 ; 
metastases of, 347 ; symptoms of, 346 ; treatment 
of, 347. 

CEsophagus, diffuse dilatation of, 339 ; after stenosis 
of the cardiac orifice, 339 ; symptoms of, 340 ; treat- 
ment of, 340. 

(Esophagus, dilatation of, 339 ; diseases of, 338. 

(Esophagus, diverticula of, 340 ; causes of, 340 ; com- 
plications of, 342 ; pressure, 340 ; symptoms of, 
341 ; symptoms of compression in, 341 ; traction, 
341 ; treatment of, 342. 

QEsophagus, paralysis of, 348 ; rupture of, 347 ; spasm 
of, 348 ; stenosis of, 342 ; auscultation of, 344 ; causes 
of, 342 ; examination of, by the sound, 344 ; prog- 
nosis and treatment of, 345 ; symptoms of, 343. 

Oidium albicans, 321. 

Oligocythaemia, 874. 

Omalgia, 864. 

Ophthalmia in diphtheria, 65 ; in exophthalmic goi- 
tre, 561 ; neuroparalytic, in anaesthesia of the tri- 
geminus, 483 ; in scrofula, 944. 

Ophthalmoplegia, progressive, 651. 

Opisthotonos, 510 ; in epilepsy, 731 ; in tetanus, 750. 

Opium in Asiatic cholera, 80 ; in cholera morbus, 
386 ; in diabetes, 924 ; in gastric ulcer, 364 ; in intes- 
tinal catarrh, 383 ; in intestinal catarrh of children, 
390 ; in intestinal obstruction, 411 ; in nephritis, 
797 ; in neuralgia, 490 ; in peritonitis, 427, 428 ; in 
tetanus, 752 ; in trigeminal neuralgia, 493 ; in typh- 
litis, 394 ; in typhoid fever, 24. 

Opium habit, 950 ; poisoning, 950. 

Optic atrophy in chronic hydrocephalus, 727 ; in dia- 
betes, 917 ; in general paralysis of the insane, 722 ; 
in locomotor ataxia, 608 ; in multiple sclerosis, 594. 

Optic neuritis. See Neuritis. 

Orchitis in typhoid fever, 16. 

Orthopaedics in pressure paralysis of the spinal cord, 
581 ; in rachitis, 870 ; in spasm of the cervical mus- 
cles, 542 ; in spinal paralysis of children, 633. 

Osmic acid in neuralgia, 490. 

Osteomalacia, 871 : diagnosis of, 872 ; examination of 
the bones in, 872 ; symptoms of, 872 ; treatment of, 
873. 

Osteomyelitis in septico-pyaemia, 101. 
Ovarian neuralgia, 497. 
Ovarie in hysteria, 759, 761, 765. 
Oxalic-acid poisoning, 946. 

Oxyuris vermicularis, 418 ; diagnosis of, 419 ; treat- 
ment of, 419. 
Ozaena, 114 ; in scrofula, 944. 

Pachymeningitis cervicalis hypertrophica, 567 ; com- 
pression of the spinal cord in, 567 ; development of, 
567 ; diagnosis of, 567 ; treatment of, 568. 

Pachymeningitis heemorrhagica, 568, 657 ; develop- 
ment of, 568 ; interna, 568, 657 ; spinalis, 568 ; symp- 
toms of, 568 ; treatment of, 568. 

Pain, sensations of, in chorea, 740 ; in chronic hydro- 
cephalus, 727 ; conduction of, 586 ; in cramps, 510 ; 
in hysteria, 759 ; in locomotor ataxia, 604 ; in pa- 
ralysis agitans, 744 ; prolonged, 479 ; rheumatoid, 
in general paralysis, 720 ; test of, 478. 

Palate, inflammation of, 328, 334. 



972 



INDEX. 



Palate, paralysis of, in compression of the medulla, 
656 ; after diphtheria, 66 ; (unilateral) in cerebral 
haemorrhage, 692. 

Palisade-worm, 823. 

Palpitation of the heart, diagnosis of nervous, 297 ; 
in hysteria, 761 ; nervous, 297 ; in neurasthenia, 
768 ; in obesity, 939 ; in pernicious anaemia, 887 ; 
in scurvy, 903 ; in tape-worm, 415 ; treatment of 
nervous, 298 ; m valvular disease of the heart, 276. 

Palsy, shaking, 742. See Paralysis Agitans. 

Pancreas, atrophy of, 473 ; in diabetes, 919. 

Pancreas, cancer of, 473 ; diagnosis of, 474 ; symp- 
toms of, 474 ; treatment of, 474. 

Pancreas, haemorrhage of, 473. 

Pancreatitis, acute, 473 ; chronic indurated, 473. 

Pancreatized meat, enemata of, in stenosis of the 
oesophagus, 345. 

Papilloma of the larynx, 131. 

Paquelin's thermo- cautery in noma, 324. 

Para-anaesthesia, 481. 

Paradoxical contraction, 514. 

Paralysie ascendante aigue, 635. See Spinal Paral- 
ysis. 

Paralysie generate spinale anterieure subaigue, 634. 
See Spinal Paralysis. 

Paralysis, 503 ; acute ascending spinal, 635, 636 ; ar- 
senical, 538 ; in articular rheumatism, 852 ; atro- 
phic, 507, 631 ; bilateral, 505 ; bulbar, 646 ; in bulbar 
haemorrhage, 652 ; central, 503 ; cerebral, 505 ; in 
cerebral haemorrhage, 689, 691, 692, 693, 694 ; in 
cerebral syphilis, 717 ; in cerebral tumor, 711, 712 ; 
in chronic hydrocephalus, 727 ; combined, of the 
upper extremity, 534 ; condition of the paralyzed 
muscles in, 508 ; in compression of the medulla, 
656 ; cortical, 505 ; of the diaphragm, 535 ; diphthe- 
ritic, 66, 506 ; in embolism and thrombosis of the 
basilar artery, 654 ; of the facial muscles in facial 
paralysis, 526 ; flaccid, 508 ; forms of peripheral, 
522 ; general, 719 ; in general paralysis of the in- 
sane, 723 ; glosso-labio-laryngeal, 646 ; in hydro- 
phobia, 103 ; hysterical, 506, 759, 764, 765, 766 ; after 
infectious diseases, 506 ; after injury to the spinal 
cord, 572 ; of the laryngeal muscles, 125 ; lead, 537 ; 
in locomotor ataxia. 600, 603, 605, 607, 612 ; of the 
lower extremity, 536 ; median, 534 ; in meningeal 
haemorrhage, 568 ; in multiple sclerosis, 594 ; of 
the muscles of the back, 531 ; in myelitis, 585 ; 
myopathic, 503 ; in neuralgia, 487 ; in neuritis, 548, 
549, 551 ; oculo-motor, 522, 523, 524 : of the oesopha- 
gus, 348 ; in pachymeningitis cervicalis hypertro- 
phica, 567 ; peripheral, 505 ; in poliomyelitis of 
adults, 633, 634, 635 ; in pressure paralysis of the 
spinal cord, 579, 580 ; in progressive bulbar paral- 
ysis, 646. 647 ; pseudo-hypertrophic muscular, 621 ; 
from psychical causes, 506 ; in purulent meningitis, 
661 ; radial, 532 ; reflex, 503 ; refrigeratory, 506 ; rheu- 
matic, 506 ; of the shoulder-muscles, 529 ; spastic, 
508 ; in spina bifida, 641 ; spinal, 505, 565, 629, 633 ; 
in spinal apoplexy, 569 ; in spinal meningitis, 565 ; 
atrophic spinal, of adults, 633 ; spinal, of children, 
629 ; in spinal paralysis of children, 630 ; of the sta- 
pedius in facial paralysis, 527 ; symptomatology of, 
507 ; toxic, 506, 537 ; traumatic. 506 ; in tumor of 
the spinal cord. 638 : in typhoid fever, 15 ; ulnar, 
533 ; unilateral, 505 ; in unilateral lesion of the spinal 
cord, 644 ; of the upper extremity, 532 ; vaso-motor, 
553, 



Paralysis agitans, 742 ; development of, 743 ; diagnosis 
of, 745 ; displacement of the center of gravity in, 
744 ; distinction of, from multiple sclerosis, 745 ; 
hereditary predisposition to, 742 ; symptoms of, 
742 ; treatment of, 743. 

Paraesthesia, 475 ; in cerebral haemorrhage, 693 ; in 
epilepsy, 731 ; in injuries of the spinal cord, 572 ; 
in locomotor ataxia, 603 ; in neurasthenia, 768 ; in 
pressure paralysis of the spinal cord, 57'8 ; in spinal 
concussion, 573 ; in spinal neurasthenia, 571 ; in 
subacute poliomyelitis, 635 ; of taste, 502 ; in tu- 
mors of the spinal cord, 638. 

Paraldehyde in neuralgia, 490 ; in neurasthenia, 770. 

Paraphasia, 679. 

Paraplegia, 505 ; in acute ascending spinal paralysis, 
636 ; in chronic hydrocephalus, 727 ; dolorosa, 581 ; 
in locomotor ataxia, 603 ; in myelitis, 585. 

Parietal convolutions, focal diseases of, 676 ; relation 
of, to cutaneous and muscular sensibility, 676. 

Parkinson's disease, 742. See Paralysis Agitans. 

Parotitis, 324 ; contagiousness of, 325 ; diagnosis of, 

325 ; duration of stage of incubation of, 325 ; meta- 
static, 325 ; primary, 324 ; in scarlet fever, 38 ; sec- 
ondary, 325 ; in small-pox, 53 ; treatment of, 325, 

326 ; in typhoid fever, 11. 

Passive congestion, kidney of, 819 ; in pulmonary 
emphysema, 165 ; in valvular disease of the heart, 
280. 

Passive congestion, liver of, 466 ; in pneumonia, 182 ; 
in pulmonary emphysema, 165 ; in valvular disease 
of the heart, 279. 

Passive congestion, spleen of, in cirrhosis of the liver, 
450 ; in pulmonary emphysema, 165 ; in valvular 
disease of the heart, 280. 

Passive motion of the extremities in hemiplegia, 697 ; 
in hysteria, 765 : in spinal paralysis of children, 633. 

Patellar reflex, 512 ; absence of, in locomotor ataxia, 
605 ; in general paralysis of the insane, 722 ; in mye- 
litis, 587 ; in neuritis, 551 ; in pressure paralysis of 
the spinal cord, 579 ; in pseudo-hypertrophic mus- 
cular paralysis, 623 ; in tetanus, 750. 

Pavement epithelium in cancer of the oesophagus, 
346. 

Pearly distemper in cattle in relation to tuberculosis 
in man, 192, 194. 

Pelioma typhosum, 16. 

Peliosis, 906 ; rheumatica, 906 ; senile, 906. 

Pelvis in osteomalacia, 872, 873 ; rachitic, 870. 

Pelvis of the kidney, dilatation of. See Pyelitis. 

Pelvis of the kidney, inflammation of. See Hydro- 
nephrosis. 

Pepsine in gastric catarrh, 356. 

Percussion, change of pitch on. over cavities, 206. 

Perforation, peritonitis from, 421 ; in purpura haem- 
orrhagica, 907. 

Peribronchitis, tubercular, 197. 

Pericardial surfaces, adhesion of, 303. 

Pericarditis, 299 ; adhesive, 303 ; in articular rheuma- 
tism, 851 ; chronic, 300 ; diagnosis of, 304 ; externa, 
299, 302 ; fibrinous, 299 ; haemorrhagic, 299 ; in 
pneumonia, 182 ; prognosis of, 305 ; in pulmonary 
tuberculosis, 211 ; purulent, 299 ; sero-fibrinous, 299 ; 
treatment of, 305 ; tubercular, 299, 304 ; in valvular 
disease of the heart, 279. 

Pericardium, air in the, 307; blood in the, 307; dropsy 
of the, 306 ; inflammation of the, 299 ; obliteration 
of the, 303. 



INDEX. 



973 



Perichondritis, laryngeal, 121 ; diagnosis of, 122 ; ex- 
ternal, 121 ; internal, 121 ; secondary, 121 ; treat- 
ment of, 122. 

Perinephric abscess, 818 ; causes of, 818 ; symptoms 

of, 818 ; treatment of, 818. 
Perinephritis, purulent, 818. 

Periosteal reflex, 513 ; in cerebral haemorrhage, 692. 

Periostitis ossificans in articular rheumatism, 859. 

Peripheral nerves, diseases of, 475 ; forms of paraly- 
sis of, 522 ; inflammation of, 546 ; new growths in, 
551. 

Peripleuritis, 249 ; diagnosis of, 249 ; prognosis of, 
249. 

Periproctitis, 381. 

Peritoneal cancer, 434 ; diagnosis of, 434 ; treatment 

of, 435. 
Peritoneal dropsy, 432. 

Peritonitis, acute, 420 ; acute circumscribed, 422, 426 ; 
adhesive, 422 ; in articular rheumatism, 421, 851 ; 
cancerous, 434 ; in children, 431 ; in cholelithiasis, 
443 ; chronic, 429 ; circumscribed, 422 ; deformans, 
429 ; diagnosis of, 427, 431 ; diffuse general, 422 ; 
fibrino-purulent, 422 ; hemorrhagic, with forma- 
tion of hsematoma, 430 ; in nephritis, 422 ; in pleu- 
risy, 421 ; prognosis of, 427 ; in pulmonary tuber- 
culosis, 211 ; sacculated, 422 ; septic, 422 ; treatment 
of, 427, 431 ; treatment of, Alonzo Clark's, 428 ; tu- 
bercular, 429 ; in typhoid fever, 9, 10. 

Peritonsillar abscess, 331. 

Perityphlitis, 391. See also Typhlitis. 

Peroneal paralysis, 536. 

Pertussis, 147. See Whooping-couc3. 

Petechial typhus, 27. See Typhus. 

Peyer's patches in typhoid fever, 8. 

Pharyngeal catarrh, chronic, 334 ; hypertrophic, 335 ; 
prognosis of, 336 ; treatment of, 336. 

Pharyngitis, chronic, 334 ; granular, 334 ; sicca, 335. 

Pharynx in measles, 44 ; in scarlet fever, 36 ; tuber- 
culosis of, 210 ; in typhoid fever, 11. 

Phlebitis, purulent, in septico-pyaemia, 99. 

Phosphatic calculi in nephrolithiasis, 832. 

Phosphorus in locomotor ataxia, 612 ; in pernicious 
anaemia, 890 ; in neuralgia, 490 ; in osteomalacia, 
873 ; in rachitis, 870. 

Phosphorus necrosis, 948. 

Phosphorus poisoning, 948 ; acute, 948 ; chronic, 948. 
Phrenic nerve, paralysis of, 535. 
Phthisis, fibroid, 206. 

Phthisis, laryngeal, 123. See Tuberculosis. 
Phthisis pulmonalis, 191. See Tuberculosis. 
Piano-players 1 cramp, 545. 
Picric acid in trichinosis, 112. 
Pigeon-breast, rachitic, 869. 

Pigment induration in pulmonary tuberculosis, 198. 
Pigment calculi in cholelithiasis, 442. 
Pilocarpine in diphtheria, 68 ; in nephritis, 795. 
Pine-needle baths in muscular rheumatism, 865. 
Pin-worms, 418. 
Piperin in leukaemia, 895. 

Pitch, change of, on percussion over cavities, 206. 
Pityriasis versicolor in pulmonary tuberculosis, 212. 
Plethora, 670. 

Pleura in leukaemia, 892 ; in pneumothorax, 251 ; in 

pulmonary tuberculosis, 209. 
Pleura, cicatricial contraction of, in pleurisy, 238, 243 ; 

fistulae of, after empyema, 246 ; new growths of, 

254. 



Pleurisy, 235 ; adhesive, 238 ; in articular rheuma- 
tism, 851 ; complications of, 243 ; diagnosis of, 245 ; 
with effusion, 240 ; fibrinous, 236, 240, 244 ; in pneu- 
monia, 181 ; primary, 235 ; prognosis of, 246 ; puru- 
lent, 245 ; secondary, 235 ; in septico-pyaemia, 101 ; 
in small-pox, 52 ; tapping in, 247 ; treatment 
of, 246 ; tubercular, 236, 241 ; in typhoid fever, 
12. 

Pleuritic effusions, 240 ; ossification, 238 ; thickening, 
238, 243. 

Pleuritis, 235 ; sicca, 236, 240. 

Pleuro-pericarditis, 302. 

Pleuro-pneumonia, 174. 

Plexus paralysis of the brachial plexus, 534. 

Pneumatic treatment in bronchitis, 141 ; in emphy- 
sema, 166. 

Pneumatometer, 164. 

Pneumonia alba in pulmonary syphilis of the new- 
born, 235 ; anomalies in course of, 185 ; asthenic, 
186 ; in articular rheumatism, 853 ; bilious, 182 ; 
catarrhal, 170 ; central, 186 ; cheesy, 173, 197 ; in 
children, 185 ; chronic interstitial, 151 ; complica- 
tions of croupous, 178 ; crossed, 177 ; croupous, 174 ; 
delayed resolution of croupous, 187 ; diagnosis of 
croupous, 188 ; in diphtheria, 65 ; disposition to 
croupous, 175 ; endemic occurrence of croupous, 
175 ; erysipelatous, 181 ; fibrinous, 175 ; genuine, 
174 ; infectious nature of croupous, 174 ; intermit- 
ting, 184 ; lobar, 174 ; lobular, 170, 197. 

Pneumonia in measles, 46 ; migrans, 181 ; in nephri- 
tis, 791 ; in old people, 185 ; pathological lesion of 
catarrhal, 171 ; of croupous, 175 ; primary, 174 ; 
prognosis of croupous, 188 ; in rachitis, 869 ; in 
scurvy, 904 ; in small-pox, 52 ; symptoms of ca- 
tarrhal, 172 ; of croupous, 178 ; in tetanus, 750 ; 
traumatic, 175 ; treatment of catarrhal, 173 ; of 
croupous, 189 ; typhoid, 186 ; wandering, 181. 

Pneumonoconiosis, 227. 

Pneumopericardium, 307. 

Pneumothorax, 250 ; circumscribed, 251 ; closed, 252 ; 
diagnosis of, 253 ; open, 252 ; in pulmonary tuber- 
culosis, 210 ; sacculated, 251 ; treatment of, 253 ; in 
typhoid fever, 12 ; valvular, 252. 

Pneumo-typhoid, 12, 187. 

Podagra, 928. See Gout. 

Points douloureux in neuralgia, 487. 

Poisoning, 946. 

Poliomyelitis, acute, of adults, 633 ; diagnosis of, 634 ; 
relation of, to neuritis, 634 ; symptoms of, 633 ; 
treatment of, 634. 

Poliomyelitis, acute, in children. See Spinal Paraly- 
sis op Children, 629. 

Poliomyelitis, subacute and chronic, 634 ; treatment 
of, 635. 

Polyaesthesia, 477 ; in locomotor ataxia, 605. 
Polyarthritis, chronic, 858. 

Polydipsia in diabetes, 912, 915, 927 ; in hysteria, 762. 
Polypi in the oesophagus, 342. 
Polysarcia adiposa, 936. 

Polyuria in anaemia, 880 ; in cerebro-spinal menin- 
gitis, 96 ; in contracted kidney, 808, 807 ; in diabetes 
insipidus, 926-928 ; in diabetes mellitus, 912, 915, 920 ; 
in epilepsy, 732 ; in hysteria, 762. 

Pomegranate in tape-worm, 416. 

Pons, haemorrhages into, 652. See also Medulla. 

Pork in relation to trichinosis, 110. 

Portal vein, purulent inflammation of, 470 (see Pyle- 



INDEX. 



phlebitis) ; thrombosis of, 471. See Pylethrom- 
bosis. 

Post-epileptic insanity, 733. 

Posterior nasal catarrh, chronic, 114. 

Potassium, acetate of, in nephritis, 796 ; chlorate of, 

in cystitis, 843 ; nitrate of, poisoning from, 947 ; 

picro-nitrate of, in chyluria, 824 ; salts, in scurvy, 

905. 

Potfs boss on the vertebral column, 576. 
Power, sense of, 79. 
Pressure diverticula, 340. 

Pressure paralysis of the spinal cord, 575 ; bending of 
the cord in, 577 ; causes of, 575 ; complications of, 
579 ; diagnosis of, 580 ; pathological lesion of the 
vertebra3 and of the cord in, 576 ; place of compres- 
sion in, 576 ; treatment of, 581. 

Pressure points in facial spasm, 540. 

Pressure, sense of, disturbances of, in locomotor 
ataxia, 605 ; partial paralysis of, 477 ; test of, 477. 

Premature delivery in chorea gravidarum, 742. 

Pregnancy in epilepsy, 733 ; nephritis of, 793. 

Proctitis, 381. 

Professional diseases, 227. 

Professional neuroses of co-ordination, 544. 

Proglottides of tape-worm, 411. 

Propulsion in paralysis agitans, 744. 

Prosopalgia, 491. See Trigeminus, Neuralgia op. 

Prostate in genito- urinary tuberculosis, 836. 

Pseudo-crises in croupous pneumonia, 184 ; in relaps- 
ing fever, 31. 

Pseudo-croup, 118. 

Pseudo-hypertrophy of the muscles, 622 ; beginning 
of, 622 ; increase of volume of different muscles in, 
623 ; symptoms of, 622, 

Pseudo-leucocythaemia, 896. 

Pseudo-leukaemia, 896 ; diagnosis of, 897 ; examina- 
tion of the blood in, 897 ; lymphatic, 896 ; relation 
of, to anaemia, 896 ; to infectious tumors, 896 ; 
symptoms of, 897 ; treatment of, 898. 

Pseudo-paralysis, spastic, 627. 

Pseudo-relapse in scarlet fever, 41. 

Pseudo -sclerosis, 595. 

Pseudo-tabes of alcoholic subjects, 550. 

Psoriasis of the tongue, 323. 

Psychical. See Mental. 

Psychical equivalent of epilepsy, 732. 

Ptosis in oculo-motor paralysis, 524. 

Pulmonary valve, insufficiency of, 273 ; stenosis of, 
274. 

Pulmonary. See Lungs. 

Pulsation, epigastric, in valvular disease of the heart, 
265. 

Pulsus bigeminus, 278 ; celer, 270 ; inequalis, 277 ; ir- 
regularis, 277 ; paradoxus, 153, 301, 303 ; tardus, 310. 

Puncture in ascites, 433 ; in chronic hydrocephalus, 
727 ; in cirrhosis of the liver, 453 ; in hydronephro- 
sis, 839 ; in nephritis, 797 ; in pericarditis, 306 ; in 
pleurisy, 247 ; in pneumonia, 181 ; in pneumotho- 
rax, 253 ; in valvular disease of the heart, 286. 

Pupils in epilepsy, 731, 736 ; in general paralysis of 
the insane, 722 ; in haematoma of the dura, 658, 659 ; 
in meningitis, 661, 665 ; in pernicious anaemia, 887 ; 
in tetanus, 750 ; in thermic fever, 707. 

Pupils, immobility of, in eclampsia of children, 738 ; 
in epilepsy, 732, 736 ; in general paralysis of the in- 
sane, 722 ; in lesions of the corpora quadrigemina, 
683 ; in locomotor ataxia, 600. 



Purpura, 906 ; Jiaemorrhagica, 907 ; hemorrhagica, 
prognosis and treatment of, 907 ; rheumatica, 906 ; 
simplex, 906 ; urticans, 908 ; variolosa, 54. 

Pus, collections of, as a cause of septico-pyaemia, 99. 

Pustule, malignant, 106. See Malignant Pustule. 

Pustules in glanders, 105 ; in small-pox, 50. 

Pyaemic symptoms in sinus thrombosis, 669 ; in sup- 
purative pylephlebitis, 471. 

Pyelitis, 829 ; calculosa, 829, 833 ; in locomotor ataxia, 
607 ; in myelitis, 588 ; origin of, 829 ; symptoms of, 
830 ; treatment of, 831. 

Pyelocystitis, 829. 

Pyelonephritis. 816, 830. 

Pylephlebitis, chronic adhesive, 471. 

Pylephlebitis, suppurative, 470 ; diagnosis of, 471 ; 
of the new-born, 470 ; symptoms of, 470. 

Pylethrombosis, 471 ; symptoms of, 472 ; treatment 
of, 473. 

Pyonephrosis, 830. 

Pyopneumothorax, 251. 

Quicksilver in intestinal obstruction, 411. 
Quincke's capillary pulse, 270. 

Quinine in asthma, 158 ; in diabetes, 925 ; in habitual 
headache, 500 ; in haemoglobinuria, 901 ; in leukae- 
mia, 895 ; in locomotor ataxia, 612 ; in malaria, 86 ; 
in Meniere's disease. 728 ; in neuralgia, 488, 489 ; in 
neurasthenia, 770 ; in neuroses of the heart, 296 ; in 
pulmonary tuberculosis, 217, 218 ; in sciatica, 489, 
497 ; after scurvy, 905 ; in trigeminal neuralgia, 
489, 492 ; in trophic disturbances, 555 ; in typhoid 
fever, 19, 22, 23 ; in whooping-cough, 150. 

Rabies, 102. See Hydrophobia. 

Race, influence of, on diabetes mellitus, 911 ; on hae- 
mophilia, 908 ; on hysteria, 757 ; on yellow fever, 
91. 

Rachitis, 866 ; acute, 870 ; chemical examination of 
the bones in, 867 ; chronic, 869 ; diagnosis and prog- 
nosis of, 870 ; foetal, 867 ; origin of, 866 ; relation 
of, to malaria, 866, 868 ; relation of, to spasm of the 
glottis, 129 ; symptoms of, 868 ; tarda, 867 ; treat- 
ment of, 870. 

Radial paralysis, 532 ; chronic thickening of the ex- 
tensor tendons in, 533 ; disturbances of function in, 
532 ; in lead paralysis, 537 ; rheumatic, 532 ; trau- 
matic, 532. 

Radiating fungus, 250. 

Rag-pickers 1 disease, 107. See Malignant Pustule. 

Railway-spine, 572. See Spinal Concussion. 

Rectal speculum in cancer of the rectum, 398. 

Rectum, cancer of, 398 ; inflammation of, 381 ; neu- 
ralgia of, 497 ; paralysis of, in injury of the spinal 
cord, 572 ; paralysis of, in myelitis, 588. 

Rectum, syphilis of, 397 ; symptoms of, 397 ; treat- 
ment of, 398. 

Recurrent fever. See Relapsing Fever. 

Recurrent nerve, paralysis of, 126. 

Reflex centers, vaso-motor, 553. 

Reflexes, 511 ; in acute ascending spinal paralysis, 
636 ; after cerebral haemorrhage, 690, 692 ; in cho- 
rea, 740 ; in facial paralysis, 528 ;,in injury of the 
spinal cord, 572 ; in locomotor ataxia, 605 ; in mye- 
litis, 586, 587 ; in neuralgia, 487 ; in neuritis, 550, 
551 ; in paralyses, 508 ; in pressure paralysis of the 
spinal cord, 579 ; in progressive bulbar paralysis, 
648 ; in progressive muscular atrophy, 620 ; in sci- 



INDEX. 



975 



atica, 496 ; in spinal apoplexy, 570 ; in spinal con- 
cussion, 573 ; in spinal meningitis, 565 ; tests and 
condition of, 511 ; in tetanus, 750 ; in trigeminal 
neuralgia, 491 ; in tubercular meningitis, 665 ; in 
unilateral lesion of the spinal cord, 645. 

Reflex epilepsy, 730 ; neuralgia, 486 ; paralyses, 506 ; 
spasm, saltatory, 543. 

Rehme bath, artificial, in myelitis, 591. 

Relapses of cholera, 77 ; of erysipelas, 60 ; of lead 
paralysis, 538 ; of scarlet fever, 41 ; of sciatica, 
496 ; of typhlitis, 392 ; of typhoid fever, 17 ; of ty- 
phus fever, 29. 

Relapsing fever, 30 ; complications of, 33 ; conta- 
giousness of, 30 ; epidemic occurrence of, in Ger- 
many, 30 ; inoculation of, 30 ; period of incubation 
of, 31 ; prognosis of, 34 ; spirilli in, 32 ; treatment 
of, 34. 

Renal crises in locomotor ataxia, 608. 
Ren mobilis, 824. 

Resonance, thoracic, in pleurisy, 241. 

Respiration in acute ascending spinal paralysis, 636 ; 
in acute bulbar paralysis, 655 ; amphoric, 252 ; in 
amyotrophic lateral sclerosis, 616 ; in anaemia, 878, 
887 ; in asthma, 155 ; bronchial, 206 ; in bronchitis, 
136, 139 ; in bulbar haemorrhage, 653 ; in cancer of 
the lungs, 233 ; in cerebral haemorrhage, 689, 690, 
692 ; in chronic poliomyelitis, 635 ; in cirrhosis of the 
liver, 451 ; in diabetic coma, 918 ; in embolism and 
thrombosis of the basilar artery, 655 ; in epilepsy, 
731 ; in exophthalmic goitre, 562 ; in hepatitis, 447 ; 
in hysteria, 758 ; interrupted, 206 ; in locomotor 
ataxia, 607 ; metallic, 252 ; metamorphosing, 206 ; 
in miliary tuberculosis, 220, 221 ; in obesity, 939 ; 
in osteomalacia, 872 ; in phthisis, 205 ; in pneumo- 
nia, 172, 179 ; in progressive bulbar paralysis, 647 ; 
in progressive muscular atrophy, 619, 620, 621 ; in 
pseudo-leukaemia lymphatica, 897 ; in scurvy, 903 ; 
in tetanus, 750 ; in thermic fever, 706 ; in trichino- 
sis, 111 ; in tubercular meningitis, 665, 666 ; in urae- 
mia, 781. 

Respiratory spasms, 543 ; complicated, 544. 
Retina in chronic nephritis, 802 ; in contracted kid- 
ney, 809 ; in diabetes, 917 ; in leukaemia, 892. 
Retinal haemorrhages in septico-pyaemia, 100. 
Retropharyngeal abscess, 337. 
Retropulsion in paralysis agitans, 744. 
Retro-tonsillar abscess, 331. 
Revaccination, 55. 
Rhabdomyoma, 820. 

Rheumatism, acute articular, 847 ; alkaline treatment 
of, 856 ; cerebral, 852 ; chronic, 858 ; diagnosis of, 
854 ; endocarditis in, 850 ; hyperpyretic, 852 ; prog- 
nosis of, 853 ; prophylaxis of, 858 ; scarlatinal, 40 ; 
symptoms, 848 ; treatment of, 854, 862. 

Rhinitis, 113 ; chronic. 114 ; in scrofula, 944. 

Rickets, 866. See Rachitis. 

Rotheln, 48 ; period of incubation of, 48 ; prognosis 

of, 48 ; relation of, to measles, 48. 
Romberg's symptom in locomotor ataxia, 600. 
Root-zones, 480. 
Rosary, rachitic, 868. 
Rosenthal-Leube meat solution, 363. 
Roseola in typhoid fever, 15 ; in typhus fever, 28. 
Round-worms. 417. 

Sac, pericardial, air in. 307 ; blood in, 307. 
Saddle-nose after ozaena, 115. 



Sage-tea in phthisis, 218. 
St. Anthony's fire, 57. 
St. Vitus's dance, 739. 
Salaam convulsions, 541. 

Salicylate of sodium in articular rheumatism, 854 ; in 
diabetes, 925 ; in gout, 636 ; in habitual headache, 
501 ; in hemicrania, 658 ; in neuralgia, 489 ; in ty- 
phoid fever, 22. 

Salicylic acid in articular rheumatism, 854 ; in dis- 
eases of the trophic nerves, 555 ; in gastric catarrh, 
356 ; in gout, 936 ; in locomotor ataxia, 612 ; in mus- 
cular rheumatism, 865 ; in neuritis, 550 ; in purpura 
haemorrhagica, 901' ; in tetanus, 752. 

Salicylic delirium, 855 ^ dyspnoea, 855 ; powder in 
phthisis, 218. 

Salivation in diabetes insipidus, 927 ; in hydrophobia, 
103 ; in stomatitis, 318 ; in ulcerative stomatitis, 
320. 

Salt in epilepsy, 737 ; in haemoptysis, 217. 
Salt-baths in gout, 935 ; in scrofula, 945. 
Saltpetre-paper in asthma, 158. 
Sand-baths in articular rheumatism, 862. 
Santonica in ascarides, 418. 
Santonin in ascarides, 418. 
Sarcina ventriculi, 353. 

Sarcoma, alveolar, of the lungs, 233 ; of the kidneys, 
820. 

Scarification of the skin in dropsy, 286. 
Scarlatina, 34. 

Scarlatinal diphtheria, 37 ; eruption, 38 ; nephritis, 

39, 42 ; poison, 35. 
Scarlet fever, 34 ; contagiousness of, 35 ; diagnosis of, 

41 ; disposition to, 35 ; epidemic occurrence of, 35 ; 

haemorrhagic, 38 ; inoculation of, 35 ; miliary, 38 ; 

papular, 38 ; period of incubation of, 35 ; prognosis 

of, 41 ; rudimentary forms of, 40 ; tenacity of the 

contagium of, 35 ; treatment of, 41 ; typhoid form 

of, 41 ; variegated, 38. 
Sciatica in diabetes, 917 ; diagnosis of, 496 ; relapses 

of, 496 ; symptoms and cause of, 496 ; treatment of, 

496. 

Sciatic paralysis, 536 ; treatment of, 537. 
Scirrhus cancer of the oesophagus, 346 ; of the stom- 
ach, 365. 

Sclerose en plaques, 592. See Sclerosis, Multiple. 

Sclerosis, amyotrophic lateral, 613 ; diagnosis of, 616 ; 
implication of the medulla in, 614 ; symptoms and 
course of, 614 ; treatment of, 616. 

Sclerosis, disseminated, 592. See Sclerosis, Multiple. 

Sclerosis, multiple, of the brain and cord, 592 ; dis- 
tinction of, from paralysis agitans, 595 ; hereditary 
predisposition to, 592 ; relation of, to chronic bul- 
bar paralysis, 595 ; to chronic myelitis, 595 ; to gen- 
eral paralysis of the insane, 595 ; to spastic spinal 
paralysis, 595 ; seat of the sclerotic nodules in, 592 ; 
symptoms of, 592 ; treatment of, 596. 

Sclerosis, primary lateral, 625. 

Sclerosis, renal, 804. 

Sclerotinic acid in phthisis, 217. 

Scoda's resonance in pleuritic effusion, 241. 

Scolex, 412. 

Scoliosis, rachitic, 869. 

Scorbutic anaemia, 904 ; ulcers, 904. 

Scorbutus, 901. See Scurvy. 

Scrofula, 943 ; relation of, to tuberculosis, 200, 944 ; 

treatment of, 944. 
Scurvy, 901 ; causes of, 902 ; contagiousness of, 902 ; 



976 



INDEX. 



distinction of, from peliosis and stomatitis, 905 ; 
epidemic occurrence of, 90.2 ; forms of, 904 ; symp- 
toms of, 903 ; treatment of, 905. 
Seat-worms, 418. 

Secondary degeneration. See Spinal Cord (second- 
ary degeneration). 

Secretion, disturbances of, 556 ; in acute ascending 
spinal paralysis. 636 ; in anaemia, 878 ; in cerebral 
haemorrhage, 695 ; in diabetes insipidus, 926 ; in ex- 
ophthalmic goitre, 562 ; in haemoglobinuria, 899 ; in 
hysteria, 762 ; in myelitis, 5S3 ; in neurasthenia, 76S ; 
in progressive bulbar paralysis, 648 ; in subacute 
poliomyelitis, 635 ; in tetanus, 751 ; in tetany, 748. 

Secretions in diabetes, 919, 92*>, 927. 

Semilunar valves, insufficiency of, 263. 

Senile emphysema, 159. 

Senile kidney, 310, 805. 

Sensation, conduction of, in acute ascending spinal 
paralysis, 636 ; delayed, 479. 

Sensation, pararysis of, in locomotor ataxia, 604 ; par- 
tial, 475. 

Sensibility, disturbances of, in acute ascending spinal 
paralysis, 636 ; in arsenical paralysis, 538 ; in bul- 
bar haemorrhage, 653 ; in caisson disease, 574 ; in 
cerebral haemorrhage, 633 ; in compression of the 
medulla, 656 ; in crural paralysis, 536 ; in epilepsy- 
731 ; in focal diseases of the crus, 683 ; of the inter- 
nal capsule, 682 ; general consideration of, 475 ; in 
general paralysis of the insane, 722 ; in injury of 
the spinal cord, 572 ; in the larynx, 130 ; in locomo- 
tor ataxia, 603 ; in median paralysis, 534 ; in multi- 
ple sclerosis, 594 : in myelitis, 586 ; in neuralgia, 
487 ; in neuritis, 550, 551 ; in obturator paralysis, 
536 ; in paralysis, 503 : in pressure paralysis of the 
spinal cord, 578 ; in radial paralysis, 533 ; in sciati- 
ca, 498 ; in sciatic paralysis, 1 537 ; in spinal concus- 
sion, 573 ; in tetanus, 750 ; in tumors of the base of 
the brain, 712 ; in ulnar paralysis, 534 ; in unilateral 
lesion of the spinal cord, 644 ; in writers 1 cramp, 
545. 

Sensory nerves, diseases of, 475. 

Septico-pyaemia, 98 ; circulatory apparatus in, 100 ; 
cryptogenetic or spontaneous, 99 ; diagnosis of, 
102 ; jaundice of the skin in, 101 ; prognosis of, 
101 : treatment of, 102. 

Sero-pneumothorax, 250. 

Serous membranes in articular rheumatism, 851. 

Serratus paralysis, 539 ; course of, 530 : rheumatic, 
530 ; traumatic, 530 ; treatment of, 531 ; wing-like 
position of the scapula in, 530. 

Serum albumen in albuminuria, 772. 

Sewing-machine girls, affection of, 546. 

Sex, influence of, in acute ascending spinal paralysis, 
636 ; in acute yellow atrophy of the liver, 455 ; in 
amyotrophic lateral sclerosis, 613 ; in anaemia, 875. 
880, 8S5 ; in cerebral haemorrhage, 636 ; in cerebral 
syphilis, 715 ; in cerebral tumor, 708 ; in cholera, 
75 ; in chorea, 733 ; in congenital myotonia, 753 ; in 
diabetes, 911 ; in exophthalmic goitre, 560 : in Fried- 
reich's ataxia, 612 ; in general paralysis of the insane, 
719 ; in gout, 929 ; in haematoma of the dura mater, 
658 ; in haemophilia, 908 ; in hepatic colic, 441 ; in 
hemicrania, 556 ; in hysteria, 757 ; in leukaemia, 
891 ; in locomotor ataxia, 597 ; in multiple sclero- 
sis, 592 ; in neuralgia, 4S6 ; in obesity, 938 ; in os- 
teomalacia, 871 ; in paralysis agitans, 742 ; in 
phthisis, 196 ; in poliomyelitis, acute, of adults. 



633 ; in pseudo-hypertrophic muscular paralysis, 
622 ; in pseudo-leukaemia, 898 ; in rachitis, 867 ; in 
tetany, 747 ; in unilateral facial atrophy, 559. 
Sexual functions in diabetes, 916 ; in functional dis- 
turbances of the spinal cord, 571 ; in injuries of the 
spinal cord, 572 ; in locomotor ataxia, 607 ; in mye- 
litis, 588. 

Sexual organs in chlorosis, 875 ; in diabetes, 916 ; 
diphtheria of, 65 ; in exophthalmic goitre. 560 ; in 
gout, 931 ; in hysteria, 757 ; neuralgia of, 497 ; in 
neurasthenia, 768 ; (female) in peritonitis, 421. 

Shadows of red blood-corpuscles in haemoglobinuria, 
900. 

Shaking, 509. 

Shaking palsy, 742. 

Ship fever, 27. See Typhus Fever. 

Shoulder, muscles of, paralysis of, 529 ; paralysis of, 
unilateral, in cerebral haemorrhage, 692 ; spasm of, 
542. 

Siderosis pulmonum, 228. 

Silver, nitrate of, in chorea, 742 ; in dysentery, 72 ; in 
intestinal catarrh of children, 390 ; in locomotor 
ataxia, 611 ; in myelitis, 591 ; in spastic spinal pa- 
ralysis, 629 ; in valvular disease of the heart, 283. 

Singultus, 543. See Hiccough. 

Siphon, in washing out the stomach, 372. 

Skin. See Cutaneous. 

Skin, care of, in diabetes, 924. 

Skin, character of, in arthritis deformans, 861. 

Skin, diseases of, in articular rheumatism, 851 ; in 
dengue, 89 ; in diabetes, 917 ; in gout, 931 ; in pneu- 
monia, 183 ; in scarlet fever, 38 ; in scrofula. 943 ; 
in scurvy, 933 ; in small-pox, 52 ; in trichinosis, 111 ; 
in typhoid fever, 15. 

Skin, itching of, in uraemia, 781. 

Sleeplessness in neurasthenia, 768. 

Small-pox, 49 ; confluent, 50 ; contagiousness of, 49 ; 
diagnosis of, 54 ; haemorrhagic, 53 ; mortality in, 
54 ; period of incubation in, 49 ; prognosis of, 54 ; 
treatment of, 54. 

Smell, sense of. anaesthesia of, 501 ; anomalies of, 
501 ; in epilepsy, 731 ; hyperaesthesia of, 501 ; in 
hysteria, 760 ; relation of, to anomalies of taste, 501 ; 
subjective sensations of, 501 ; test of, 501 ; treat- 
ment of anomalies of, 502. 

Sneezing spasm, 544. 

Sodic bicarbonate in diabetic coma, 925 ; bicarbonate 
in gastric catarrh, 357 ; carbonate in nephrolithia- 
sis, 835 ; hydrate in sulphuric-acid poisoning, 946 ; 
phosphate in nephrolithiasis, 835 ; sulphate in car- 
bolic-acid poisoning, 950. 

Soil theory in relation to typhoid fever. 2. 

Soil water in relation to cholera, 74 ; in relation to 
typhoid fever, 2, 3. 

Somnambulism in hysteria, 763. 

Soor, 321. 

Sore throat, 323 (see Tonsillitis) ; catarrhal, 329 ; 
croupous (benign), 331 ; follicular, 329 ; haemor- 
rhagic, 330 ; necrotic, 331 : parenchymatous, 330 ; 
phlegmonous, 330 ; in scarlet fever, 36 ; in small- 
pox, 53 ; in typhoid fever, 11. 

Soul-blindness, 677. 

Soul-deafness, 677. 

Southey's trocar in dropsy, 286. 

Spasm, 508 (see Convulsions) ; of the cervical mus- 
cles, 541 ; clonic, 509 : co-ordinated, 510 ; of the fa- 
cial nerves, 539 ; forms of localized, 508 ; of the 



INDEX. 



977 



muscles of the lower extremity, 542 ; of the oesoph- 
agus, 348 ; of the respiratory muscles, 543 ; tome, 
509, 510 ; tonic-dome, 509. 

Spasm of the glottis, 129. See Glottis, Spasm of. 

Spastic-paretic gait in multiple sclerosis, 594 ; in spas- 
tic spinal paralysis, 627. 

Speech, disturbances of, 677 ; in acute bulbar myeli- 
tis, 655 ; in amyotrophic lateral sclerosis, 615 ; in 
athetosis, 745 ; in bulbar haemorrhage, 653 ; in 
cerebral embolism, 700 ; in cerebral haemorrhage, 
689, 696 ; in cerebral syphilis, 717 ; in cerebral 
tumors, 710, 712 ; in chorea, 739 ; in compression of 
the medulla, 656 ; in embolism and thrombosis of 
the basilar artery, 655 ; in epilepsy, 731 ; in focal 
diseases of the centrum ovale, 681 ; in general 
paralysis of the insane, 721, 725 ; in haematoma of 
the dura, 658 ; in hereditary ataxia, 612 ; in menin- 
gitis, 665 ; in multiple sclerosis, 593 ; in progressive 
bulbar paralysis, 646, 648. 

Sphincter, reflex spasm of, in cystitis, 841. 

Spina bifida, 640; complication of, with purulent 
meningitis, 641 ; seat of, 640 ; surgical treatment 
of, 641 ; tumor formation in, 641. 

Spinal apoplexy, 569 ; symptoms of, 570 ; treatment 
of, 570. 

Spinal cord, anaemia of, 569. 

Spinal cord, cavity and fissure formation in, 639 ; in 
cerebro-spinal meningitis, 94, 95 ; circulatory dis- 
turbances of, 569 ; concussion of, 572 ; consumption 
of, 596 ; diffuse diseases of, 582 ; diseases of, 564 ; 
functional disturbances of, 570 ; in gout, 932 ; haem- 
orrhages into, 569 ; new growths of, 638 ; systemic 
diseases of, 582 ; traumatic lesions of, 571 . 

Spinal cord, compression of, 575 ; origin of, 575 ; seat 
of, 576 ; in spina bifida, 641. 

Spinal cord, concussion of. 572 ; implication of the 
brain in, 573 ; origin of, after railway accidents, 
573 ; symptoms of, 573 ; treatment of, 574. 

Spinal cord, degeneration of, in amyotrophic lateral 
sclerosis, 613. 

Spinal cord, disease of, after sudden lowering of at- 
mospheric pressure, 574. 
Spinal cord, hyperaemia of, 569. 

Spinal cord, injuries of, 571 ; complication of, with 
secondaiy inflammation, 572 ; symptoms of, 572 ; 
treatment of, 572. 

Spinal cord, membranes of, acute inflammation of, 
564 ; haemorrhages of, 568 ; new growths of, 638. 

Spinal cord, secondary degeneration of, 641 ; after 
cerebral haemorrhage, 692, 694 ; after cerebral le- 
sions, 641 ; in compression of the cord, 577 ; in mul- 
tiple sclerosis, 592 ; in transverse affections of the 
cord, 642 ; in tumors of the cord, 638. 

Spinal cord, softening of, 585. 

Spinal cord, tumors of, 638 ; differential diagnosis of, 
from transverse myelitis, 639 ; forms of, 638 ; ori- 
gin of, 638 ; prognosis and treatment of, 639 ; rela- 
tion of, to unilateral lesion of the spinal cord, 639. 

Spinal irritation, 570 ; in hysteria, 761 ; in neurasthe- 
nia, 767. 

Spinal meningitis, 564, 566 ; origin of, 564, 566 ; prog- 
nosis of, 565 ; symptoms of, 565, 566 ; treatment of, 
566. 

Spinal muscles, paralysis of. 531 ; in pseudo-hyper- 
trophic spinal paralysis, 531, 623. 

Spinal neurasthenia, 570 ; diagnosis of, 571 ; sensi- 
tiveness of the vertebrae in, 571 ; symptoms of, 571. 



Spinal paralysis, acute ascending, 635 ; acute infec- 
tion in, 637 ; diagnosis and prognosis of, 637 ; symp- 
toms of, 636 ; treatment of, 638. 

Spinal paralysis, atrophic, 633. 

Spinal paralysis of children, 629 (see Infantile 
Paralysis) ; from acute infection, 629 ; diagnosis 
and prognosis of, 632 ; relation of, to primary neu- 
ritis, 630 ; spinal cord in, 629 ; symptoms of, 630 ; 
treatment of, 632. 

Spinal paralysis, spastic, 625 ; diagnosis of, 628 ; 
pathological lesion in the cord in, 627 ; relation of, 
to chronic hydrocephalus, 627 ; treatment of, 628. 

Spine, stiffness of, in sinus thrombosis, 668 ; (tonic) in 
tetanus, 750 ; in tubercular meningitis, 664. 

Spirilli in relapsing fever, 32. 

Spirometer in pulmonary emphysema, 164. 

Spleen in acute ascending spinal paralysis, 637 ; in 
acute yellow atrophy of the liver, 456 ; in Addi- 
son's disease, 827 ; in articular rheumatism, 853 ; 
in cerebro-spinal meningitis, 96 ; in cirrhosis of 
the liver, 450 ; in erysipelas, 60 ; in hemoglo- 
binuria, 900 ; in hepatic syphilis, 461 ; in leukae- 
mia, 891 ; in malaria, 84, 86 ; in miliary tubercu- 
losis, 222 ; in pernicious anaemia, 886 ; in phthisis, 
211 ; in pneumonia, 182 ; in pseudo-leukaemia, 897 ; 
in pylephlebitis, 470 ; in rachitis, 868 ; in relapsing 
fever, 31 ; in scarlet fever, 36, 40 ; in scurvy, 904 ; 
in septico-pyaemia, 98, 101 ; in tubercular meningi- 
tis, 666 ; in typhoid fever, 10 ; in typhus fever, 28 ; 
in yellow fever, 91. 

Spleen, extirpation of, in leukaemia, 896. 

Splenic fever, 106. 

Splenization of the lung in atelectasis, 167. 
Spondylitis deformans in chronic articular rheuma- 
tism, 861. 
Spoonwort in scurvy, 905. 

Spotted fever, 27, 93. See Typhus Fever and Cere- 
bro-spinal Meningitis. 
Stasis, oedema from, in renal diseases, 778. 
Status epilepticus, 733, 734. 

Stenocardia in hysteria, 761 ; in valvular disease of 

the heart, 277. 
Stenson's experiment in spinal anaemia, 569. 
Stimulants in cholera morbus, 386 ; in pneumonia, 

191 ; in tetanus, 752. 
Stinknase, 114. 

Stitch in the side in pleurisy, 238 ; in pneumonia, 177. 
Stomacace, 319. See Stomatitis. 
Stomach. See also Gastric. 

Stomach, adhesions of, 361 ; in chlorosis, 880 ; in 
dysentery, 71 ; in erysipelas, 60 ; perforation of, 
361, 367 : in phthisis, 210 ; in pulmonary gangrene, 
226 ; in purpura haemorrhagica, 907 ; purulent in- 
flammation of, 357 ; in yellow fever, 91. 

Stomach, abscess of, 357. 

Stomach-bougie in dilatation, 371. 

Stomach, cancer of, 364. 

Stomach, dilatation of, 369. 

Stomach, haemorrhage from, 374 ; in gastric cancer, 

365 ; in gastric ulcer, 360. 
Stomach, nervous affections of, 375 ; diagnosis of, 

376 ; in hysteria, 761 ; nervous complications of, 

375 ; peristaltic disturbance of the stomach in, 375 ; 

prognosis and treatment of, 376. 
Stomach-pump in chronic gastric catarrh, 353 ; in 

dilatation of the stomach, 372. 
Stomach, softening of, 358. 



62 



978 



INDEX. 



Stomach, ulcer of, 358. 

Stomachics in gastric catarrh, 357 ; in jaundice, 439 ; 
in neurasthenia, 770. 

Stomatitis, 318 ; acute, 319 ; aphthous, 320 ; chronic, 
319 ; in diabetes, 915 ; mercurial, 318 ; in scarlet 
fever, 37 ; scorbutic, 903 ; treatment of, 319, 320, 
321 ; in typhoid fever, 11 ; ulcerative, 319. 

Strabismus convergens in abducens paralysis, 524 ; 
in sinus thrombosis, 668. 

Stonecutters' lung, 228. 

Stramonium cigarettes in asthma, 158. 

Strangulation, internal, 405. 

Stricture of the intestine, cicatricial, 404. 

Stripe-pneumonia, 173. 

Stroke, apoplectic, 689. 

Strongylus duodenalis, 419. 

Strongylus gigas, 823. 

Struma in exophthalmic goitre, 561 ; extirpation of, 
563 ; of the supra-renal capsules, 827. 

Strychnine in acute bulbar paralysis, 656 ; in cere- 
bral haemorrhage, 697 ; in diphtheria, 69 ; in facial 
paralysis, 529 ; in laryngeal paralysis, 129 ; in mye- 
litis, 591 ; in neuritis, 551 ; in oculo-motor paralysis, 
525 ; in spinal concussion, 574 ; in spinal paralysis 
of children, 633. 

Strychnine poisoning, 950. 

Subsultus tendinum in typhoid fever, 13. 

Succussion of Hippocrates in pyo-pneumothorax, 252. 

Sudamina in articular rheumatism, 851. 

Sugar formation in diabetes, 914 ; influence of febrile 
diseases on, 915 ; influence of mental excitement 
on, 915 ; influence of physical exertion on, 915. 

Suggestion in catalepsy, 754 ; in hysteria, 763. 

Sulphur in haemorrhoids, 401. 

Sulphur baths in lead paralysis, 538. 

Sulphuretted hydrogen poisoning, 949. 

Sulphuric acid in purpura hemorrhagica, 907. 

Sulphuric-acid poisoning, 946. 

Sulphurous-acid poisoning, 946. 

Sunstroke, 706 ; causes of, 706 ; symptoms of, 706 ; 
treatment of, 707. 

Support, mechanical, in spasm of the cervical mus- 
cles, 542 ; for the vertebral column in pressure 
paralysis of the spinal cord, 581. 

Suppositories in dysentery, 72. 

Suppurative fever in small-pox, 52. 

Supra-renal capsules, diseases of, 826. 

Swamp fever, 81. See Malaria. 

Sweat-glands in jaundice, 438 ; in typhoid fever, 16 ; 
in uraemia, 781. 

Sweating in articular rheumatism, 851 ; in diabetes, 
917 ; in haemoglobinaemia, 899 ; in phthisis, 209, 
212 ; in trichinosis, 111. 

Sympathetic, irritation of, 556 ; in exophthalmic 
goitre, 562 ; trophic disturbances in, 556 ; paralysis 
of, 556 ; contraction of the pupils in, 556 ; in 
exophthalmic goitre, 562 ; in hemicrania, 557 ; 
vaso-motor disturbances in, 556. 

Synovitis in articular rheumatism, 849 ; scarlatinal, 
40. 

Syphilis of the larynx, 132 ; of the rectum, 397. 
Syphiloma, formation of, in syphilis of the liver, 460. 
Syringomyelia, 639 ; extent of, 640 ; origin of, 639. 

Tabes dorsalis, 596. See Locomotor Ataxia. 
Tabes mesenterica, 431. 

Tabes spastica, 625. See Lateral Sclerosis. 



Taches bleuatres, 16. 
Taches cerebrales, 666. 
Tachycardia, 298. 
Tactile circles, 476. 
Tactile compasses, 476. 

Taenia echinococcus, 464 ; medio -canellata, 413 ; sagi- 

nata, 413 ; solium, 411. 
Tailors' cramp, 546. 
Tampons in nasal catarrh, 115. 

Tannin in chronic pharyngeal catarrh, 336 ; in ne- 
phritis, 794. 

Tape-worms, 411 ; cures for, 415. 

Taste, disturbances of, 502 ; central, 502 ; diagnosis 
of, 502 ; in epilepsy, 731 ; in facial paralysis, 527, 
528 ; in hysteria, 760 ; partial, 502 ; test of, 502 ; 
treatment of, 502. 

Teeth, anomalies of, in diabetes, 916 ; in rachitis, 
868. 

Teething, 326 ; convulsions in, 327. 
Telegraphers' cramp, 546. 

Temperature, sense of, in locomotor ataxia, 605 ; in 
paralysis agitans, 744 ; partial paralysis of, 478 ; 
perverse, 478 ; test of, 478. 

Temporal convolutions, focal diseases of, 677 ; rela- 
tion of, to deafness, 677 ; relation of, to word-deaf- 
ness, 677, 680. 

Temporal convolutions, seat of the cortical center 
for hearing in, 677. 

Tendinous spots on the pericardium, 300. 

Tendon reflexes, 512 ; absence of, 513 ; in amyotro- 
phic lateral sclerosis, 615 ; in cerebral haemorrhage, 
692 ; in cerebral paralysis of children, 705 ; in 
chronic hydrocephalus, 727 ; in epilepsy, 732 ; in- 
crease of, 513 ; in locomotor ataxia, 605 ; in the 
lower extremities, 513 ; in multiple sclerosis, 594 ; 
in myelitis, 587 ; in poliomyelitis of adults, 633 ; in 
pressure paralysis of the spinal cord, 579 ; in pro- 
gressive bulbar paralysis, 648 ; in secondary degen- 
eration of the spinal cord, 643 ; in spastic spinal 
paralysis, 625, 627 ; in spinal paralysis of children, 
631 ; in unilateral lesion of the spinal cord, 645 ; in 
the upper extremities, 513. 

Tendons, sheaths of, in articular rheumatism, 849 ; 
thickening of, in radial paralysis, 533. 

Tenesmus in dysentery, 70 ; in intestinal catarrh, 381. 

Terminal phalanges, thickening of, in pulmonary 
stenosis, 274. 

Testicles in genito-urinary tuberculosis, 836. 

Tetanus, 749 ; diagnosis of, 751 ; distinction of, from 
hydrophobia, 752 ; from meningitis, 751 ; from 
strychnine poisoning, 751 ; endemic and epidemic, 
749 ; hydrophobic, 750 ; idiopathic, 749 ; influence 
of external conditions on, 749 ; intermittent (see 
Tetany), 747 ; nature of, 751 ; neonatorum, 749 ; par- 
oxysms of, 750 ; prodromal symptoms of, 749 ; 
rheumatic, 749 ; symptoms of, 749 ; traumatic, 749 ; 
treatment of, 752. 

Tetany, 747 ; diagnosis of, 748 ; distinction of, from 
ergotism, 748 ; from professional neuroses, 749 ; 
epidemic, 747 ; origin of, 747 ; symptoms of, 748 ; 
treatment of, 749. 

Thermaesthesiometer, 478. 

Thermic fever, 706 ; pathology of, 706 ; symptoms of, 

707 ; treatment of, 707. 
Thermo-cautery in noma, 324 ; in pressure paralysis 

of the spinal cord, 581. 
Thomsen's disease, 752. See Myotonia. 



INDEX. 



979 



Thoracotomy, 248. 

Thoracic aorta, aneurism of, 311 ; causes of, 311 ; 
diagnosis of, 314 ; prognosis of, 314; symptoms of, 
312 ; treatment of, 315. 

Thorax, barrel-shaped, 163 ; compression of, in pul- 
monary emphysema, 166 ; deformity of, in osteoma- 
lacia, 872 ; in rachitis, 868 ; phthisical, 204 ; in pleu- 
risy, 241 ; rigid dilatation of, 161. 

Thrombi in typhoid fever, 15 ; in valvular disease of 
the heart, 280. 

Thrombosis of the portal vein, 471. 

Thrush, 321. 

Tibialis paralysis, 536. 

Tic convulsif , 539 (see Spasm, Facial) ; douloureux, 
491 (see Trigeminus, Neuralgia of) ; rotatoire, 
541. See Spasm of the Cervical Muscles. 

Tissue metamorphosis, anomalies of, 874 ; in anaemia, 
879 ; in diabetes mellitus, 914. 

Tissue, necrosis of, in gout, 932. 

Toe-drop in peroneal paralysis, 536. 

Tongue, atrophy of, in amyotrophic lateral sclerosis, 
615 ; in progressive bulbar paralysis, 646 ; in pro- 
gressive muscular atrophy, 620. 

Tongue, ulcer on the fraenum of, in whooping-cough, 
148. 

Tongue, injuries to, in epilepsy, 732. 

Tongue, paralysis of, in acute bulbar paralysis, 655 ; 
in bulbar haemorrhage, 653 ; (unilateral) in cerebral 
haemorrhage, 692 ; in compression of the medulla, 
656 ; in embolism and thrombosis of the basilar 
artery, 655. 

Tongue, spasm of, 540. 

Tonics in scurvy, 905. 

Tonsillitis, 328 (see Sore Throat) ; diagnosis of, 332 ; 
follicular, 329 ; necrotic, 331 ; parenchymatous, 
330 ; treatment of, 333. 

Tonsils, abscess of, 330 ; chronic hypertrophy of, 333 ; 
treatment of, 334 ; extirpation of, 334 ; in leukae- 
mia, 892 ; in pseudo-leukaemia, 897. 

Torpid habitus, 943. 

Torticollis, rheumatic, 541 ; spastic, 541. 
Torulaceae in urine, 841. 

Touch, sense of, 476 ; condition of, 586 ; diminished 
in the tongue in facial paralysis, 527 ; in locomotor 
ataxia, 604 ; test of, 476. 

Tracheal catarrh, 133 ; stenosis, 152. 

Tracheitis, 133. 

Tracheotomy in diphtheria, 68 ; in oedema of the 

glottis, 123 ; in perichondritis, 122. 
Traction diverticula in the oesophagus, 341. 
Transfer in hysteria, 766. 

Transudation in diabetes, 919 ; in leukaemia, 894. 

Transverse myelitis, 581. See Myelitis. 

Traube's double sound in aortic insufficiency, 270. 

Tremor, 509 ; alcoholic, 509 ; in amyotrophic lateral 
sclerosis, 614 ; in epilepsy, 734 ; in exophthalmic 
goitre, 561 ; intention, 509 ; mercurial, 948 ; in mul- 
tiple sclerosis. 592 ; in osteomalacia, 872 ; in paraly- 
sis agitans, 742 ; senile, 509 ; in typhoid fever, 13. 

Trephining the skull in cerebral abscess, 703 ; in trau- 
matic epilepsy, 736 ; the vertebral column in in- 
juries to the cord, 572. 

Triceps paralysis, 532. 

Trichina spiralis, 109. 

Trichinosis, 109 ; treatment of, 111. 

Tricocephalus dispar, 420. 

Tricuspid insufficiency, 272. 



Trigeminus, anaesthesia of, 482 ; in locomotor ataxia, 
605 ; neuroparalytic ophthalmia in, 483 ; occlusive 
bandage in, 484 ; skin of the face in, 483. 

Trigeminus, neuralgia of, 491 ; in compression of the 
medulla, 656 ; in diabetes, 917 ; diagnosis of, 492 ; 
epileptiform, 492 ; infra-maxillary, 492 ; infra-orbi- 
tal, 492 ; ligature of the carotid for, 493 ; operative 
treatment of, 493 ; prognosis of, 492 ; supra-orbital, 
491 ; symptoms and course of, 491 ; treatment of, 
492. 

Trigeminus, paralysis of, 525 ; in bulbar haemor- 
rhage, 653 ; in progressive bulbar paralysis, 648. 

Trigeminus, spasm of, 538 ; treatment of, 539. 

Trismus, 538 ; artificial feeding in, 539 ; in cerebro- 
spinal meningitis, 95 ; in tetanus, 750 ; in tubercular 
meningitis, 666. 

Trochlear paralysis, 524. 

Trophic disturbances, 553 ; in arsenical paralysis, 
538 ; of the bones and joints, 555 ; in cerebral 
haemorrhage, 695 ; in cervico-brachial neuralgia, 
494 ; in cutaneous anaesthesia, 482 ; in facial hemi- 
atrophy, 559 ; of the hair and nails, 555 ; in inter- 
costal neuralgia, 494 ; in locomotor ataxia, 608 ; in 
median paralysis, 534 ; in myelitis, 588 ; in neural- 
gia, 487 ; in neuritis, 549 ; in occipital neuralgia, 
493 ; in paralysis, 507 ; in pressure paralysis of the 
spinal cord, 579 ; in progressive muscular atrophy, 
618 ; in pseudo-hypertrophic muscular paralysis, 
623 ; in sciatic paralysis, 537 ; of the skin, 554 ; in 
spinal paralysis of children, 631 ; treatment of, 555 ; 
in trigeminal anaesthesia, 483 ; in trigeminal neu- 
ralgia, 491. 

Trousseau's phenomenon in tetany, 748. 

Trousseau's spots in tubercular meningitis, 666. 

Tubercle bacilli, 192 ; detection of, 203. 

Tubercula dolorosa of the peripheral nerves, 552. 

Tuberculosis, 191. See also Miliary Tuberculosis. 

Tuberculosis of the genito-urinary apparatus, 836; 
diagnosis of, 837 ; prognosis and treatment of, 837. 

Tuberculosis of the intestines, 395 ; treatment of, 396. 

Tuberculosis of the larynx, 123 ; diagnosis of, 124 ; 
treatment of, 125. 

Tuberculosis of the lungs, 191 ; causes of, 193 ; com- 
plications of, 201 ; diagnosis of, 212 ; heredity of, 
195 ; infectiousness of, 193 ; local, 196 ; physical ex- 
amination in, 204 ; predisposition to, 194 ; prognosis 
of, 213 ; prophylaxis of, 213 ; symptoms of, 201 ; 
treatment of, 213. 

Tuberculosis of the peritoneum, 429 ; of the pharynx, 
210 ; of the serous membranes, 244, 304, 429 ; of the 
supra-renal capsules, 826. 

Turpentine, inhalations of, in asthma, 158 ; in whoop- 
ing-cough, 150. 

Turpentine, oil of, in acute phosphorus poisoning, 
948 ; in cystitis, 843 ; in foetid bronchitis, 145 ; in 
sciatica, 497 ; in tape-worm, 416. 

Turpentine pipes in bronchitis, 141. 

Tussis convulsiva, 147. See Whooping-cough. 

Tylosis of the tongue, 323. 

Typhlitis, 391 ; diagnosis of, 393 ; prognosis of, 393 ; 
treatment of, 394. 

Typhoid, bilious, 34. See also Relapsing Fever. 

Typhoid fever, 1 ; abortive, 17 ; bacilli of, 1 ; baths 
in, 20 ; in children, 17 ; contagiousness of, 2 ; in 
the corpulent, 17 ; diagnosis of, 18 ; disinfection 
in. 25 ; disposition to, 4 ; in drunkards, 17 ; immu- 
nity toward, 4 ; influence of age upon, 4 ; influence 



980 



INDEX. 



of season upon, 4 ; in old people, 17 ; outcry of 
children in, 17 ; peculiarities in the course of, 17 ; 
period of incubation of, 4 ; prodromal symptoms 
of, 4 ; prognosis of, 18 ; prophylaxis of, 24 ; recur- 
rent fever-attack in, 8 ; relapses of, 17 ; relapses of, 
duration of, 18 ; relapses of, frequency of, 18 ; sopor 
in children in, 17 ; temperature curve in, 5 ; treat- 
ment of, 19 ; walking, 17. 
Typho-malarial fever, 88. 

Typhus abdominalis, 1 (see Typhoid Fever) ; levissi- 
mus, 17. 

Typhus exanthematicus, 27 (see Typhus Fever) ; le- 
vissimus, 29. 

Typhus fever, 27 ; contagiousness of, 27 ; diagnosis 
of, 29 ; distinction of, from typhoid fever, 29 ; epi- 
demic occurrence of, 27 ; immunity toward, 27 ; 
period of incubation of, 28 ; prodromal symptoms 
of, 28 ; prognosis of, 29 ; treatment of, 30. 

Typhus recurrens, 30. See Relapsing Fever. 

Tyrosine crystals in acute yellow atrophy of the liver, 
458. 

Ulcers, atheromatous, 309 ; in laryngeal syphilis, 

132 ; in laryngeal tuberculosis, 124 ; tubercular, 

197 ; typhoid, 8. 
Ulnar paralysis, 533 ; disturbance of function in, 533 ; 

traumatic, 533. 
Umbilical haemorrhage in relation to haemophilia, 

908. 

Umbilical vein, inflammation of, in the new-born, 470. 
Unilateral lesion of the spinal cord, 643. 
Upper extremities, thickening and deformity of, in 
rachitis, 869. 

Uraemia, 778 ; chronic, 780 ; in contracted kidney, 
809 ; duration of, 782 ; in gout, 932 ; origin of, 779 ; 
in scarlet fever, 40 ; termination of, 782 ; in yellow 
fever, 92. 

Urates in gout, 932. 

Urea, deposit of, on the skin in uraemia, 781 ; in dia- 
betes insipidus, 927 ; in diabetes mellitus, 913. 

Ureter, obstruction of, in relation to hydronephrosis, 
838. 

Ureteritis, 829. 

Urethan in neurasthenia, 770. 

Urethra, stricture of, in hydronephrosis, 838. 

Urethral crises in locomotor ataxia, 608. 

Uric acid in diabetes, 913 ; in gout, 932 ; in relation 
to contracted kidney, 806. 

Urinary casts in renal disease, 775. 

Urinary passages, parasites of, 822. 

Urinary tests, Bottger's, 913 ; with chloroform, 438 ; 
in diabetes mellitus, 912 ; Fehling's, 913 ; with fer- 
ric chloride, for acetone, 914 ; Gmelin's, 438 ; heat, 
773 ; Moore's, 913 ; with thread in gout, 934 ; Trom- 
mels, 912. 

Urine, in acute yellow atrophy of the liver, 457 ; 
amount of, in diabetes insipidus, 926 ; amount of, 
in diabetes mellitus, 912 ; in amyloid kidney, 814 ; 
in anaemia, 880 ; in cancer of the stomach, 367 ; in 
cerebral haemorrhage, 690 ; in chlorosis, 881 ; in 
chorea, 740 ; in chyluria, 823 ; in cirrhosis of the 
liver, 451 ; in contracted kidney, 806 ; in cystitis, 
841 ; in diabetes insipidus, 926 ; in diabetes mellitus, 
912 ; in diphtheria, 66 ; in epilepsy, 732 ; in erysipe- 
las, 60 ; in functional diseases of the spinal cord, 
571 ; in gastric catarrh, 354 ; in genito-urinary tu- 
berculosis, 837 ; in gout, 930 ; in haemoglobinaemia, 



899 ; in hydronephrosis, 839 ; in injuries of the spinal 
cord, 572 ; in jaundice, 438 ; in leukaemia, 894 ; in 
locomotor ataxia, 607 ; in malaria, 84 ; in meningeal 
haemorrhage, 568 ; in meningitis, 662, 666 ; in myeli- 
tis, 587 ; in nephritis, 789, 800 ; in osteomalacia, 872 ; 
in passive congestion of the kidney, 819 ; in perni- 
cious anaemia, 888 ; in pneumonia, 182 ; in pressure 
paralysis of the spinal cord, 579 ; in pseudo-leukae- 
mia, 897 ; in pyelitis, 830 ; in pylephlebitis, 471 ; in 
rachitis, 869 ; in renal diseases, 772 ; in renal tumors, 
821 ; in scarlet fever, 39 ; in small-pox, 53 ; in spinal 
concussion, 573 ; in spinal meningitis, 565 ; in spinal 
paralysis of children, 631 ; in tetanus, 751 ; in ty- 
phoid fever, 16 ; in typhus fever, 28 ; in ulcer of the 
stomach, 361 ; in unilateral lesion of the spinal 
cord, 645 ; in whooping-cough, 148 ; in yellow fever, 
92. 

Urticaria in articular rheumatism, 851 ; in erysipelas, 
60 ; in exophthalmic goitre, 562 ; in haemoglobinae- 
mia, 899 ; in jaundice, 437 ; in neuralgia, 487 ; in 
pneumonia, 183 ; in scarlet fever, 38. 

Uterine neuralgia, 497. 

Uva ursa in nephritis, 794. 

Vaccination, 54. 

Vagus paralysis in relation to tachycardia, 298. 

Valerian in diabetes insipidus, 928 ; in epilepsy, 737 ; 
in hysteria, 765. 

Valvular disease of the heart, 261. 

VariceUa, 57 ; period of incubation of, 57 ; prognosis 
of, 57 ; treatment of, 57. 

Variola, 49 (see Small-pox) ; haemorrhagica pustulo- 
sa, 54 ; vaccina, 55 ; vera, 50. 

Varioloid, 51. See Small-pox. 

Variolois miliaris, 51 ; verrucosa, 51. 

Vaso-motor disturbances, 553 ; in bulbar haemor- 
rhage, 653 ; in cerebral haemorrhage, 695 ; in cere- 
bral hyperaemia, 671 ; in cervico-brachial neuralgia, 
494 ; in epilepsy, 731 ; in exophthalmic goitre, 562 ; 
in hemicrania, 557 ; in hysteria, 761 ; in intercostal 
neuralgia, 494 ; in myelitis, 588 ; in neuralgia, 487 ; 
in neuritis, 549 ; in occipital neuralgia, 493 ; in pa- 
ralysis, 508 ; in progressive bulbar paralysis, 648 ; 
in progressive muscular atrophy, 620 ; in sciatic 
paralysis, 537 ; in spinal neurasthenia, 571 ; symp- 
toms of, 553 ; in trigeminal neuralgia, 491. 

Vaso-motor paralysis, 553 ; redness of the skin with 
heightened temperature in, 553 ; in unilateral lesion 
of the spinal cord, 645. 

Vaso-motor spasm, 554 ; relation of, to spontaneous 
symmetrical gangrene, 554 ; relation of, to sclero- 
derma, 554 ; symptoms of, 554. 

Veal, diseased, as a cause of typhoid fever, 3. 

Vegetable acids in scurvy, 905. 

Veins, diastolic collapse of, in obliteration of the peri- 
cardial cavity, 303. 
Venesection. See Blood-letting. 
Venous murmurs, anaemic, 879, 880; in leukaemia, 894. 
Venous pulse, 272. 
Venous stasis, 279. 
Veratrine in pneumonia, 189. 

Vermiform process in relation to intestinal obstruc- 
tion, 405. 

Vertebral column in arthritis deformans, 861 ; in 
cerebro-spinal meningitis, 95 ; in osteomalacia, 872; 
in rachitis, 869. 
j Vertigo in anaemia, 878 ; in bulbar haemorrhage, 652 ; 



INDEX. 



981 



in cerebellar disease, 684 ; in cerebellar tumor, 
713 ; in cerebral abscess, 702 ; in cerebral haemor- 
rhage, 688 ; in cerebral tumor, 710 ; in chlorosis, 
880 ; in compression of the medulla, 656 ; in epilep- 
sy, 732 ; in insolation, 706 ; in leukaemia, 894 ; in 
Meniere's disease, 728 ; in multiple sclerosis, 594 ; 
in neurasthenia, 768 ; in oculo-motor paralysis, 523 ; 
in pernicious anaemia, 887 ; in purulent meningitis, 
661 : in spinal concussion, 573. 

"Vertigo ab aure laesa, 728 ; a stomacho laeso, 354. 

Vesical. See Bladdeh. 

Vesicatory. See Blister. 

Villous cancer in the bladder, 844. 

Violin-players' cramp, 546. 

Vocal cords, paralysis of, in diphtheria, 66 ; in hyste- 
ria, 759 ; in mediastinal tumor, 256 ; in pericarditis, 
302.' 

Vocal fremitus in pleurisy, 243, 245 ; in pneumonia, 
180 ; in pneumothorax, 252. 

Volume, increased, of the lungs, 161. 

Vomiting in acute yellow atrophy of the liver, 456 ; 
in Addison's disease, 828 ; in anaemia, 878 ; in can- 
cer of the stomach, 365 ; in cerebellar disease, 684 ; 
in cerebral abscess, 702 ; in cerebral anaemia, 670 ; 
in cerebral haemorrhage, 690 ; in cerebral tumor, 
710 ; in cholera, 76 ; in cholera morbus, 385 ; in 
compression of the medulla, 656 ; in dilatation of 
the stomach, 370 ; in dysentery, 71 ; in erysipelas, 
60 ; in exophthalmic goitre, 562 ; in gastric catarrh, 
352 ; in haematoma of the dura, 658 ; in haemoglo- 
binaemia, 899 ; in hemicrania, 558 ; in hepatic colic, 
442 ; in hepatitis, 447 ; in intestinal obstruction, 
407 ; in Meniere's disease, 728 ; in meningitis, 94, 
662, 666 ; in miliary tuberculosis, 222 ; morning, of 
drunkards, 353 ; in nephritis, 791, 802 ; in nephro- 
lithiasis, 834 ; in nervous affections of the stomach, 
375 ; in peritonitis, 425, 426 ; in pleurisy, 240 ; in 
pneumonia, 182 ; in phthisis, 210 ; in pulmonary 
gangrene, 226 ; in pylephlebitis, 471 ; in scarlet 
fever, 35 ; in small-pox, 49 ; in tape-worm, 415 ; in 
thermic fever, 707 ; in typhlitis, 392 ; in typhoid 
fever, 10, 11 ; in typhus fever, 28 ; in ulcer of the 
stomach, 360 ; in uraemia, 781 ; in whooping-cough, 
148 ; in yellow fever, 92. 

Voracity in tape-worm, 414. 



Vox choleraica, 76. 

Warmth, feeling of, increased in paralysis agitans, 
744. 

Water cancer, 323. 

Water cushions in myelitis, 591. 

Water-pipe sound in open pneumothorax, 253. 

Waxy kidney, 812. See Amyloid. 

Weakened heart, 291. 

Weeping spasms, 544 ; in hysteria, 758. 

Wet-nurse, milk of, 389. 

Whip-worm, 420. 

Whooping-cough, 147 ; catarrhal stage in, 147 ; con- 
tagiousness of, 147 ; convulsive stage in, 147 ; diag- 
nosis of, 149 ; prognosis of, 149 ; sequelae of, 149 ; 
treatment of, 149. 

Williams's tracheal tone in pleuritic effusion, 242. 
[ Wine in cholera morbus, 386 ; in typhoid fever, 20. 

Word-deafness, 679 ; in abscesses of the temporal 
lobes, 703. 

Worm abscess, 418. 

Worms, intestinal, 411. 

Writers' cramp, 544 ; diagnosis of, 545 ; Nussbaum's 
bracelet for, 545 ; origin of, 544 ; paralytic, 545 ; 
prognosis of, 545 ; spastic, 544 ; symptoms of, 544 ; 
treatment of, 545 ; tremulous, 545. 

Xanthelasma in jaundice, 437. 
Xanthine calculi in nephrolithiasis, 832. 

Yawning in paroxysmal haemoglobinaemia, 899. 
Yawning spasm, 544. 

Yellow fever, 90 ; black vomit in, 92 ; causes of, 90 ; 
contagiousness of, 91 ; diagnosis of, 92 ; epidemic 
character of, 90 ; pathology of, 91 ; prognosis of, 
92 ; symptoms and cause of, 91 ; treatment of, 92. 

Zinc, oxide of, in chorea, 742 ; in epilepsy, 737 ; in 

facial spasm, 540. 
Zinc paralysis, 538. 

Zinc, sulphate of, in angina pectoris, 296 ; in gastric 
catarrh, 357. 

Zinc, valerianate of, in chorea, 742 ; in hiccough, 544 ; 
j in spasm of the cervical muscles, 542 ; in trigeminal 
J spasm, 539. 



THE END. 



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On the Antagonism between Medicines and between 

REMEDIES AND DISEASES. Being the Cartwright Lectures for the 
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TEXT-BOOK OF OPHTHALMOSCOPY. 



By EDWARD G. LORING, M. D. 

PART I. 

The Normal Eye, Determination of Refraction, Diseases of 
the Media, Physiological Optics, and Theory of 
the Ophthalmoscope. 

8vo, 267 pages, with 131 Illustrations, and Four Chromo-Lithograph Plates, 

CONTAINING FOURTEEN FIGURES. PRICE, CLOTH, $5.00. 



CONTENTS: 

I. Remarks on the Ophthalmoscope. — Examination hy Daylight. — Examina- 
tion of the Eye by Artificial Light. II. Examination with the Ophthalmoscope. 
— Method of Examination. — Examination by the Inverted Image. — Examination 
by the Upright Image. III. The Anatomy of the Fundus of the Normal Eye. 
IV. The Fundus of the Normal Eye as seen with the Ophthalmoscope. — Anom- 
alies. Y. Determination of the Optical Condition of the Eye with the Ophthal- 
moscope. — Refraction. — Astigmatism. — Refraction, according to the Standard 
of the Inch. — Directions in case the Observer is Ametropic. — Determination of 
the Refraction of the Eye by the Mirror alone, and by means of the Inverted 
Image. — Astigmatism with the Mirror alone. — Astigmatism with the Inverted 
Image. — Amount of Enlargement produced by Upright Image. VI. Examina- 
tion of the Media of the Eye. — Oblique Illumination. — The Aqueous Humor. — 
The Iris. — The Lens. — Opacities of the Lens. — Examination of the Media by the 
Ophthalmoscope. — The Iris. — The Lens. — Vitreous Humor, and Fundus of the 
Eye. — Differential Diagnosis of Troubles in the Media. — Entozoa. 

Appendix. — General Principles of the Ophthalmoscope. — Physiological Op- 
tics. — Theory of the Ophthalmoscope. — The Metric System. — Ophthalmoscopes. 
— Adjuncts to the Ophthalmoscope. 

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easy. Avoiding the Scylla of too much technicality, he has not plunged into 
the Oharybdis of too little. He will be doing a proper thing who adds this book 
to his working library." — American Lancet. 



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